| 90376424 | as only weakly stimulated by phorbol ester or TNF-alpha, multimers of the PRDII | NF-kappa B | -binding domain were inducible by both agents. TNF-alpha was able to increase ex |
| 90376424 | id not induce the HIV LTR above a constitutive level of activity. This level of | NF-kappa B | -independent activity appears to be sufficient for virus multiplication, since T |
| 91321794 | nvestigated the effects of cysteine and related thiols on HIV-1 replication and | NF-kappa B | expression. The experiments in this report show that cysteine or N-acetylcystei |
| 91321794 | and chloramphenicol acetyl-transferase ( CAT ) gene expression under control of | NF-kappa B | binding sites in uninfected cells. This suggests that the cysteine deficiency i |
| 91321794 | steine deficiency in HIV-1-infected individuals may cause an over-expression of | NF-kappa B | -dependent genes and enhance HIV-1 replication. NAC may be considered for the tr |
| 92052106 | deficiency virus type 1 expression in monocytes: role of the 65-kDa plus 50-kDa | NF-kappa B | dimer. Although monocytic cells can provide a reservoir for viral production in |
| 92052106 | arkedly less viral RNA production. This absence of binding was localized to the | NF-kappa B | region of the HIV-1 enhancer; the 65-kDa plus 50-kDa NF-kappa B heterodimer was |
| 92052106 | ocalized to the NF-kappa B region of the HIV-1 enhancer; the 65-kDa plus 50-kDa | NF-kappa B | heterodimer was preferentially lost. Adding purified NF-kappa B protein to nucl |
| 92052106 | ride increased viral production and NF-kappa B activity. Antiserum specific for | NF-kappa B | binding proteins, but not c-rel-specific antiserum, disrupted heterodimer compl |
| 92052106 | t c-rel-specific antiserum, disrupted heterodimer complex formation. Thus, both | NF-kappa B | -binding complexes are needed for optimal viral transcription. Binding of the 65 |
| 92135145 | F-kappa B ( consisting of subunits p50 an dp65 ) and the DNA-binding subunit of | NF-kappa B | ( p50 ) by itself, also called KBF1, are constitutively expressed and localized |
| 92135145 | ids between IARC 301.5 and a murine myeloma. Most hybrids express both KBF1 and | NF-kappa B | in their nuclei, but one hybrid expresses only KBF1. The kappa B enhancer of th |
| 92135145 | nal only in the hybrids expressing nuclear NF-kappa B. These findings show that | nuclear NF-kappa B | is necessary to activate the kappa B enhancer, while KBF1 by itself is not suff |
| 92135145 | by itself is not sufficient. We propose that KBF1 is a competitive inhibitor of | NF-kappa B | and discuss how these factors may be involved in the transient expression of IL |
| 93024468 | e-specific transcription factor binding to the simian virus 40 enhancer TC-II ( | NF-kappa B | ) element. We have biochemically and functionally characterized a new transcrip |
| 93024468 | matopoietic cells. This factor has a DNA-binding specificity similar to that of | NF-kappa B | but is unrelated to this or other Rel proteins by functional and biochemical cr |
| 94107268 | or by a phorbol ester to induce interleukin 2 production. Pervanadate activated | NF-kappa B | , as shown by an increase in DNA-binding activity of this transcription factor. |
| 94254835 | posure of monocytic cells to bacterial lipopolysaccharide ( LPS ) activates the | NF-kappa B | / Rel family of proteins and leads to the rapid induction of inflammatory gene |
| 94254835 | 5 dimers but instead comigrated with c-Rel / p65 dimers. Antibodies against the | NF-kappa B | and Rel proteins and UV cross-linking studies revealed the presence of c-Rel an |
| 95000924 | cated LTRs confirmed that inhibition of LTR activation was not mediated through | NF-kappa B | -binding activity but through the region containing the negative responding elem |
| 95202809 | Aspirin inhibits | nuclear factor-kappa B | mobilization and monocyte adhesion in stimulated human endothelial cells. BACKG |
| 95202809 | s mediated by mobilization of the transcription factor nuclear factor-kappa B ( | NF-kappa B | ) . Since salicylates have been reported to inhibit NF-kappa B activation by pr |
| 95202809 | SULTS: Gel-shift analyses demonstrated dose-dependent inhibition of TNF-induced | NF-kappa B | mobilization by aspirin at concentrations ranging from 1 to 10 mmol / L. Induct |
| 95202809 | domethacin was ineffective. CONCLUSIONS: Our data suggest that aspirin inhibits | NF-kappa B | mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhes |
| 95332324 | iption factor, to activation of a reporter gene driven by a promoter containing | NF-kappa B | sites, and to increased levels of mRNAs for immediate-early genes, including th |
| 95399771 | ssion in endothelial cells, even though the E-selectin promoter is activated by | NF-kappa B | rather than NFAT. Hence, induction of cell surface expression of this leukocyte |
| 96074632 | D3 [1,25 ( OH ) 2 ) D3], a steroid hormone with immunomodulating properties, on | nuclear factor kappa B | ( NF-kappa B ) proteins was examined in in vitro activated normal human lymphoc |
| 96074632 | a steroid hormone with immunomodulating properties, on nuclear factor kappa B ( | NF-kappa B | ) proteins was examined in in vitro activated normal human lymphocytes by Weste |
| 96074632 | blot analysis. Over a 72-hr period of activation, the expression of the 50-kDa | NF-kappa B | , p50, and its precursor, p105, was increased progressively. When cells were act |
| 96074632 | transiently transfected with a construct containing four tandem repeats of the | NF-kappa B | binding sequence of the immunoglobulin kappa light chain gene linked to the chl |
| 96074632 | ene. These observations demonstrate directly that there is de novo synthesis of | NF-kappa B | during human lymphocyte activation and suggest that this process is hormonally |
| 96075792 | e cells as determined by electrophoretic mobility shift assay using a consensus | NF-kappa B | oligonucleotide. An additional significant finding was than TNF mRNA induced in |
| 96211859 | that were composed of c-Fos / c-Jun AP-1. The resting and stimulated levels of | NF kappa B | were reduced in T cells from certain elderly individuals; however, alterations |
| 96211859 | re reduced in T cells from certain elderly individuals; however, alterations of | NF kappa B | did not correlate with changes in IL-2 expression. Thus, these results show tha |
| 96279111 | nd inducible expression of the IL-9 gene in C5MJ2 cells. Within this region, an | NF-kappa B | site at -59 to -50 and its adjacent 20-base pair upstream sequence were demonst |
| 96279111 | role for the IL-9 promoter activity. DNA-protein binding studies indicated that | NF-kappa B | , c-Jun, and potentially novel proteins ( around 35 kDa ) can bind to this impor |
| 96303658 | ene transcription and translation in leukocytes. Transcription factors, such as | NF kappa B | and AP-1, are activated upon stimulation of the cells with several chemoattract |
| 97054651 | terminal repeat ( HIV-1 LTR ) , a promoter largely dependent on the binding of | nuclear factor kappa B | ( NF- kappa B ) . In contrast, the cAMP-dependent protein kinase specific inhib |
| 97054651 | LTR ) , a promoter largely dependent on the binding of nuclear factor kappa B ( | NF- kappa B | ) . In contrast, the cAMP-dependent protein kinase specific inhibitor H-89 tota |
| 97054651 | on. Electrophoretic mobility shift assay ( EMSA ) and supershift assay using an | NF-kappa B | binding sequence from the kappa light chain as a probe, revealed that both p65 |
| 97054651 | were present in CD40-stimulated B cells. While PKC depletion did not alter the | NF-kappa B | level, treatment of B lymphocytes with H-89 or herbimycin A provoked a decrease |
| 97054651 | treatment of B lymphocytes with H-89 or herbimycin A provoked a decrease in the | NF-kappa B | level. These observations establish the importance of different signal transduc |
| 97162234 | Nuclear factor-kappa B | activation in human monocytes stimulated with lipopolysaccharide is inhibited b | |
| 97162234 | accharide is inhibited by fibroblast conditioned medium and exogenous PGE2. The | nuclear factor kappa B | ( NF-kappa B ) is thought to be crucially involved in the gene activation of se |
| 97162234 | fibroblast conditioned medium and exogenous PGE2. The nuclear factor kappa B ( | NF-kappa B | ) is thought to be crucially involved in the gene activation of several cytokin |
| 97162234 | -kappa B activation in PBM. Furthermore, we show that exogenous PGE2 mimics the | NF-kappa B | inhibitory effect of FCM. On the other hand, FCM produced in the presence of in |
| 97211823 | c-Rel protein complexes are differentially distributed within human thymocytes. | Nuclear factor-kappa B | ( NF-kappa B ) /Rel proteins are inducible transcriptional regulators of numero |
| 97211823 | re differentially distributed within human thymocytes. Nuclear factor-kappa B ( | NF-kappa B | ) /Rel proteins are inducible transcriptional regulators of numerous cellular g |
| 97211823 | rescent staining of thymus sections using specific Abs allowed visualization of | nuclear NF-kappa B | proteins in both thymocytes and nonthymocyte cells. This detection suggested a |
| 97211823 | d c-Rel complexes play distinct roles in gene expression and that both forms of | NF-kappa B | play critical roles during late stages of the intrathymic maturation of T cells |
| 97307577 | verexpression of Ikappa B alpha. A role in thymic maturation for factors of the | NF-kappa B | family has long been suspected, but not yet proven. Transgenic mice with a lymp |
| 97307577 | re severely affected. These data provide direct evidence for the involvement of | NF-kappa B | / Rel family proteins in late stages of T lymphocyte development, coincident wi |
| 97376857 | up-regulating the activity of several transcription factors, including AP-1 and | nuclear factor-kappa B | ( NF-kappa B ) /Rel family members as well as an uncharacterized transcription |
| 97376857 | y of several transcription factors, including AP-1 and nuclear factor-kappa B ( | NF-kappa B | ) /Rel family members as well as an uncharacterized transcription factor called |
| 97376857 | CD28 response complex. While several lines of investigation have suggested that | NF-kappa B | / Rel family members make up the CD28 response complex transcription factor, ot |
| 97376857 | se complexes is specific for both the CD28RE and the adjacent AP-1 site. Of the | NF-kappa B | / Rel family members tested, this CD28RE / AP-1-specific complex contains predo |
| 98001571 | ption factor in the regulation of gene expression in the inflammatory response, | NF-kappa B | inhibitors have been suggested as potential therapeutic drugs for inflammatory |
| 98001571 | experiments at the IL-2 promoter level, and involved not only the inhibition of | NF-kappa B | -driven reporter activation but also that of nuclear factor of activated T cells |
| 98001571 | bility shift assays ( EMSAs ) indicated that pyrrolidine DTC ( PDTC ) prevented | NF-kappa B | , and NFAT DNA-binding activity in T cells stimulated with either phorbol myrist |
| 98012705 | Dysregulation of monocytic | nuclear factor-kappa B | by oxidized low-density lipoprotein. Nuclear factor-kappa B ( NF-kappa B ) /Rel |
| 98012705 | lation of monocytic nuclear factor-kappa B by oxidized low-density lipoprotein. | Nuclear factor-kappa B | ( NF-kappa B ) /Rel transcription factors may be involved in atherosclerosis, a |
| 98012705 | ar factor-kappa B by oxidized low-density lipoprotein. Nuclear factor-kappa B ( | NF-kappa B | ) /Rel transcription factors may be involved in atherosclerosis, as is suggeste |
| 98012705 | ay be involved in atherosclerosis, as is suggested by the presence of activated | NF-kappa B | in human atherosclerotic lesions. The aim of the present study was to investiga |
| 98012705 | e present study was to investigate the effects of oxidized LDL ( oxLDL ) on the | NF-kappa B | system in human THP-1 monocytic cells as well as adherent monocytes. Our result |
| 98012705 | short-term incubation of these cells with oxLDL activated p50 / p65 containing | NF-kappa B | dimers and induced the expression of the target gene IL-8. This activation of N |
| 98012705 | is a potent modulator of gene expression and suggest that ( dys ) regulation of | NF-kappa B | / Rel is likely to play an important role in atherogenesis. |
| 98090689 | Constitutive expression c-fos, c-jun, and | NF kappa B | mRNA is in nucleated fetal blood cells and up-regulation of c-fos and c-jun wit |
| 98090689 | three transcription factors implicated in T-cell activation: c-jun, c-fos, and | NF kappa B | ( p50 subunit ) . We demonstrate that mRNAs for all three of these regulatory f |
| 98104459 | NF-kappa B | / Rel family members regulating the ICAM-1 promoter in monocytic THP-1 cells. A | |
| 98104462 | 3' cytosins are required in the DNA binding motif for detection of upregulated | NF-kappa B | p50 homodimers. When monocytes are stimulated with LPS ( lipopolysaccharide ) r |
| 98104462 | lls still express the CD14 receptor and they can still be activated to mobilize | NF-kappa B | into nucleus. Analysis of the binding proteins employing the -605 motif of the |
| 99118181 | and in vivo: role of 26S proteasome. It is becoming increasingly apparent that | NF-kappa B | plays a critical role in regulating the inflammatory response. Data obtained fr |
| 99118181 | e inhibitors should prove useful in delineating the roles of the proteasome and | NF-kappa B | in other pathophysiological conditions such as cancer and heart disease. |
| 99172186 | ts primary human T cell responses at the dendritic cell level: association with | NF-kappa B | inhibition. N-acetyl-L-cysteine ( NAC ) is an antioxidant molecule endowed with |
| 99201482 | volved and, in a broader sense, in pathological situations in which genes under | nuclear factor-kappa B | control are up-regulated. |
| 99207658 | o interact with transcriptional factors such as AP-1 ( activator protein-1 ) of | NF-kappa B | ( nuclear factor-kappa B ) . Through these actions glucocorticosteroids are sus |
| 99207658 | th transcriptional factors such as AP-1 ( activator protein-1 ) of NF-kappa B ( | nuclear factor-kappa B | ) . Through these actions glucocorticosteroids are susceptible to modify functi |
| 99228708 | transduction in human monocytes leads to activation of nuclear factor-kappa B ( | NF-kappa B | ) and TNF-alpha release. Previous studies have implicated activation of both pr |
| 99356019 | pecific mRNA were inhibited by antioxidants. These data suggest a ROI-dependent | NF-kappa B | mediated transcription of inflammatory cytokines in bronchial epithelial cells. |
| 99386936 | proteins IKK-alpha, IKK-beta, NF-kappa B-inducing kinase ( NIK ) , IKK-gamma ( | NF-kappa B | essential modulator ) , and IKK complex-associated protein. Kinase assays showe |
| 99386936 | K complex-associated protein inhibited stimulus-mediated transcription, whereas | NF-kappa B | essential modulator enhanced it. The understanding of LPS- and TNF-induced sign |
| 93204975 | by the alpha globin regulatory element ( HS-40 ) : functional role of specific | nuclear factor | -DNA complexes. We studied the functional interaction between human embryonic ze |
| 93204975 | l core of HS-40, as mapped by transient expression analysis, appeared to bind a | nuclear factor | ( s ) in living K562 cells but not in nonerythroid cells. On the other hand, on |
| 93204975 | ts from adult human bone marrow exhibited a similar but nonidentical pattern of | nuclear factor | binding in vivo at the HS-40 region. These data suggest that transcriptional ac |
| 93204975 | n genes is mediated by erythroid cell-specific and developmental stage-specific | nuclear factor | -DNA complexes which form at the enhancer ( HS-40 ) and the globin promoters. |
| 95399771 | in endothelial cells by cyclosporin A and the T-cell transcription factor NFAT. | Nuclear factor | of activated T cells ( NFAT ) was originally described as a T-cell-specific tra |
| 96184791 | IL-4 P element sites specifically bound the transcriptional activator protein, | nuclear factor | -activated T cells, preformed ( NF-ATp ) , when incubated with nuclear protein e |
| 96211859 | anscriptional factors AP-1 and NF-AT. Although transcriptional factors AP-1 and | nuclear factor | of activated T cells ( NF-AT ) are important for the normal induction of IL-2, |
| 97263762 | ablation / supershift assays revealed that it is similar to a recently reported | nuclear factor | designated SAF. These results demonstrated that LPS-mediated SAA gene induction |
| 97456880 | optimal transcription of the mouse IL-4 gene: involvement of a distinct set of | nuclear factor | of activated T cells and activator protein-1 family proteins. We previously ide |
| 97456880 | body supershift assays in EMSA, complexes formed with P or P2 proved to contain | nuclear factor | of activated T cells ( NFAT ) family proteins as major components. Activator pr |
| 97458245 | ing member of the tumor necrosis factor receptor superfamily. Activation of the | nuclear factor | of activated T cells transcription factor ( NF-AT ) is a key event underlying l |
| 97468093 | moters, defined Interferon Stimulated Response Element ( ISRE ) , which binds a | nuclear factor | ( s ) translocated from the cytoplasm to the nucleus ( ISGF3 ) after the bindin |
| 98001571 | -cell activation by dithiocarbamates involves novel mechanisms of inhibition of | nuclear factor | of activated T cells. Dithiocarbamates ( DTCs ) have recently been reported as |
| 98001571 | t only the inhibition of NF-kappa B-driven reporter activation but also that of | nuclear factor | of activated T cells ( NFAT ) . Accordingly, electrophoretic mobility shift ass |
| 98230439 | irus type 1 long terminal repeat quasispecies differ in basal transcription and | nuclear factor | recruitment in human glial cells and lymphocytes. The generation of genomic div |
| 90376424 | atory elements of human immunodeficiency virus and beta interferon promoters by | tumor necrosis factor | . Three aspects of the involvement of tumor necrosis factor in human immunodefic |
| 90376424 | erferon promoters by tumor necrosis factor. Three aspects of the involvement of | tumor necrosis factor | in human immunodeficiency virus ( HIV ) pathogenesis were examined. Tumor necro |
| 95202809 | adhesion molecule-1 ( VCAM-1 ) and E-selectin by tumor necrosis factor-alpha ( | TNF | ) is mediated by mobilization of the transcription factor nuclear factor-kappa |
| 95202809 | THODS AND RESULTS: Gel-shift analyses demonstrated dose-dependent inhibition of | TNF | -induced NF-kappa B mobilization by aspirin at concentrations ranging from 1 to |
| 95202809 | from 1 to 10 mmol / L. Induction of VCAM-1 and E-selectin surface expression by | TNF | was dose-dependently reduced by aspirin over the same range, while induction of |
| 95202809 | transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by | TNF | . As a functional consequence, adhesion of U937 monocytes to TNF-stimulated HUVE |
| 95202809 | VCAM-1 mRNA by TNF. As a functional consequence, adhesion of U937 monocytes to | TNF | -stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 |
| 95202809 | E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by | TNF | , thereby providing an additional mechanism for therapeutic effects of aspirin. |
| 95399771 | ce, induction of cell surface expression of this leukocyte adhesion molecule by | tumor necrosis factor | ( TNF ) -alpha was reduced by 40% in the presence of CsA, and this was reflecte |
| 95399771 | rface expression of this leukocyte adhesion molecule by tumor necrosis factor ( | TNF | ) -alpha was reduced by 40% in the presence of CsA, and this was reflected by a |
| 96075792 | IFN-gamma priming of monocytes enhances LPS-induced | TNF | production by augmenting both transcription and MRNA stability. The induction o |
| 96075792 | . However, the mechanism ( s ) by which priming occurs is poorly defined. Using | tumour necrosis factor | ( TNF ) induction as a model, experiments were designed to analyse in detail th |
| 96075792 | ( s ) by which priming occurs is poorly defined. Using tumour necrosis factor ( | TNF | ) induction as a model, experiments were designed to analyse in detail the prim |
| 96075792 | human monocytes. Priming by IFN-gamma was primarily manifested at the level of | TNF | mRNA accumulation. IFN-gamma pre-treatment affected the magnitude rather than t |
| 96075792 | uced by either IFN-gamma or GM-CSF, but not M-CSF. Primed monocytes transcribed | TNF | mRNA at a higher rate than freshly isolated monocytes upon activation with LPS. |
| 96075792 | onsensus NF-kappa B oligonucleotide. An additional significant finding was than | TNF | mRNA induced in primed cells was much more stable than in unprimed cells ( T1 / |
| 96075792 | itivity to the kinase inhibitor H-89. H-89 substantially suppressed LPS-induced | TNF | mRNA accumulation in unprimed cells, but had no effect on primed monocytes foll |
| 97162234 | e gene activation of several cytokines, including tumor necrosis factor alpha ( | TNF | ) . Previously, we showed that fibroblast conditioned medium ( FCM ) is able to |
| 97162234 | y, we showed that fibroblast conditioned medium ( FCM ) is able to inhibit both | TNF | mRNA accumulation and protein release in peripheral blood-derived human monocyt |
| 97458245 | NF-AT activation induced by a CAML-interacting member of the | tumor necrosis factor | receptor superfamily. Activation of the nuclear factor of activated T cells tra |
| 97458245 | ducer of NF-AT activation when overexpressed in Jurkat T cells. A member of the | tumor necrosis factor | receptor superfamily was isolated by virtue of its affinity for CAML. Cross-lin |
| 98104462 | LPS ( lipopolysaccharide ) repeatedly then the initially high expression of the | TNF | ( tumor necrosis factor ) gene is only very low, i.e. the cells are tolerant to |
| 98104462 | lipopolysaccharide ) repeatedly then the initially high expression of the TNF ( | tumor necrosis factor | ) gene is only very low, i.e. the cells are tolerant to LPS. Tolerant cells sti |
| 98104462 | nucleus. Analysis of the binding proteins employing the -605 motif of the human | TNF | promoter () revealed that in tolerant cells of the human monocytic cell line Mo |
| 98104462 | urine P388D1 macrophage cell line when tested with the -516 motif of the murine | TNF | promoter () . Here the wild type motif gives efficient binding of p50p50 that a |
| 99305241 | GM-CSF and FMLP, and Sos1 and c-Raf-1 were not phosphorylated by GM-CSF, IL-3, | TNF | , and FMLP in monocytes, whereas all these signaling molecules were affected and |
| 99386936 | Differential effects of lipopolysaccharide and | tumor necrosis factor | on monocytic Ikappa B kinase signalsome activation and Ikappa B proteolysis. Th |
| 99386936 | Ikappa B proteolysis. The inflammatory mediators lipopolysaccharide ( LPS ) and | tumor necrosis factor | ( TNF ) are potent activators of NF-kappa B. This study compared the effect of |
| 99386936 | e inflammatory mediators lipopolysaccharide ( LPS ) and tumor necrosis factor ( | TNF | ) are potent activators of NF-kappa B. This study compared the effect of these |
| 99386936 | ial modulator ) , and IKK complex-associated protein. Kinase assays showed that | TNF | elicited a rapid but short-lived induction of IKK activity with a 3-fold greate |
| 99386936 | with NIK, Ikappa B-alpha and -epsilon in unstimulated cells. Exposure to LPS or | TNF | led to differential patterns of Ikappa B-alpha and Ikappa B-epsilon disappearan |
| 99386936 | ereas NF-kappa B essential modulator enhanced it. The understanding of LPS- and | TNF | -induced signaling may allow the development of specific strategies to treat sep |
| 90376424 | ble by both agents. TNF-alpha was able to increase expression of the HIV LTR in | T cells | , but in monocytic cells, TNF-alpha did not induce the HIV LTR above a constitut |
| 90376424 | rough the cell population and increased viral RNA synthesis, indicating that in | T cells | HIV-1 multiplication was stimulated by TNF-alpha treatment. |
| 91190842 | tor C alpha gene enhancer in a context-dependent manner. The differentiation of | T cells | into functionally diverse subpopulations is controlled in part, by transcriptio |
| 93183827 | ve transcription factor, requires two signals and is cyclosporin A sensitive in | T cells | . Few known genes ( IL-2, members of the IL-8 family, interferon-gamma ) are ind |
| 93183827 | own genes ( IL-2, members of the IL-8 family, interferon-gamma ) are induced in | T cells | only through the combined effect of phorbol myristic acetate ( PMA ) and a Ca ( |
| 93183827 | requirement for expression. Induction of the PILOT gene is detectable in human | T cells | 20 min following activation in the presence of cycloheximide and is fully suppr |
| 93183827 | er regions of the transcription factors EGR1, EGR2, and pAT 133. In contrast to | T cells | , in fibroblasts PILOT gene expression requires only one signal ( PMA ) and is n |
| 93183827 | signal-dependent regulatory element obligatory for expression of some genes in | T cells | but not in fibroblasts. This differential expression model will be valuable in |
| 93183827 | pression model will be valuable in the dissection of the dual signal pathway in | T cells | and the effects of CyA upon it. |
| 93321228 | became refractory to activation via the CD3 / T cell receptor ( TcR ) complex. | T cells | preincubated with phorbol 12-myristate 13-acetate ( PMA ) and dibutyryl cAMP ( |
| 94107268 | peroxide ( pervanadate ) , on the activation cascade of Jurkat human leukaemic | T-cells | . Pervanadate induced activation of the tyrosine kinases lck and fyn ( 4- and 3- |
| 94238882 | described to induce differentiation of murine thymocytes to cytolytic effector | T-cells | by stimulating IL-6 release from adherent cells. This study shows that human pe |
| 95000924 | Role of HIV-1 Nef expression in activation pathways in CD4+ | T cells | . The role of the human immunodeficiency virus ( HIV-1 ) Nef protein in T cell a |
| 95000924 | f downmodulates LTR activation without significantly inhibiting the capacity of | T cells | to respond to immunological activations. |
| 95166251 | Expression of the Runt domain-encoding PEBP2 alpha genes in | T cells | during thymic development. The PEBP2 alpha A and PEBP2 alpha B genes encode the |
| 95166251 | - CD8+ cell populations. The results indicated that both genes are expressed in | T cells | throughout their development, supporting the notion that PEBP2 is a T-cell-spec |
| 95222739 | e nonleukemogenic virus, Akv. This difference strongly affects transcription in | T cells | and leukemogenicity of SL3. However, no combination of CBF alpha and CBF beta s |
| 95222739 | 1-bp difference in transcription assays. Thus, a complete understanding of how | T cells | recognize the SL3 core remains to be elucidated. |
| 95399771 | osporin A and the T-cell transcription factor NFAT. Nuclear factor of activated | T cells | ( NFAT ) was originally described as a T-cell-specific transcription factor ath |
| 96038813 | Cloning a cDNA from human NK / | T cells | which codes for a protein with high proline content. A cDNA clone, B4-2, was is |
| 96079922 | ulate proliferation and activate transcription of over-lapping sets of genes of | T cells | . PRL and IL-2 receptor activation are both linked to the Jak / Stat ( signal tr |
| 96085174 | eukin-7 can induce the activation of Jak 1, Jak 3 and STAT 5 proteins in murine | T cells | . The activation of Janus protein tyrosine kinases ( Jak ) and STAT ( signal tra |
| 96184791 | chromosome 5q23-31. Interleukin-13 ( IL-13 ) and IL-4 are cytokines produced by | T cells | that are encoded by the q23-31 region of human chromosome 5. To investigate the |
| 96184791 | f human chromosome 5. To investigate the regulation of IL-13 gene expression by | T cells | , we isolated and sequenced the human IL-13 gene, analyzed its 5'-flanking regio |
| 96184791 | gy to P elements of the IL-4 promoter involved in transcriptional activation in | T cells | . Mutation of the IL-13 P element site significantly reduced IL-13 promoter acti |
| 96184791 | cifically bound the transcriptional activator protein, nuclear factor-activated | T cells | , preformed ( NF-ATp ) , when incubated with nuclear protein extracts from activ |
| 96184791 | formed ( NF-ATp ) , when incubated with nuclear protein extracts from activated | T cells | . Similar to IL-4, IL-13 mRNA expression was highest in T-cell populations enric |
| 96184791 | pression of the IL-13 and IL-4 genes in a coordinate manner. Because the primed | T cells | contain higher levels of nuclear NF-ATp, capable of binding to P elements of th |
| 96184791 | binding to P elements of the IL-4 and IL-13 promoters, than do freshly-isolated | T cells | , the NF-AT-binding P elements are attractive candidates to mediate the coordina |
| 96195006 | hway exerts an inhibitory effect on the proliferation and effector functions of | T cells | . The ability of T cells to form high intracellular levels of cAMP is acquired d |
| 96195006 | y effect on the proliferation and effector functions of T cells. The ability of | T cells | to form high intracellular levels of cAMP is acquired during development in the |
| 96195006 | y of mature peripheral T lymphocytes. Here we show that elevated cAMP levels in | T cells | correlate with the expression of the potent transcriptional repressor ICER ( in |
| 96195006 | T-lymphotropic virus type I ( HTLV-I ) promoter. Thus, the induction of ICER in | T cells | may play an important role in the cAMP-induced quiescence and the persistent la |
| 96211859 | Age-related decreases in IL-2 production by human | T cells | are associated with impaired activation of nuclear transcriptional factors AP-1 |
| 96211859 | nd NF-AT. Although transcriptional factors AP-1 and nuclear factor of activated | T cells | ( NF-AT ) are important for the normal induction of IL-2, it is unknown if the |
| 96211859 | it is unknown if the age-related decline in IL-2 production by activated human | T cells | may be associated with aberrancies in transcriptional regulatory proteins. In t |
| 96211859 | transcriptional regulatory proteins. In the current studies, IL-2 production by | T cells | from elderly ( mean 78 years ) and young ( mean 37 years ) humans was measured |
| 96211859 | from other elderly individuals were equivalent to those observed for stimulated | T cells | of young subjects. Analyses of nuclear extracts by electrophoretic DNA mobility |
| 96211859 | ociated with impairments in the activation of both AP-1 and NF-AT. By contrast, | T cells | from elderly subjects with normal levels of IL-2 production exhibited normal ac |
| 96279111 | ranscription factors are required for activation of human interleukin 9 gene in | T cells | . The genetic elements and regulatory mechanisms responsible for human interleuk |
| 96279111 | ion of different transcription factors is essential for IL-9 gene expression in | T cells | . |
| 96322726 | ibition of transcription factor Stat1 activity in mononuclear cell cultures and | T cells | by the cyclic AMP signaling pathway. Activation of T cells results in a cascade |
| 96322726 | ( STAT ) family was analyzed in PHA-activated mononuclear cells and in purified | T cells | activated by cross-linking cell surface CD3. Cell activation resulted in a dela |
| 97025698 | he proliferation of human lymphocytes in a non-specific manner and may activate | T cells | to express CD40 antigen. |
| 97211823 | kappa B play critical roles during late stages of the intrathymic maturation of | T cells | . |
| 97376857 | ng activity to the IL-2 promoter CD28 response element / AP-1 sequence in human | T cells | . CD28 is an important costimulatory molecule in the activation of human T cells |
| 97376857 | T cells. CD28 is an important costimulatory molecule in the activation of human | T cells | . Costimulation of T cells through both the Ag receptor and CD28 leads to high l |
| 97376857 | ant costimulatory molecule in the activation of human T cells. Costimulation of | T cells | through both the Ag receptor and CD28 leads to high level IL-2 production, whic |
| 97376857 | nd the AP-1-binding sites influence IL-2 promoter activity in CD28-costimulated | T cells | . |
| 97456880 | e mouse IL-4 gene: involvement of a distinct set of nuclear factor of activated | T cells | and activator protein-1 family proteins. We previously identified the P sequenc |
| 97456880 | SA, complexes formed with P or P2 proved to contain nuclear factor of activated | T cells | ( NFAT ) family proteins as major components. Activator protein ( AP ) -1 famil |
| 97458245 | osis factor receptor superfamily. Activation of the nuclear factor of activated | T cells | transcription factor ( NF-AT ) is a key event underlying lymphocyte action. The |
| 97458245 | igand ) protein is a coinducer of NF-AT activation when overexpressed in Jurkat | T cells | . A member of the tumor necrosis factor receptor superfamily was isolated by vir |
| 98001571 | rbamates involves novel mechanisms of inhibition of nuclear factor of activated | T cells | . Dithiocarbamates ( DTCs ) have recently been reported as powerful inhibitors o |
| 98001571 | kappa B-driven reporter activation but also that of nuclear factor of activated | T cells | ( NFAT ) . Accordingly, electrophoretic mobility shift assays ( EMSAs ) indicat |
| 98001571 | Tp and NFATc, leading to their accelerated export from the nucleus of activated | T cells | . We propose that the activation of an NFAT kinase by PDTC could be responsible |
| 98380286 | Stimulation of B and | T cells | activates expression of transcription and differentiation factors. During B and |
| 99081619 | zed the effects of interleukin-10 ( IL-10 ) on the entry of quiescent CD4 ( + ) | T cells | into the cell cycle upon stimulation with the superantigen staphylococcal enter |
| 99081619 | n. Cell separation experiments suggest that IL-10 can effect purified CD4 ( + ) | T cells | directly, providing functional evidence for the presence of IL-10 receptors on |
| 99081619 | providing functional evidence for the presence of IL-10 receptors on CD4 ( + ) | T cells | . IL-10 also inhibited expression of IL-2 transcriptional regulators c-fos and c |
| 99091536 | Functional testosterone receptors in plasma membranes of | T cells | . T cells are considered to be unresponsive to testosterone due to the absence o |
| 99091536 | Functional testosterone receptors in plasma membranes of T cells. | T cells | are considered to be unresponsive to testosterone due to the absence of androge |
| 99091536 | ( AR ) . Here, we demonstrate the testosterone responsiveness of murine splenic | T cells | in vitro as well as the presence of unconventional cell surface receptors for t |
| 99091536 | ites for testosterone on the surface of both CD4 ( + ) and CD8 ( + ) subsets of | T cells | are directly revealed with the impeded ligand testosterone-BSA-FITC by confocal |
| 99091536 | sterone-BSA conjugate induces a rapid rise ( <5 s ) in [Ca2+]i of Fura-2-loaded | T cells | . This rise reflects influx of extracellular Ca2+ through non-voltage-gated and |
| 99091536 | blocker of the AR. In addition, AR are not detectable on the surface of intact | T cells | when using anti-AR antibodies directed against the amino and carboxy terminus o |
| 99091536 | antibodies directed against the amino and carboxy terminus of the AR, although | T cells | contain AR, as revealed by reverse transcription-polymerase chain reactions and |
| 99091536 | can be visualized with the anti-AR antibodies in the cytoplasm of permeabilized | T cells | by using CLSM, though AR are not detectable in cytosol fractions when using the |
| 99091536 | ay with 3H-R1881 as ligand. Cytoplasmic AR do not translocate to the nucleus of | T cells | in the presence of testosterone, in contrast to cytoplasmic AR in human cancer |
| 99091536 | er LNCaP cells. These findings suggest that the classical AR present in splenic | T cells | are not active in the genomic pathway. By contrast, the cell surface receptors |
| 99091536 | surface receptors for testosterone are in a functionally active state, enabling | T cells | a nongenomic response to testosterone. |
| 99102590 | vities to the immunodominant and subdominant lytic cycle epitopes identified by | T cells | during primary EBV infection are regularly detectable in the CTL memory of viru |
| 99146379 | a novel, phosphorylated, zinc finger transcription factor that is expressed in | T cells | 3 days after activation, coincident with RANTES expression. While Rel proteins |
| 99146379 | ene expression in fibroblasts, RFLAT-1 is a strong transactivator for RANTES in | T cells | . |
| 99168986 | pregulates proliferation-associated IL-2Ralpha, c-myc, and pim-1 genes in human | T cells | . Interferon-alpha ( IFN-alpha ) is a pleiotropic cytokine that has antiviral, a |
| 99168986 | gulated IL-2Ralpha, c-myc, and pim-1 gene expression. IFN-alpha also sensitized | T cells | to IL-2-induced proliferation, further suggesting that IFN-alpha may be involve |
| 99168986 | est that IFN-alpha, IL-2, IL-12, and IL-15 have overlapping activities on human | T cells | . These findings thus emphasize the importance of IFN-alpha as a T-cell regulato |
| 99172186 | odified by NAC. Finally, we found that the addition of NAC to MLR between naive | T cells | and allogeneic DC resulted in a profound inhibition of alloreactive responses, |
| 99369970 | lation by antibody and bacterial superantigen induces Stat3 activation in human | T cells | . Recent data show that TCR / CD3 stimulation induces activation of Stat5 in mur |
| 99369970 | cent data show that TCR / CD3 stimulation induces activation of Stat5 in murine | T cells | . Here, we show that CD3 ligation by mAb and Staphylococcal enterotoxin ( SE ) i |
| 99369970 | rapid, PP1-sensitive tyrosine and serine phosphorylation of Stat3 in human CD4+ | T cells | . Moreover, we provide evidence that TCR / CD3 and IL-2 induce Stat3 activation |
| 90376424 | osis factor in human immunodeficiency virus ( HIV ) pathogenesis were examined. | Tumor necrosis factor alpha | ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplifi |
| 90376424 | iciency virus ( HIV ) pathogenesis were examined. Tumor necrosis factor alpha ( | TNF-alpha | ) mRNA production was analyzed by polymerase chain reaction amplification in mo |
| 90376424 | cytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ) . | TNF-alpha | RNA was undetectable in U937 cells, whereas a low constitutive level was detect |
| 90376424 | xovirus infection induced a 5- to 10-fold increase in the steady-state level of | TNF-alpha | RNA in U9-IIIB cells compared with U937 cells, suggesting that HIV-infected mon |
| 90376424 | 7 cells, suggesting that HIV-infected monocytic cells produced higher levels of | TNF-alpha | than did normal cells after a secondary virus infection. The effects of TNF-alp |
| 90376424 | F-alpha than did normal cells after a secondary virus infection. The effects of | TNF-alpha | on gene expression were examined by transient expression assays using reporter |
| 90376424 | Jurkat T lymphoid cells, the inducibility of the different hybrid promoters by | TNF-alpha | or phorbol ester varied in a cell type- and promoter context-specific manner; t |
| 90376424 | intact beta interferon promoter was only weakly stimulated by phorbol ester or | TNF-alpha | , multimers of the PRDII NF-kappa B-binding domain were inducible by both agents |
| 90376424 | multimers of the PRDII NF-kappa B-binding domain were inducible by both agents. | TNF-alpha | was able to increase expression of the HIV LTR in T cells, but in monocytic cel |
| 90376424 | able to increase expression of the HIV LTR in T cells, but in monocytic cells, | TNF-alpha | did not induce the HIV LTR above a constitutive level of activity. This level o |
| 90376424 | B-independent activity appears to be sufficient for virus multiplication, since | TNF-alpha | treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infecti |
| 90376424 | 1 ) infection and viral RNA production in U937 cells. However, in Jurkat cells, | TNF-alpha | dramatically enhanced the spread of HIV-1 through the cell population and incre |
| 90376424 | NA synthesis, indicating that in T cells HIV-1 multiplication was stimulated by | TNF-alpha | treatment. |
| 91321794 | kappa B. HIV-1-infected individuals have, on average, abnormally high levels of | tumour necrosis factor alpha | ( TNF alpha ) and abnormally low plasma cysteine levels. We therefore investiga |
| 91321794 | uals have, on average, abnormally high levels of tumour necrosis factor alpha ( | TNF alpha | ) and abnormally low plasma cysteine levels. We therefore investigated the effe |
| 94238882 | d monocytes ( PBMo ) also respond to MDHM with increases in IL-1 beta, IL-6 and | TNF alpha | expression, both at the mRNA and protein level. The induced expression of IL-1 |
| 95000924 | ell line stably transfected with a Nef expression vector. Secretion of IL-2 and | TNF-alpha | , surface expression of IL-2R, and DNA-binding activity of NF-kappa B and AP-1 ( |
| 95000924 | appa B and AP-1 ( Fos / Jun ) complex in response to phorbol myristate acetate, | TNF-alpha | , or immobilized antibodies to CD3 were monitored. These parameters were not mod |
| 95202809 | The induction of vascular cell adhesion molecule-1 ( VCAM-1 ) and E-selectin by | tumor necrosis factor-alpha | ( TNF ) is mediated by mobilization of the transcription factor nuclear factor- |
| 96303658 | The underlying signaling pathways appear to be different from those utilized by | TNF-alpha | , a better characterized cytokine that induces the transcription of immediate-ea |
| 97162234 | to be crucially involved in the gene activation of several cytokines, including | tumor necrosis factor alpha | ( TNF ) . Previously, we showed that fibroblast conditioned medium ( FCM ) is a |
| 98012705 | ccompanied by an inhibition of both NF-kappa B activation and the expression of | tumor necrosis factor-alpha | and interleukin-1 beta genes. These observations provide additional evidence th |
| 98104459 | cule-1 ( ICAM-1 ) gene, which is involved in regulation of ICAM-1 expression by | tumor necrosis factor alpha | ( TNF-alpha ) and glucocorticoids. We now report on the transcription factors w |
| 98104459 | is involved in regulation of ICAM-1 expression by tumor necrosis factor alpha ( | TNF-alpha | ) and glucocorticoids. We now report on the transcription factors which bind an |
| 98104459 | to transactivate an ICAM-1 kappa B-reporter construct. In monocytic THP-1 cells | TNF-alpha | induced two nuclear complexes which in vitro bound to the ICAM-1 kappa B site. |
| 98104459 | er. We argue that in vivo RelA homodimers are likely to play a dominant role in | TNF-alpha | -induced ICAM-1 transcription in monocytic cells. |
| 99228708 | protein tyrosine kinase dependent and protein kinase C independent. BACKGROUND: | Tumor necrosis factor alpha | ( TNF-alpha ) is an important mediator of septic shock. Endotoxin ( LPS ) signa |
| 99228708 | ent and protein kinase C independent. BACKGROUND: Tumor necrosis factor alpha ( | TNF-alpha | ) is an important mediator of septic shock. Endotoxin ( LPS ) signal transducti |
| 99228708 | ) and protein tyrosine kinases ( PTK ) in LPS-induced NF-kappa B activation and | TNF-alpha | production. We hypothesized that inhibition of either PKC or PTK would decrease |
| 99228708 | PTK inhibition with Gen attenuated both LPS-induced NF-kappa B DNA binding and | TNF-alpha | production in human monocytes. Direct activation of PKC with PMA induced both N |
| 99228708 | cytes. Direct activation of PKC with PMA induced both NF-kappa B activation and | TNF-alpha | production by human monocytes. CONCLUSIONS: These results suggest that LPS-indu |
| 99356019 | kinase activity, protein activity of NF-kappa B and cytokine ( IL-1beta, IL-6, | TNF-alpha | ) specific mRNA levels in BEAS-2B cells. We observed an increase in protein tyr |
| 99406845 | laddering, and typical morphology by means of transmission electron microscopy. | TNF-alpha | and IL-1beta were measured by ELISA. GC receptor was blocked with mifepristone. |
| 99406845 | ed by propidium iodide staining. Proinflammatory cytokines such as IL-1beta and | TNF-alpha | were down-regulated by GC treatment. Continuous treatment of monocytes with IL- |
| 99406845 | by GC treatment. Continuous treatment of monocytes with IL-1beta, but not with | TNF-alpha | , could almost completely prevent GC-induced cell death. The addition of mifepri |
| 90376424 | Cell-specific differences in | activation of NF-kappa B | regulatory elements of human immunodeficiency virus and beta interferon promote |
| 90376424 | varied in a cell type- and promoter context-specific manner; the levels of gene | activity of NF-kappa B | -containing plasmids correlated directly with induction of NF-kappa B DNA-bindin |
| 91321794 | Inhibition of HIV-1 replication and | NF-kappa B activity | by cysteine and cysteine derivatives. HIV-1 proviral DNA contains two binding s |
| 91321794 | rs not to be directly correlated with GSH levels. Cysteine and NAC also inhibit | NF-kappa B activity | as determined by electrophoretic mobility shift assays and chloramphenicol acet |
| 92052106 | eir ability to form the heterodimer, suggesting the presence of an inhibitor of | NF-kappa B activity | . Furthermore, treatment of nuclear extracts from these cells that had restricte |
| 92052106 | ad restricted expression with lipopolysaccharide increased viral production and | NF-kappa B activity | . Antiserum specific for NF-kappa B binding proteins, but not c-rel-specific ant |
| 95000924 | . Secretion of IL-2 and TNF-alpha, surface expression of IL-2R, and DNA-binding | activity of NF-kappa B | and AP-1 ( Fos / Jun ) complex in response to phorbol myristate acetate, TNF-al |
| 95202809 | factor-kappa B ( NF-kappa B ) . Since salicylates have been reported to inhibit | NF-kappa B activation | by preventing the degradation of its inhibitor I kappa B, we studied a potentia |
| 95332324 | rtant component of an integrin signaling pathway in monocytic cells, leading to | activation of NF-kappa B | and to increased levels of cytokine messages. |
| 96075792 | th LPS. The increased transcriptional rate correlated with a marked increase in | nuclear factor-kappa B activity | in these cells as determined by electrophoretic mobility shift assay using a co |
| 97162234 | his study we have investigated the effect of FCM on the LPS-induced DNA-binding | activity of NF-kappa B | , by means of electrophoretic shift assay ( EMSA ) . We provide evidence that FC |
| 97162234 | assay ( EMSA ) . We provide evidence that FCM strongly inhibits the LPS-induced | NF-kappa B activation | in PBM. Furthermore, we show that exogenous PGE2 mimics the NF-kappa B inhibito |
| 97162234 | n the other hand, FCM produced in the presence of indomethacin does not inhibit | NF-kappa B activation | by LPS. Our results lend further support to the hypothesis that inflammatory an |
| 97211823 | volved in immune and inflammatory responses. We have reported previously that a | nuclear NF-kappa B activity | was present in freshly extracted human thymocytes in the absence of in vitro tr |
| 97307577 | ected, but not yet proven. Transgenic mice with a lymphocyte-specific defect in | NF-kappa B activation | were produced by targeted expression of human Ikappa B alpha. The thymic cellul |
| 98001571 | Dithiocarbamates ( DTCs ) have recently been reported as powerful inhibitors of | NF-kappa B activation | in a number of cell types. Given the role of this transcription factor in the r |
| 98012705 | ning NF-kappa B dimers and induced the expression of the target gene IL-8. This | activation of NF-kappa B | was inhibited by the antioxidant and H2O2 scavenger pyrrolidine dithiocarbamate |
| 98012705 | pyrrolidine dithiocarbamate and the proteasome inhibitor PSI. The oxLDL-induced | NF-kappa B activation | was accompanied by an initial depletion of I kappa B-alpha followed by a slight |
| 98012705 | ride-induced depletion of I kappa B-alpha, accompanied by an inhibition of both | NF-kappa B activation | and the expression of tumor necrosis factor-alpha and interleukin-1 beta genes. |
| 99118181 | Inhibition of | NF-kappa B activation | in vitro and in vivo: role of 26S proteasome. It is becoming increasingly appar |
| 99228708 | LPS-Induced | NF-kappa B activation | and TNF-alpha release in human monocytes are protein tyrosine kinase dependent |
| 99228708 | septic shock. Endotoxin ( LPS ) signal transduction in human monocytes leads to | activation of nuclear factor-kappa B | ( NF-kappa B ) and TNF-alpha release. Previous studies have implicated activati |
| 99228708 | th protein kinase C ( PKC ) and protein tyrosine kinases ( PTK ) in LPS-induced | NF-kappa B activation | and TNF-alpha production. We hypothesized that inhibition of either PKC or PTK |
| 99228708 | pha release in human monocytes. Nonspecific protein kinase inhibition inhibited | NF-kappa B activation | and TNF-alpha release, while specific PKC inhibition with Bis had no effect on |
| 99228708 | a production in human monocytes. Direct activation of PKC with PMA induced both | NF-kappa B activation | and TNF-alpha production by human monocytes. CONCLUSIONS: These results suggest |
| 99228708 | duction by human monocytes. CONCLUSIONS: These results suggest that LPS-induced | NF-kappa B activation | and TNF-alpha release in human monocytes are independent of PKC activity. Furth |
| 99228708 | Furthermore, our results provide evidence that PTK plays a role in LPS-induced | NF-kappa B activation | and TNF-alpha release in human monocytes and thus could be a potential therapeu |
| 99356019 | nocytes increases inflammatory cytokine-mRNA level, protein tyrosine kinase and | NF-kappa B activity | in co-cultured bronchial epithelial cells ( BEAS-2B ) . Some pulmonary diseases |
| 99356019 | say ) and RT-PCR were used to measure protein tyrosine kinase activity, protein | activity of NF-kappa B | and cytokine ( IL-1beta, IL-6, TNF-alpha ) specific mRNA levels in BEAS-2B cell |
| 99356019 | A were elevated ( up to 1.9 +/- 0.58-fold ) . Protein tyrosine kinase activity, | NF-kappa B activity | , and the synthesis of cytokine-specific mRNA were inhibited by antioxidants. Th |
| 90140708 | Two distinct | transcription factors | that bind the immunoglobulin enhancer microE5 / kappa 2 motif. Activity of the |
| 91190842 | vity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) | transcription factors | and the context of its binding site within the TCR alpha enhancer. |
| 91321794 | and cysteine derivatives. HIV-1 proviral DNA contains two binding sites for the | transcription factor | NF-kappa B. HIV-1-infected individuals have, on average, abnormally high levels |
| 93024468 | Characterization of a new tissue-specific | transcription factor | binding to the simian virus 40 enhancer TC-II ( NF-kappa B ) element. We have b |
| 93024468 | F-kappa B ) element. We have biochemically and functionally characterized a new | transcription factor | , NP-TCII, which is present in nuclei from unstimulated T and B lymphocytes but |
| 93183827 | Expression of PILOT, a putative | transcription factor | , requires two signals and is cyclosporin A sensitive in T cells. Few known gene |
| 93183827 | an be fully suppressed by Cyclosporin A ( CyA ) . We have identified a putative | transcription factor | , designated PILOT, with an identical dual signal requirement for expression. In |
| 93183827 | carboxyl-terminus which are highly homologous to the zinc finger regions of the | transcription factors | EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT gene expr |
| 93204975 | F-E2 / AP1 motifs of HS-40 is mediated through its binding to NF-E2 but not AP1 | transcription factor | . Finally, we did genomic footprinting of the HS-40 enhancer region in K562 cell |
| 93321228 | D3-dependent T cell activation and leads to a persistent expression of the AP-1 | transcription factor | . The effects mediated by a combined stimulation of cAMP -and protein kinase C ( |
| 94107268 | e activated NF-kappa B, as shown by an increase in DNA-binding activity of this | transcription factor | . We thus conclude that PTPases play a crucial role in the negative regulation o |
| 95166251 | EBP2 alpha A and PEBP2 alpha B genes encode the DNA-binding subunit of a murine | transcription factor | , PEBP2, which is implicated as a T-cell-specific transcriptional regulator. The |
| 95222739 | lyomavirus enhancer-binding protein 2 and SL3 enhancer factor 1, is a mammalian | transcription factor | that binds to an element termed the core within the enhancers of the murine leu |
| 95261059 | B. PU.1 ( the Spi-1 oncogene ) and Spi-B are closely related members of the ets | transcription factor | family, sharing similar DNA binding specificities mediated by similar DNA bindi |
| 95399771 | and E-selectin expression in endothelial cells by cyclosporin A and the T-cell | transcription factor | NFAT. Nuclear factor of activated T cells ( NFAT ) was originally described as |
| 96079922 | in and interleukin-2 receptors in T lymphocytes signal through a MGF-STAT5-like | transcription factor | . The cell surface receptors for PRL and interleukin-2 ( IL-2 ) are structurally |
| 96079922 | rameters were indistinguishable for one of the PRL- and IL-2-induced factors. A | transcription factor | closely related to mammary gland factor-Stat5 is rapidly activated upon interac |
| 96211859 | production by human T cells are associated with impaired activation of nuclear | transcriptional factors | AP-1 and NF-AT. Although transcriptional factors AP-1 and nuclear factor of act |
| 96211859 | impaired activation of nuclear transcriptional factors AP-1 and NF-AT. Although | transcriptional factors | AP-1 and nuclear factor of activated T cells ( NF-AT ) are important for the no |
| 96279111 | Multiple | transcription factors | are required for activation of human interleukin 9 gene in T cells. The genetic |
| 96279111 | inding. Taken together, these results suggest that the cooperation of different | transcription factors | is essential for IL-9 gene expression in T cells. |
| 96303658 | transduce signals leading to gene transcription and translation in leukocytes. | Transcription factors | , such as NF kappa B and AP-1, are activated upon stimulation of the cells with |
| 96322726 | Inhibition of | transcription factor | Stat1 activity in mononuclear cell cultures and T cells by the cyclic AMP signa |
| 96322726 | t proliferation and differentiation into effector phenotypes. The regulation of | transcription factors | belonging to the signal transducer and activator of transcription ( STAT ) fami |
| 96322726 | eceptor alpha-chain and CD69 expression or the induction of activator protein 1 | transcription factors | . cAMP signaling inhibited Stat1 at several different levels, including suppress |
| 96329553 | ediate effects in monocytes by activation of the Janus kinase ( JAK2 ) and STAT | transcription factor | ( STAT5 ) pathway. Recent studies have identified homologues of STAT5, STAT5A, |
| 97064186 | phorylation of STAT4 ( signal transducer and activator of transcription-4 ) , a | transcription factor | that is typically involved in IL-12 signaling. Consequently, IL-12 also failed |
| 97263762 | Involvement of an SAF-like | transcription factor | in the activation of serum amyloid A gene in monocyte / macrophage cells by lip |
| 97324097 | ive nuclear localization of the ETS protein Elf-1. Elf-1 is a lymphoid-specific | transcription factor | that belongs to the ETS protein family. It can bind to DNA target sequences wit |
| 97376857 | to the activation of the IL-2 promoter by up-regulating the activity of several | transcription factors | , including AP-1 and nuclear factor-kappa B ( NF-kappa B ) /Rel family members a |
| 97376857 | factor-kappa B ( NF-kappa B ) /Rel family members as well as an uncharacterized | transcription factor | called CD28 response complex. While several lines of investigation have suggest |
| 97376857 | uggested that NF-kappa B / Rel family members make up the CD28 response complex | transcription factor | , other work has not supported this conclusion. Recent studies suggest that the |
| 97436422 | ve stages of commitment and differentiation. From analyses of mice deficient in | transcription factor | genes and from the characterizations of chromosome breakpoints in human leukemi |
| 97436422 | ations of chromosome breakpoints in human leukemias, it has become evident that | transcription factors | are important regulators of hematopoiesis. During myelopoiesis, which includes |
| 97436422 | poiesis, which includes the development of granulocytic and monocytic lineages, | transcription factors | from several families are active, including AML1 / CBF beta, C / EBP, Ets, c-My |
| 97458245 | tor receptor superfamily. Activation of the nuclear factor of activated T cells | transcription factor | ( NF-AT ) is a key event underlying lymphocyte action. The CAML ( calcium-modul |
| 97458245 | transfected Jurkat cells with TACI-specific antibodies led to activation of the | transcription factors | NF-AT, AP-1, and NFkappa B. TACI-induced activation of NF-AT was specifically b |
| 97468093 | . These results suggest that in human T lymphocytes IFN-beta can activate other | transcription factor | ( s ) distinct from ISGF3 to regulate PLC gamma 1 expression. In addition, the |
| 98001571 | tors of NF-kappa B activation in a number of cell types. Given the role of this | transcription factor | in the regulation of gene expression in the inflammatory response, NF-kappa B i |
| 98001571 | he NFAT, therefore transiently converting the sustained transactivation of this | transcription factor | that occurs during lymphocyte activation, and show that c-Jun NH2-terminal kina |
| 98012705 | by oxidized low-density lipoprotein. Nuclear factor-kappa B ( NF-kappa B ) /Rel | transcription factors | may be involved in atherosclerosis, as is suggested by the presence of activate |
| 98038749 | k-2-dependent phosphorylation. The functions of basic helix-loop-helix ( bHLH ) | transcription factors | in activating differentiation-linked gene expression and in inducing G1 cell cy |
| 98090689 | o examine both fetal and term neonatal cord bloods for mRNA expression of three | transcription factors | implicated in T-cell activation: c-jun, c-fos, and NF kappa B ( p50 subunit ) . |
| 98090689 | shown in fetal blood cells. Quantitative experiments comparing binding of these | transcription factors | to the IL-2 promoter are currently under investigation. |
| 98104459 | r necrosis factor alpha ( TNF-alpha ) and glucocorticoids. We now report on the | transcription factors | which bind and transactivate this enhancer sequence. In vitro, the ICAM-1 kappa |
| 98230439 | red to the LAI LTR. Differences in LTR sequence also resulted in differences in | transcription factor | recruitment to cis-acting sites within the U3 region of the LTR, as demonstrate |
| 98230439 | ty shift assays. In particular, naturally occurring sequence variation impacted | transcription factor | binding to an activating transcription factor / cAMP response element binding ( |
| 98230439 | ggest that LTR sequence changes can significantly affect basal LTR function and | transcription factor | recruitment, which may, in turn, alter the course of viral replication in cells |
| 99007236 | y could regulate transcription of specific genes. Multiple cellular DNA-binding | transcription factors | are required by HIV type 1 for RNA synthesis. Two pyrrole-imidazole polyamides |
| 99007236 | re designed to bind DNA sequences immediately adjacent to binding sites for the | transcription factors | Ets-1, lymphoid-enhancer binding factor 1, and TATA-box binding protein. These |
| 99007236 | nding protein. These synthetic ligands specifically inhibit DNA-binding of each | transcription factor | and HIV type 1 transcription in cell-free assays. When used in combination, the |
| 99146379 | RFLAT-1: a new zinc finger | transcription factor | that activates RANTES gene expression in T lymphocytes. RANTES ( Regulated upon |
| 99146379 | sing expression cloning, we identified the first "late" T lymphocyte associated | transcription factor | and named it "RANTES Factor of Late Activated T Lymphocytes-1" ( RFLAT-1 ) . RF |
| 99146379 | T Lymphocytes-1" ( RFLAT-1 ) . RFLAT-1 is a novel, phosphorylated, zinc finger | transcription factor | that is expressed in T cells 3 days after activation, coincident with RANTES ex |
| 99172186 | that NAC inhibited the constitutive as well as the LPS-induced activity of the | transcription factor | NF-kappa B. In parallel, NAC was shown to down-regulate the production of cytok |
| 99207658 | ion or gene repression. Glucocorticoid receptors are also able to interact with | transcriptional factors | such as AP-1 ( activator protein-1 ) of NF-kappa B ( nuclear factor-kappa B ) . |
| 99310627 | operate to promote erythroid cell survival by regulating bcl-xL expression. The | transcription factor | GATA-1 is essential for normal erythropoiesis. By examining in vitro-differenti |
| 91321794 | GSH levels. Cysteine and NAC also inhibit NF-kappa B activity as determined by | electrophoretic mobility shift assays | and chloramphenicol acetyl-transferase ( CAT ) gene expression under control of |
| 96075792 | ked increase in nuclear factor-kappa B activity in these cells as determined by | electrophoretic mobility shift assay | using a consensus NF-kappa B oligonucleotide. An additional significant finding |
| 97054651 | y at a concentration as low as 100 nM without affecting cellular proliferation. | Electrophoretic mobility shift assay | ( EMSA ) and supershift assay using an NF-kappa B binding sequence from the kap |
| 97054651 | ithout affecting cellular proliferation. Electrophoretic mobility shift assay ( | EMSA | ) and supershift assay using an NF-kappa B binding sequence from the kappa ligh |
| 97162234 | d DNA-binding activity of NF-kappa B, by means of electrophoretic shift assay ( | EMSA | ) . We provide evidence that FCM strongly inhibits the LPS-induced NF-kappa B a |
| 97263762 | SAA promoter sequence between -280 and -226 can confer LPS responsiveness. Gel | electrophoretic mobility shift assay | detected an induced DNA-binding activity in these cells in response to LPS. Cha |
| 97456880 | their binding factors in the native promoter, we did transient transfection and | electrophoretic mobility shift assays | ( EMSA ) . Transfection of EL-4 cells with the IL-4 promoter-reporter construct |
| 97456880 | oter, we did transient transfection and electrophoretic mobility shift assays ( | EMSA | ) . Transfection of EL-4 cells with the IL-4 promoter-reporter constructs carry |
| 97456880 | and P4, but not P3, were required for optimal activation of the IL-4 promoter. | EMSA | showed that both constitutive and inducible complexes bound to CLE0, P, P2 and |
| 97456880 | stitutive complex bound to P3. In competition and antibody supershift assays in | EMSA | , complexes formed with P or P2 proved to contain nuclear factor of activated T |
| 98001571 | on but also that of nuclear factor of activated T cells ( NFAT ) . Accordingly, | electrophoretic mobility shift assays | ( EMSAs ) indicated that pyrrolidine DTC ( PDTC ) prevented NF-kappa B, and NFA |
| 98001571 | tivated T cells ( NFAT ) . Accordingly, electrophoretic mobility shift assays ( | EMSAs | ) indicated that pyrrolidine DTC ( PDTC ) prevented NF-kappa B, and NFAT DNA-bi |
| 98089072 | ion of erythroid-specific genes, and, in particular, the histone H5 gene. Using | electrophoretic mobility shift assays | , we found that in the presence of rabbit reticulocyte lysate, human ER reduced |
| 98230439 | uitment to cis-acting sites within the U3 region of the LTR, as demonstrated by | electrophoretic mobility shift assays | . In particular, naturally occurring sequence variation impacted transcription f |
| 99228708 | supernatants was measured by an ELISA. NF-kappa B DNA binding was evaluated by | electrophoretic mobility shift assay | . RESULTS: LPS increased NF-kappa B DNA binding and TNF-alpha release in human m |
| 99356019 | tration of 100 microg / 10 ( 6 ) cells. After up to 90 min exposure time ELISA, | EMSA | ( electromobility shift assay ) and RT-PCR were used to measure protein tyrosin |
| 90376424 | did normal cells after a secondary virus infection. The effects of TNF-alpha on | gene expression | were examined by transient expression assays using reporter chloramphenicol ace |
| 91321794 | rophoretic mobility shift assays and chloramphenicol acetyl-transferase ( CAT ) | gene expression | under control of NF-kappa B binding sites in uninfected cells. This suggests th |
| 92052106 | scription can be either latent, restricted, or productive. These differences in | gene expression | have not been molecularly defined. In THP-1 cells with restricted HIV expressio |
| 92052106 | be negatively regulated in monocytes, providing one mechanism restricting HIV-1 | gene expression | . |
| 93183827 | n factors EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT | gene expression | requires only one signal ( PMA ) and is not affected by CyA. This observation d |
| 93321228 | ata provide the evidence that both pathways complement each other in regulating | gene expression | and, conversely, downregulate the TcR transduction mechanisms. |
| 94209654 | s in T and B lymphocytes initiates signal transduction cascades which alter the | expression of genes | that regulate cellular proliferation and differentiation. The transmission of s |
| 94254835 | Lipopolysaccharide induction of tissue factor | gene expression | in monocytic cells is mediated by binding of c-Rel / p65 heterodimers to a kapp |
| 94254835 | el / p65 heterodimers to a novel kappa B-like site mediated LPS induction of TF | gene expression | in monocytic cells. |
| 95065655 | tion by BMLF1 proteins has been controversial but SM was shown to transactivate | gene expression | from a CAT reporter construct by increasing the amount of cytoplasmic CAT mRNA. |
| 95261059 | unlikely that Spi-B plays a significant role in myeloid lineage development and | gene expression | . In contrast, PU.1 is expressed at high levels not only in monocytes and macrop |
| 95261059 | ytes and macrophages but also in neutrophils, indicating that PU.1 can activate | gene expression | in both major myeloid lineages. |
| 95399771 | T-cell-specific transcription factor athat supported the activation of cytokine | gene expression | and mediated the immunoregulatory effects of cyclosporin A ( CsA ) . As we obse |
| 96079922 | t factors mammary gland factor-Stat5 and Stat1 play a role in the regulation of | gene expression | during T cell development. |
| 96184791 | the q23-31 region of human chromosome 5. To investigate the regulation of IL-13 | gene expression | by T cells, we isolated and sequenced the human IL-13 gene, analyzed its 5'-fla |
| 96239534 | molecules. These data suggest that Tax stimulates RNA polymerase III-dependent | gene expression | by accelerating the rate and / or extent of transcription initiation complex as |
| 96279111 | elements and regulatory mechanisms responsible for human interleukin 9 ( IL-9 ) | gene expression | in a human T cell leukemia virus type I-transformed human T cell line, C5MJ2, w |
| 96279111 | nsformed human T cell line, C5MJ2, were investigated. We demonstrated that IL-9 | gene expression | is controlled, at least in part, by transcriptional activation. Transient expre |
| 96279111 | t that the cooperation of different transcription factors is essential for IL-9 | gene expression | in T cells. |
| 96303658 | nitiate an autocrine regulatory mechanism for persistent cytokine and chemokine | gene expression | . |
| 97211823 | These observations suggest that p65 and c-Rel complexes play distinct roles in | gene expression | and that both forms of NF-kappa B play critical roles during late stages of the |
| 98001571 | of cell types. Given the role of this transcription factor in the regulation of | gene expression | in the inflammatory response, NF-kappa B inhibitors have been suggested as pote |
| 98012705 | se observations provide additional evidence that oxLDL is a potent modulator of | gene expression | and suggest that ( dys ) regulation of NF-kappa B / Rel is likely to play an im |
| 98038749 | -loop-helix ( bHLH ) transcription factors in activating differentiation-linked | gene expression | and in inducing G1 cell cycle arrest are negatively regulated by members of the |
| 98038749 | is not simply a function of its ability to modulate bHLH heterodimer-dependent | gene expression | and establish a biologically important mechanism through which Cdk2 and Id-bHLH |
| 98230439 | f the impact of long terminal repeat ( LTR ) sequence diversity on LTR-directed | gene expression | in cells of the central nervous system ( CNS ) and immune system, we amplified |
| 98380286 | ely expressed. To investigate processes related to B and T cell activation, the | gene expression | of stimulated and nonstimulated Ramos and Jurkat cells was studied using cDNA m |
| 98406200 | ransfection of Rta leads to synthesis of ZEBRA, viral DNA replication, and late | gene expression | . However, Rta by itself is less potent than ZEBRA in the ability to activate mo |
| 99007236 | ithin RNA polymerase II promoters suggests a general approach for regulation of | gene expression | , as well as a mechanism for the inhibition of viral replication. |
| 99083144 | hat display agonist activity in reproductive tissue also have an effect on IL-1 | gene expression | in hemopoietic-derived tissue. |
| 99146379 | RFLAT-1: a new zinc finger transcription factor that activates RANTES | gene expression | in T lymphocytes. RANTES ( Regulated upon Activation, Normal T cell Expressed a |
| 99146379 | ent with RANTES expression. While Rel proteins play the dominant role in RANTES | gene expression | in fibroblasts, RFLAT-1 is a strong transactivator for RANTES in T cells. |
| 99168986 | with IFN-alpha, IL-2, IL-12, and IL-15 upregulated IL-2Ralpha, c-myc, and pim-1 | gene expression | . IFN-alpha also sensitized T cells to IL-2-induced proliferation, further sugge |
| 99310627 | equired for erythroid cell survival, cooperates with GATA-1 to stimulate bcl-xL | gene expression | and to maintain erythroid cell viability during terminal maturation. Together, |
| 99408303 | ng the vitamin A derivative, retinoic acid. Retinoic acid can directly modulate | gene expression | via binding to its nuclear receptors, which can, in turn, activate transcriptio |
| 91164434 | Glucocorticoid receptors | on mononuclear leukocytes in Alzheimer's disease. Several lines of evidence sug | |
| 91164434 | in Alzheimer's disease ( AD ) . In an exploration of the potential role of the | glucocorticoid receptor | ( GR ) in AD, GR density and affinity were assessed on mononuclear leukocytes o |
| 91164434 | AD ) . In an exploration of the potential role of the glucocorticoid receptor ( | GR | ) in AD, GR density and affinity were assessed on mononuclear leukocytes of 12 |
| 91164434 | exploration of the potential role of the glucocorticoid receptor ( GR ) in AD, | GR | density and affinity were assessed on mononuclear leukocytes of 12 AD patients |
| 91164434 | e assessed on mononuclear leukocytes of 12 AD patients and 12 healthy controls. | GR | binding characteristics did not differ between patients and controls or between |
| 91164434 | ata suggest that the abnormalities of the HPA system in AD are not related to a | GR | deficiency. |
| 91363265 | Regulation of | glucocorticoid receptors | in human mononuclear cells: effects of glucocorticoid treatment, Cushing's dise |
| 91363265 | cells: effects of glucocorticoid treatment, Cushing's disease and ketoconazole. | Glucocorticoid receptors | ( GcR ) were determined by a whole cell assay in human mononulear leukocytes ( |
| 91363265 | icoid treatment, Cushing's disease and ketoconazole. Glucocorticoid receptors ( | GcR | ) were determined by a whole cell assay in human mononulear leukocytes ( hMNL ) |
| 91363265 | zole therapy. Prolonged corticosteroid treatment resulted in down-regulation of | GcR | , while the mean level of GcR in Cushing's disease was normal. In this group, ho |
| 91363265 | costeroid treatment resulted in down-regulation of GcR, while the mean level of | GcR | in Cushing's disease was normal. In this group, however, receptor levels and mo |
| 91363265 | negative correlation, indicating a subtle down-regulatory effect. Furthermore, | GcR | were unaltered after these patients received ketoconazole, in spite of a marked |
| 91363265 | nary free cortisol. We also observed that ketoconazole was a weak competitor of | GcR | in intact cells, although it significantly inhibited [3H] dexamethasone binding |
| 91363265 | binding in cytosolic preparations from rat tissues. The results suggested that | GcR | in hMNL are down-regulated by synthetic steroids given in vivo, but they showed |
| 91363265 | g's disease. Finally, we did not observed either up-regulation or antagonism of | GcR | by ketoconazole treatment, at the time that cortisol levels of patients with Cu |
| 91363265 | g's disease are due to adrenal cortisol suppression and not to interaction with | GcR | of target cells, and that the process of GcR regulation in hMNL is a complex ph |
| 91363265 | ession and not to interaction with GcR of target cells, and that the process of | GcR | regulation in hMNL is a complex phenomenon awaiting further elucidation. |
| 92362919 | hy persons and patients with hypertension] It has been found that the number of | glucocorticoid receptors | in lymphocytes of the peripheral blood of healthy elderly subjects increases, w |
| 98104459 | ed higher affinity towards the ICAM-1 kappa B than to the HIV kappa B site. The | glucocorticoid receptor | was shown to repress activity of both the RelA homodimer and the NF-kappa B1 / |
| 98133462 | Glucocorticoid receptors | in cord blood lymphocytes of healthy neonates and of preterms suffering from re | |
| 98133462 | reterms suffering from respiratory distress syndrome. We measured the number of | glucocorticoid receptors | ( GR ) in cord blood lymphocytes and the binding affinity ( Kd ) in 15 term and |
| 98133462 | iratory distress syndrome. We measured the number of glucocorticoid receptors ( | GR | ) in cord blood lymphocytes and the binding affinity ( Kd ) in 15 term and in 2 |
| 98133462 | terms developed neonatal respiratory distress syndrome ( NRDS ) . The number of | GR | and the Kd were similar in the term and preterm ( with and without NRDS ) babie |
| 98133462 | thasone was the same in all groups. In this study on the number and function of | GR | in lymphocytes, we were unable to find a relation between the functionality of |
| 98133462 | lymphocytes, we were unable to find a relation between the functionality of the | GR | and the development of NRDS. |
| 99207658 | se of allergic reaction. The action of glucocorticosteroids is mediated through | glucocorticoid receptors | present in the cellular cytoplasm. When activated, glucocorticoid receptors for |
| 99207658 | ugh glucocorticoid receptors present in the cellular cytoplasm. When activated, | glucocorticoid receptors | form a dimer and bind to DNA after migration into the nucleus. Interaction to D |
| 99207658 | in the transcription rate, leading to either gene induction or gene repression. | Glucocorticoid receptors | are also able to interact with transcriptional factors such as AP-1 ( activator |
| 99294118 | Binding characteristics of the | glucocorticoid receptor | in peripheral blood lymphocytes in multiple sclerosis. Although the exact etiol |
| 99294118 | uitary-adrenal system in a substantial proportion of patients. We characterized | glucocorticoid receptor | ( GR ) binding in peripheral blood lymphocytes from 39 MS patients and 14 age- |
| 99294118 | substantial proportion of patients. We characterized glucocorticoid receptor ( | GR | ) binding in peripheral blood lymphocytes from 39 MS patients and 14 age- and s |
| 99294118 | apacity, using a whole-cell binding assay with [3H]dexamethasone as the ligand. | GR | binding parameters did not differ significantly between patients ( Kd 8.98 +/- |
| 99294118 | rse, duration or severity of disease, or prior steroid treatments was detected. | GR | binding parameters were analyzed in relation to the results of the combined dex |
| 99294118 | s. While controls showed a moderate correlation between binding affinity of the | GR | in lymphocytes and regulatory function at the hypothalamic level, the patients |
| 99294118 | suggest that the physiological relationship between binding and function of the | glucocorticoid receptor | is disturbed in MS. |
| 96437028 | tic-specific transcript directly regulated by the retinoic acid receptor alpha. | Retinoic acid | ( RA ) -induced maturation mediated by the retinoic acid receptor alpha ( RAR a |
| 96437028 | nscript directly regulated by the retinoic acid receptor alpha. Retinoic acid ( | RA | ) -induced maturation mediated by the retinoic acid receptor alpha ( RAR alpha |
| 96437028 | fferential hybridization analysis of a cDNA library constructed from the murine | RA | -inducible MPRO promyelocyte cell line to identify immediate-early genes induced |
| 96437028 | ucible MPRO promyelocyte cell line to identify immediate-early genes induced by | RA | during granulocytic differentiation. E3, one of nine sequences identified, was |
| 96437028 | diate-early manner, with transcript levels peaking after 60 minutes exposure to | RA | . E3 transcripts were RA-inducible in HL60 cells, but not in an RA-resistant sub |
| 96437028 | transcript levels peaking after 60 minutes exposure to RA. E3 transcripts were | RA | -inducible in HL60 cells, but not in an RA-resistant subclone, HL60R, that harbo |
| 96437028 | s exposure to RA. E3 transcripts were RA-inducible in HL60 cells, but not in an | RA | -resistant subclone, HL60R, that harbors a mutated RAR alpha gene. However, when |
| 96437028 | when HL60R cells were transduced with a functional copy of the RAR alpha gene, | RA | induced a 10-fold increase in E3 mRNA levels. E3 transcripts are present in the |
| 96437028 | n expressed in myeloid cells. The murine E3 promoter harbors a single bipartite | retinoic acid | response element which in transient transfection assays conferred RA sensitivit |
| 96437028 | retinoic acid response element which in transient transfection assays conferred | RA | sensitivity. These results indicate that E3 is a hematopoietic-specific gene th |
| 97028169 | Dual action of | retinoic acid | on human embryonic / fetal hematopoiesis: blockade of primitive progenitor prol |
| 97028169 | investigated the role of all-trans retinoic acid ( ATRA ) and its isomer 9-cis | RA | in FL hematopoiesis. Both compounds modulate the growth of purified FL HPCs, wh |
| 97028169 | of the HPC differentiation program to the granulopoietic pathway ( rather than | RA | -induced down-modulation of multipotent /erythroid / monocytic HPC growth couple |
| 97028169 | tic HPC growth coupled with recruitment of granulocytic HPCs ) . ATRA and 9-cis | RA | also exert their effect on the proliferation of primitive HPCs ( high-prolifera |
| 97028169 | anulocytic differentiation. Altogether, these results suggest that ATRA / 9-cis | RA | may play a key role in FL hematopoiesis via a dual effect hypothetically mediat |
| 99408303 | Neutrophil maturation and the role of | retinoic acid | . Neutrophil maturation occurs in well defined morphological stages that correla |
| 99408303 | y a role in terminal neutrophil maturation, including the vitamin A derivative, | retinoic acid | . Retinoic acid can directly modulate gene expression via binding to its nuclear |
| 99408303 | minal neutrophil maturation, including the vitamin A derivative, retinoic acid. | Retinoic acid | can directly modulate gene expression via binding to its nuclear receptors, whi |
| 99408303 | ceptors, which can, in turn, activate transcription of target genes. A role for | retinoic acid | during neutrophil maturation has been suggested from a variety of sources. Here |
| 96085174 | of Jak 1, Jak 3 and STAT 5 proteins in murine T cells. The activation of Janus | protein tyrosine kinases | ( Jak ) and STAT ( signal transducer and activator of transcription ) proteins |
| 97054651 | own to be directly involved in mediating CD40-dependent signals. The use of the | protein tyrosine kinase | ( PTK ) -specific inhibitor herbimycin A dramatically decreased cellular prolif |
| 97054651 | d in mediating CD40-dependent signals. The use of the protein tyrosine kinase ( | PTK | ) -specific inhibitor herbimycin A dramatically decreased cellular proliferatio |
| 97468093 | ivity of the enzyme appear to be affected by pretreatment of the cells with the | protein tyrosine kinase | inhibitor genistein, which is known to prevent the association of ISGF3 compone |
| 99228708 | LPS-Induced NF-kappa B activation and TNF-alpha release in human monocytes are | protein tyrosine kinase | dependent and protein kinase C independent. BACKGROUND: Tumor necrosis factor a |
| 99228708 | revious studies have implicated activation of both protein kinase C ( PKC ) and | protein tyrosine kinases | ( PTK ) in LPS-induced NF-kappa B activation and TNF-alpha production. We hypot |
| 99228708 | ated activation of both protein kinase C ( PKC ) and protein tyrosine kinases ( | PTK | ) in LPS-induced NF-kappa B activation and TNF-alpha production. We hypothesize |
| 99228708 | tion and TNF-alpha production. We hypothesized that inhibition of either PKC or | PTK | would decrease LPS-induced NF-kappa B DNA binding and TNF-alpha release in huma |
| 99228708 | , a specific pan-PKC inhibitor bisindolylmaleimide ( Bis ) , or an inhibitor of | PTK | genistein ( Gen ) . TNF-alpha release in culture supernatants was measured by a |
| 99228708 | h Bis had no effect on LPS-induced NF-kappa B DNA binding or TNF-alpha release. | PTK | inhibition with Gen attenuated both LPS-induced NF-kappa B DNA binding and TNF- |
| 99228708 | are independent of PKC activity. Furthermore, our results provide evidence that | PTK | plays a role in LPS-induced NF-kappa B activation and TNF-alpha release in huma |
| 99356019 | -release of fibre-exposed monocytes increases inflammatory cytokine-mRNA level, | protein tyrosine kinase | and NF-kappa B activity in co-cultured bronchial epithelial cells ( BEAS-2B ) . |
| 95202809 | ectin by tumor necrosis factor-alpha ( TNF ) is mediated by mobilization of the | transcription factor nuclear factor-kappa B | ( NF-kappa B ) . Since salicylates have been reported to inhibit NF-kappa B act |
| 95332324 | grin ligation leads to nuclear translocation of the p50 and p65 subunits of the | NF-kappa B transcription factor | , to activation of a reporter gene driven by a promoter containing NF-kappa B si |
| 97445683 | Rel / | NF-kappa B transcription factors | and the control of apoptosis. The process of apoptosis is used to eliminate unw |
| 97445683 | ific fashion. Recent work from several laboratories has demonstrated that Rel / | NF-kappa B transcription factors | regulate apoptosis in many cell types. In most cells, Rel / NF-kappa B transcri |
| 97445683 | anscription factors regulate apoptosis in many cell types. In most cells, Rel / | NF-kappa B transcription factors | appear to mediate survival signals that protect cells from apoptosis; however, |
| 98230439 | ment binding ( ATF / CREB ) binding site ( located between the LEF-1 and distal | NF-kappa B transcription factor | binding sites ) that we identified in previous studies of the HIV-1 LTR. These |
| 99201482 | in part, due to the ability of HTB and triflusal to block the activation of the | transcription factor nuclear factor-kappa B | to a higher extent than aspirin and sodium salicylate. Thus, in addition to inh |
| 90376424 | Cell-specific differences in activation of NF-kappa B regulatory elements of | human immunodeficiency virus | and beta interferon promoters by tumor necrosis factor. Three aspects of the in |
| 90376424 | r necrosis factor. Three aspects of the involvement of tumor necrosis factor in | human immunodeficiency virus | ( HIV ) pathogenesis were examined. Tumor necrosis factor alpha ( TNF-alpha ) m |
| 90376424 | s of the involvement of tumor necrosis factor in human immunodeficiency virus ( | HIV | ) pathogenesis were examined. Tumor necrosis factor alpha ( TNF-alpha ) mRNA pr |
| 90376424 | erase chain reaction amplification in monocytic U937 cells and in a chronically | HIV | infected U937 cell line ( U9-IIIB ) . TNF-alpha RNA was undetectable in U937 ce |
| 90376424 | vel of TNF-alpha RNA in U9-IIIB cells compared with U937 cells, suggesting that | HIV | -infected monocytic cells produced higher levels of TNF-alpha than did normal ce |
| 90376424 | loramphenicol acetyltransferase plasmids linked to regulatory elements from the | HIV | long terminal repeat ( LTR ) and the beta interferon promoter. In U937 and Jurk |
| 90376424 | were inducible by both agents. TNF-alpha was able to increase expression of the | HIV | LTR in T cells, but in monocytic cells, TNF-alpha did not induce the HIV LTR ab |
| 90376424 | of the HIV LTR in T cells, but in monocytic cells, TNF-alpha did not induce the | HIV | LTR above a constitutive level of activity. This level of NF-kappa B-independen |
| 90376424 | tiplication, since TNF-alpha treatment had no effect on the kinetics of de novo | HIV | type 1 ( HIV-1 ) infection and viral RNA production in U937 cells. However, in |
| 92052106 | Negative regulation of | human immunodeficiency virus | type 1 expression in monocytes: role of the 65-kDa plus 50-kDa NF-kappa B dimer |
| 92052106 | cells can provide a reservoir for viral production in vivo, their regulation of | human immunodeficiency virus | type 1 ( HIV-1 ) transcription can be either latent, restricted, or productive. |
| 92052106 | ne expression have not been molecularly defined. In THP-1 cells with restricted | HIV | expression, there is an absence of DNA-protein binding complex formation with t |
| 95000924 | of HIV-1 Nef expression in activation pathways in CD4+ T cells. The role of the | human immunodeficiency virus | ( HIV-1 ) Nef protein in T cell activation pathways was investigated using a Ju |
| 98104459 | and RelA, and to bind with higher affinity to the consensus kappa B site in the | HIV | long terminal repeat. The second complex contained RelA, and exhibited higher a |
| 98104459 | ined RelA, and exhibited higher affinity towards the ICAM-1 kappa B than to the | HIV | kappa B site. The glucocorticoid receptor was shown to repress activity of both |
| 98230439 | Human immunodeficiency virus | type 1 long terminal repeat quasispecies differ in basal transcription and nucl | |
| 99007236 | ific genes. Multiple cellular DNA-binding transcription factors are required by | HIV | type 1 for RNA synthesis. Two pyrrole-imidazole polyamides were designed to bin |
| 99007236 | hetic ligands specifically inhibit DNA-binding of each transcription factor and | HIV | type 1 transcription in cell-free assays. When used in combination, the polyami |
| 99146379 | tokine ( chemokine ) important in the generation of inflammatory infiltrate and | human immunodeficiency virus | entry into immune cells. RANTES is expressed late ( 3-5 days ) after activation |
| 93321228 | Costimulation of cAMP and | protein kinase C | pathways inhibits the CD3-dependent T cell activation and leads to a persistent |
| 93321228 | anscription factor. The effects mediated by a combined stimulation of cAMP -and | protein kinase C | ( PKC ) -dependent pathways have been investigated in different cellular system |
| 93321228 | The effects mediated by a combined stimulation of cAMP -and protein kinase C ( | PKC | ) -dependent pathways have been investigated in different cellular systems, and |
| 94209654 | inducer of Fos kinase activity in all of the above populations, suggesting that | PKC | plays a role in the regulation of this enzyme. Fos kinase phosphorylates c-Fos |
| 94209654 | t from other identified serine / threonine kinases, including protein kinase A, | protein kinase C | , casein kinase II, MAP kinases, p70S6K and p90RSK. Fos kinase was purified by a |
| 97054651 | system was used to examine the role of different signal transduction elements. | Protein kinase C | ( PKC ) depletion generated by a long-term phorbol 12 myristate 13-acetate trea |
| 97054651 | examine the role of different signal transduction elements. Protein kinase C ( | PKC | ) depletion generated by a long-term phorbol 12 myristate 13-acetate treatment |
| 97054651 | that both p65 ( RelA ) and c-Rel were present in CD40-stimulated B cells. While | PKC | depletion did not alter the NF-kappa B level, treatment of B lymphocytes with H |
| 99228708 | TNF-alpha release in human monocytes are protein tyrosine kinase dependent and | protein kinase C | independent. BACKGROUND: Tumor necrosis factor alpha ( TNF-alpha ) is an import |
| 99228708 | B ) and TNF-alpha release. Previous studies have implicated activation of both | protein kinase C | ( PKC ) and protein tyrosine kinases ( PTK ) in LPS-induced NF-kappa B activati |
| 99228708 | release. Previous studies have implicated activation of both protein kinase C ( | PKC | ) and protein tyrosine kinases ( PTK ) in LPS-induced NF-kappa B activation and |
| 99228708 | activation and TNF-alpha production. We hypothesized that inhibition of either | PKC | or PTK would decrease LPS-induced NF-kappa B DNA binding and TNF-alpha release |
| 99228708 | / threonine protein kinase inhibitor staurosporine ( Stauro ) , a specific pan- | PKC | inhibitor bisindolylmaleimide ( Bis ) , or an inhibitor of PTK genistein ( Gen |
| 99228708 | nhibition inhibited NF-kappa B activation and TNF-alpha release, while specific | PKC | inhibition with Bis had no effect on LPS-induced NF-kappa B DNA binding or TNF- |
| 99228708 | B DNA binding and TNF-alpha production in human monocytes. Direct activation of | PKC | with PMA induced both NF-kappa B activation and TNF-alpha production by human m |
| 99228708 | -kappa B activation and TNF-alpha release in human monocytes are independent of | PKC | activity. Furthermore, our results provide evidence that PTK plays a role in LP |
| 94107268 | ascade of Jurkat human leukaemic T-cells. Pervanadate induced activation of the | tyrosine kinases | lck and fyn ( 4- and 3-fold respectively ) and a dramatic increase in tyrosine |
| 95332324 | possible signaling role for the Syk tyrosine kinase. Activation of cytoplasmic | tyrosine kinases | is an important aspect of signal transduction mediated by integrins. In the hum |
| 95332324 | r immediate-early genes, including the cytokine interleukin ( IL ) -1 beta. The | tyrosine kinase | inhibitors genistein and herbimycin A block both integrin-mediated tyrosine pho |
| 97054651 | Tyrosine kinase | and cAMP-dependent protein kinase activities in CD40-activated human B lymphocy |
| 90376424 | on amplification in monocytic U937 cells and in a chronically HIV infected U937 | cell line | ( U9-IIIB ) . TNF-alpha RNA was undetectable in U937 cells, whereas a low const |
| 91190842 | t, CCRF-CEM ) and not in mature B cells ( JY, Namalwa ) or nonlymphoid ( HeLa ) | cell lines | . A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 |
| 94209654 | normal human T lymphocytes and in response to IL-6 and anti-IgM in the human B | cell lines | AF10 and Ramos, respectively. The phorbol ester, PMA, was also a potent inducer |
| 94238882 | e and cytokine expression in human peripheral blood monocytes and the monocytic | cell line | THP-1 after stimulation with mycoplasma-derived material MDHM. Mycoplasma ferme |
| 94238882 | . The induced expression of IL-1 beta and TNF alpha mRNA in the monocytic THP-1 | cell line | increased as quickly as in primary cells. In contrast to PBMo, THP-1 and 14 oth |
| 94238882 | s. In contrast to PBMo, THP-1 and 14 other monocytic / myeloid leukemia-derived | cell lines | did not secrete measurable amounts of the cytokines upon treatment with MDHM. I |
| 95000924 | Nef protein in T cell activation pathways was investigated using a Jurkat CD4+ | cell line | stably transfected with a Nef expression vector. Secretion of IL-2 and TNF-alph |
| 95036290 | ession, we investigated tal-1 chromatin structure in erythroid / megakaryocytic | cell lines | and in T-cell lines either with or without tal-1 rearrangements. Tal-1 transcri |
| 95036290 | ls, and methylated de novo on transcriptionally inactive alleles in established | cell lines | . Five major DNase-I hypersensitive sites ( HS ) were mapped in the tal-1 locus. |
| 95036290 | us. HS I, IV, and V were exclusively observed in the erythroid / megakaryocytic | cell lines | that express tal-1 from the promoters 1a and 1b. HS II was weak in hematopoieti |
| 95036290 | hat express tal-1 from the promoters 1a and 1b. HS II was weak in hematopoietic | cell lines | , absent in Hela, and greatly enhanced in Jurkat, suggesting that this region mi |
| 95036290 | s region might be implicated in the cis-activation of tal-1 promoter 1b in this | cell line | . HS III was weak in HEL and Jurkat, and greatly enhanced in DU528, a T-cell lin |
| 95261059 | U.1 expression is maintained at stable levels during differentiation of myeloid | cell lines | U937 and HL-60 to monocytic and neutrophilic cells. PU.1 is expressed at highes |
| 95261059 | to PU.1, significant levels of Spi-B mRNA and protein are found only in some B- | cell lines | and spleen but are not found in myeloid cell lines, neutrophils, or macrophages |
| 95261059 | ein are found only in some B-cell lines and spleen but are not found in myeloid | cell lines | , neutrophils, or macrophages. In vitro translated Spi-B protein can bind to PU. |
| 95332324 | ant aspect of signal transduction mediated by integrins. In the human monocytic | cell line | THP-1, either integrin-dependent cell adhesion to fibronectin or ligation of be |
| 96038813 | showed that B4-2 is not a lymphoid specific gene and is expressed in a hepatoma | cell line | and also weakly transcribed or absent in a variety of other cells. A polyclonal |
| 96437028 | is of a cDNA library constructed from the murine RA-inducible MPRO promyelocyte | cell line | to identify immediate-early genes induced by RA during granulocytic differentia |
| 97303223 | k1 ) activation, STAT6 activation, and Cepsilon germline transcripts in human B | cell line | BJAB. Disruption of the Jak1-binding proline-rich Box1 region of IL-4Ralpha abo |
| 98104462 | he human TNF promoter () revealed that in tolerant cells of the human monocytic | cell line | Mono Mac 6 there is a predominance of p50p50 of NF-kappa B. We now show that a |
| 98104462 | . The same is true for nuclear extracts taken from the murine P388D1 macrophage | cell line | when tested with the -516 motif of the murine TNF promoter () . Here the wild t |
| 98230439 | which varied significantly from the LAI LTR in U-373 MG cells ( an astrocytoma | cell line | ) as well as in Jurkat cells ( a CD4-positive lymphocyte cell line ) . While LT |
| 98230439 | astrocytoma cell line ) as well as in Jurkat cells ( a CD4-positive lymphocyte | cell line | ) . While LTRs which demonstrated the highest activities in U-373 MG cells also |
| 98406200 | xpression of Rta is also sufficient for disruption of latency in a permissive B- | cell line | . In HH514-16 cells, transfection of Rta leads to synthesis of ZEBRA, viral DNA |
| 99083144 | Effect of environmental estrogens on IL-1beta promoter activity in a macrophage | cell line | . Environmental estrogens or estrogen disrupters have recently received a great |
| 99083144 | the modulation of the interleukin-1beta ( IL-1beta ) gene in a model monocytic | cell line | , hER + IL-1beta-CAT+. This cell line stably transfected with the human estrogen |
| 99083144 | eta ( IL-1beta ) gene in a model monocytic cell line, hER + IL-1beta-CAT+. This | cell line | stably transfected with the human estrogen receptor, and an IL-1beta promoter c |
| 99102590 | y, by in vitro stimulation with the latently infected autologous lymphoblastoid | cell line | ( LCL ) , has important limitations. First, it gives no information on memory t |
| 93321228 | Costimulation of cAMP and protein kinase C pathways inhibits the CD3-dependent | T cell activation | and leads to a persistent expression of the AP-1 transcription factor. The effe |
| 94107268 | Induction of tyrosine phosphorylation and | T-cell activation | by vanadate peroxide, an inhibitor of protein tyrosine phosphatases. Rapid tyro |
| 95000924 | T cells. The role of the human immunodeficiency virus ( HIV-1 ) Nef protein in | T cell activation | pathways was investigated using a Jurkat CD4+ cell line stably transfected with |
| 96184791 | -13 P element site significantly reduced IL-13 promoter activity in response to | T-cell activation | . Oligonucleotides containing the IL-13 or IL-4 P element sites specifically bou |
| 96322726 | y in mononuclear cell cultures and T cells by the cyclic AMP signaling pathway. | Activation of T cells | results in a cascade of gene activation and subsequent proliferation and differ |
| 98001571 | Blockade of | T-cell activation | by dithiocarbamates involves novel mechanisms of inhibition of nuclear factor o |
| 98001571 | ( IL-2 ) synthesis and membrane expression of antigens which are induced during | T-cell activation | . This inhibition, which occurred with a parallel activation of c-Jun transactiv |
| 98001571 | icated that pyrrolidine DTC ( PDTC ) prevented NF-kappa B, and NFAT DNA-binding | activity in T cells | stimulated with either phorbol myristate acetate plus ionophore or antibodies a |
| 98090689 | clearly elucidated. We have hypothesized that such defects in fetal / neonatal | T-cell activation | may be due to lack of expression of the transcriptional regulatory elements req |
| 98090689 | e to lack of expression of the transcriptional regulatory elements required for | T-cell activation | . We used reverse transcriptase-polymerase chain reaction to examine both fetal |
| 98090689 | al cord bloods for mRNA expression of three transcription factors implicated in | T-cell activation | : c-jun, c-fos, and NF kappa B ( p50 subunit ) . We demonstrate that mRNAs for a |
| 98380286 | n genes are constitutively expressed. To investigate processes related to B and | T cell activation | , the gene expression of stimulated and nonstimulated Ramos and Jurkat cells was |
| 99081619 | Our studies show that the mechanism of IL-10 regulation of quiescent CD4 ( + ) | T-cell activation | is mainly by blocking induction of IL-2 that is critical to downregulation of p |
| 99081619 | is critical to downregulation of p27 ( Kip1 ) and upregulation of D cyclins in | T-cell activation | and entry into the cell cycle. |
| 99228708 | LPS-Induced NF-kappa B activation and | TNF-alpha release in human monocytes | are protein tyrosine kinase dependent and protein kinase C independent. BACKGRO |
| 99228708 | tion of either PKC or PTK would decrease LPS-induced NF-kappa B DNA binding and | TNF-alpha release in human monocytes | . MATERIALS AND METHODS: Human monocytes were stimulated with PMA ( 50 ng / ml ) |
| 99228708 | horetic mobility shift assay. RESULTS: LPS increased NF-kappa B DNA binding and | TNF-alpha release in human monocytes | . Nonspecific protein kinase inhibition inhibited NF-kappa B activation and TNF- |
| 99228708 | . CONCLUSIONS: These results suggest that LPS-induced NF-kappa B activation and | TNF-alpha release in human monocytes | are independent of PKC activity. Furthermore, our results provide evidence that |
| 99228708 | provide evidence that PTK plays a role in LPS-induced NF-kappa B activation and | TNF-alpha release in human monocytes | and thus could be a potential therapeutic target in inflammatory states. |
| 90140708 | tive helix-loop-helix motifs and each possesses a distinct domain that dictates | transcription activation | . |
| 91190842 | n of T cells into functionally diverse subpopulations is controlled in part, by | transcriptional activation | and silencing; however, little is known in detail about the proteins that influ |
| 91190842 | positioned in one or more copies upstream of a heterologous promoter. Thus, the | transcriptional activity | of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) tran |
| 92135145 | ne the roles of these two factors, which bind to the same kappa B enhancers, in | transcription activation | we have prepared somatic cell hybrids between IARC 301.5 and a murine myeloma. |
| 93204975 | Transcriptional activation | of human zeta 2 globin promoter by the alpha globin regulatory element ( HS-40 | |
| 93204975 | of nuclear factor binding in vivo at the HS-40 region. These data suggest that | transcriptional activation | of human embryonic zeta 2 globin gene and the fetal / adult alpha globin genes |
| 95222739 | Transcriptional activity | of core binding factor-alpha ( AML1 ) and beta subunits on murine leukemia viru | |
| 95222739 | ic determinants of the ability of this virus to induce T-cell lymphomas and the | transcriptional activity | of the viral long terminal repeat in T lymphocytes. CBF consists of two subunit |
| 95222739 | gh the core elements. Three different isoforms of CBF beta were also tested for | transcriptional activity | on the SL3 enhancer. The longest form, CBF beta-187, increased the transcriptio |
| 95222739 | CBF alpha 2-451 twofold in HeLa cells, although it had no effect in P19 cells. | Transcriptional activation | by CBF beta required binding to the CBF alpha subunit, as a form of CBF beta th |
| 96074632 | a labeled NF-kappa B DNA binding motif. Further, 1,25 ( OH ) 2D3 inhibited the | transcriptional activity | of NF-kappa B in Jurkat cells transiently transfected with a construct containi |
| 96079922 | 2 receptor activation are both linked to the Jak / Stat ( signal transducer and | activator of transcription | ) pathway. We investigated the ability of PRL and IL-2 to activate Stat protein |
| 96085174 | tion of Janus protein tyrosine kinases ( Jak ) and STAT ( signal transducer and | activator of transcription | ) proteins has recently been linked to the signal transduction mechanism of sev |
| 96184791 | d sequenced the human IL-13 gene, analyzed its 5'-flanking region for potential | transcriptional activation | elements, and examined its expression in nontransformed T-lineage cell populati |
| 96184791 | a segment with sequence homology to P elements of the IL-4 promoter involved in | transcriptional activation | in T cells. Mutation of the IL-13 P element site significantly reduced IL-13 pr |
| 96184791 | nucleotides containing the IL-13 or IL-4 P element sites specifically bound the | transcriptional activator | protein, nuclear factor-activated T cells, preformed ( NF-ATp ) , when incubate |
| 96239534 | Transcriptional activation | of RNA polymerase III-dependent genes by the human T-cell leukemia virus type 1 | |
| 96279111 | . We demonstrated that IL-9 gene expression is controlled, at least in part, by | transcriptional activation | . Transient expression of the luciferase reporter gene linked to serially delete |
| 96322726 | The regulation of transcription factors belonging to the signal transducer and | activator of transcription | ( STAT ) family was analyzed in PHA-activated mononuclear cells and in purified |
| 97207294 | and IRS-1 were phosphorylated. Additionally, we detected signal transducers and | activators of transcription | 6 ( STAT6 ) tyrosine phosphorylation and DNA binding activity in X-SCID B cells |
| 97324097 | Transcriptional activity | and constitutive nuclear localization of the ETS protein Elf-1. Elf-1 is a lymp | |
| 97324097 | fusion proteins revealed that the N-terminal 86 amino acids of Elf-1 contain a | transcriptional activation | domain, the activity of which is attenuated by an internal repression domain. F |
| 97456880 | element-binding complexes are not identical and may coordinately contribute to | transcriptional activity | . |
| 98400423 | R for erythroid cell development, dominant interfering mutant RXRs, lacking the | transcriptional activator | functions AF-1 and AF-2, or AF-2 only, or the entire DNA-binding domain, were i |
| 98406200 | ion of lytic cycle genes, including BRLF1. The BRLF1 product Rta functions as a | transcriptional activator | in both B lymphocytes and epithelial cells. However, Rta has recently been repo |
| 99386936 | cells and investigated the role of the signalsome proteins IKK-alpha, IKK-beta, | NF-kappa B-inducing kinase | ( NIK ) , IKK-gamma ( NF-kappa B essential modulator ) , and IKK complex-associ |
| 99386936 | le of the signalsome proteins IKK-alpha, IKK-beta, NF-kappa B-inducing kinase ( | NIK | ) , IKK-gamma ( NF-kappa B essential modulator ) , and IKK complex-associated p |
| 99386936 | ermore, our studies showed association of the IKK-alpha / beta heterodimer with | NIK | , Ikappa B-alpha and -epsilon in unstimulated cells. Exposure to LPS or TNF led |
| 99386936 | rance from and reassembly with the signalsome, whereas IKK-alpha, IKK-beta, and | NIK | remained complex-associated. NIK cannot phosphorylate Ikappa B-alpha directly, |
| 99386936 | e signalsome, whereas IKK-alpha, IKK-beta, and NIK remained complex-associated. | NIK | cannot phosphorylate Ikappa B-alpha directly, but it appears to be a functional |
| 99386936 | irectly, but it appears to be a functionally important subunit, because mutated | NIK | inhibited stimulus-induced kappa B-dependent transcription more effectively tha |
| 90376424 | ctivity of NF-kappa B-containing plasmids correlated directly with induction of | NF-kappa B DNA-binding | activity. Although the intact beta interferon promoter was only weakly stimulat |
| 96074632 | d upon incubation of nuclear extracts from activated lymphocytes with a labeled | NF-kappa B DNA binding | motif. Further, 1,25 ( OH ) 2D3 inhibited the transcriptional activity of NF-ka |
| 99228708 | We hypothesized that inhibition of either PKC or PTK would decrease LPS-induced | NF-kappa B DNA binding | and TNF-alpha release in human monocytes. MATERIALS AND METHODS: Human monocyte |
| 99228708 | n ( Gen ) . TNF-alpha release in culture supernatants was measured by an ELISA. | NF-kappa B DNA binding | was evaluated by electrophoretic mobility shift assay. RESULTS: LPS increased N |
| 99228708 | g was evaluated by electrophoretic mobility shift assay. RESULTS: LPS increased | NF-kappa B DNA binding | and TNF-alpha release in human monocytes. Nonspecific protein kinase inhibition |
| 99228708 | ha release, while specific PKC inhibition with Bis had no effect on LPS-induced | NF-kappa B DNA binding | or TNF-alpha release. PTK inhibition with Gen attenuated both LPS-induced NF-ka |
| 99228708 | nding or TNF-alpha release. PTK inhibition with Gen attenuated both LPS-induced | NF-kappa B DNA binding | and TNF-alpha production in human monocytes. Direct activation of PKC with PMA |
| 97376857 | olvement of Rel, Fos, and Jun proteins in binding activity to the IL-2 promoter | CD28 response element | / AP-1 sequence in human T cells. CD28 is an important costimulatory molecule i |
| 97376857 | , other work has not supported this conclusion. Recent studies suggest that the | CD28 response element | ( CD28RE ) does not function independently but works instead in conjunction wit |
| 97376857 | ported this conclusion. Recent studies suggest that the CD28 response element ( | CD28RE | ) does not function independently but works instead in conjunction with the adj |
| 97376857 | ypothesis is confirmed here. Also in the current study, binding activity to the | CD28RE | / AP-1 sequence of the IL-2 promoter is evaluated. Although four specific compl |
| 97376857 | binding to this sequence, only one of these complexes is specific for both the | CD28RE | and the adjacent AP-1 site. Of the NF-kappa B / Rel family members tested, this |
| 97376857 | and the adjacent AP-1 site. Of the NF-kappa B / Rel family members tested, this | CD28RE | / AP-1-specific complex contains predominantly c-Rel, despite the fact that bot |
| 97376857 | ntly c-Rel, despite the fact that both p50 and RelA can efficiently bind to the | CD28RE | . c-Fos and c-Jun are also found in this CD28RE / AP-1-specific complex. These d |
| 97376857 | RelA can efficiently bind to the CD28RE. c-Fos and c-Jun are also found in this | CD28RE | / AP-1-specific complex. These data indicate that functional complexes encompas |
| 97376857 | ic complex. These data indicate that functional complexes encompassing both the | CD28RE | and the AP-1-binding sites influence IL-2 promoter activity in CD28-costimulate |
| 99168986 | Interferon-alpha | activates multiple STAT proteins and upregulates proliferation-associated IL-2R | |
| 99168986 | s proliferation-associated IL-2Ralpha, c-myc, and pim-1 genes in human T cells. | Interferon-alpha | ( IFN-alpha ) is a pleiotropic cytokine that has antiviral, antiproliferative, |
| 99168986 | ociated IL-2Ralpha, c-myc, and pim-1 genes in human T cells. Interferon-alpha ( | IFN-alpha | ) is a pleiotropic cytokine that has antiviral, antiproliferative, and immunore |
| 99168986 | roliferative, and immunoregulatory functions. There is increasing evidence that | IFN-alpha | has an important role in T-cell biology. We have analyzed the expression of IL- |
| 99168986 | eukin-2 ( IL-2 ) -induced T-cell proliferation. Treatment of T lymphocytes with | IFN-alpha | , IL-2, IL-12, and IL-15 upregulated IL-2Ralpha, c-myc, and pim-1 gene expressio |
| 99168986 | L-2, IL-12, and IL-15 upregulated IL-2Ralpha, c-myc, and pim-1 gene expression. | IFN-alpha | also sensitized T cells to IL-2-induced proliferation, further suggesting that |
| 99168986 | also sensitized T cells to IL-2-induced proliferation, further suggesting that | IFN-alpha | may be involved in the regulation of T-cell mitogenesis. When we analyzed the n |
| 99168986 | -2Ralpha, pim-1, and IRF-1 GAS elements after cytokine stimulation, we observed | IFN-alpha | -induced binding of STAT1, STAT3, and STAT4, but not STAT5 to all of these eleme |
| 99168986 | inding of STAT1, STAT3, and STAT4, but not STAT5 to all of these elements. Yet, | IFN-alpha | was able to activate binding of STAT5 to the high-affinity IFP53 GAS site. IFN- |
| 99168986 | lpha was able to activate binding of STAT5 to the high-affinity IFP53 GAS site. | IFN-alpha | enhanced tyrosine phosphorylation of STAT1, STAT3, STAT4, STAT5a, and STAT5b. I |
| 99168986 | ced STAT5 binding to the GAS elements. Taken together, our results suggest that | IFN-alpha | , IL-2, IL-12, and IL-15 have overlapping activities on human T cells. These fin |
| 99168986 | ng activities on human T cells. These findings thus emphasize the importance of | IFN-alpha | as a T-cell regulatory cytokine. |
| 90110496 | Anti-Ro ( SSA ) autoantibodies are associated with | T cell receptor | beta genes in systemic lupus erythematosus patients. Several of the heterogeneo |
| 90110496 | molecules present antigen to T cell receptors ( TCRs ) , we have searched for a | TCR | gene associated with the production of anti-Ro ( SSA ) antibodies. A pair of re |
| 90110496 | iction fragment length polymorphisms ( RFLPs ) , one of which hybridizes to the | TCR | constant region C beta 1 and the other to the C beta 2 gene, has been identifie |
| 90110496 | tified, suggesting these may be genotypic markers for an extended region of the | TCR | beta locus. This RFLP pair occurs in 76% of patients with Ro ( SSA ) precipitin |
| 90110496 | Ps are not disease susceptibility markers, but rather are important markers for | TCR | genes whose products are involved in the production of anti-Ro ( SSA ) antibodi |
| 91190842 | ation of TCF-1 alpha, a T-cell-specific transcription factor that activates the | T-cell receptor | C alpha gene enhancer in a context-dependent manner. The differentiation of T c |
| 91190842 | s implicated in the activation of genes encoding a major component of the human | T-cell receptor | ( TCR ) . TCF-1 alpha, originally identified and purified through its binding s |
| 91190842 | e activation of genes encoding a major component of the human T-cell receptor ( | TCR | ) . TCF-1 alpha, originally identified and purified through its binding sites o |
| 91190842 | genes expressed at significantly earlier stages of T-cell development than the | TCR | alpha gene ( e.g., p56 lck and CD3 delta ) . Sequences related to the TCF-1 alp |
| 91190842 | related to the TCF-1 alpha binding motif ( 5'--3' ) are also found in the human | TCR | delta ( and possibly TCR beta ) enhancers. Southwestern and gel renaturation ex |
| 91190842 | a binding motif ( 5'--3' ) are also found in the human TCR delta ( and possibly | TCR | beta ) enhancers. Southwestern and gel renaturation experiments with the use of |
| 91190842 | JY, Namalwa ) or nonlymphoid ( HeLa ) cell lines. A small 95-bp fragment of the | TCR | alpha control region that contains the TCF-1 alpha binding site juxtaposed betw |
| 93321228 | on of both pathways T lymphocytes became refractory to activation via the CD3 / | T cell receptor | ( TcR ) complex. T cells preincubated with phorbol 12-myristate 13-acetate ( PM |
| 93321228 | s T lymphocytes became refractory to activation via the CD3 / T cell receptor ( | TcR | ) complex. T cells preincubated with phorbol 12-myristate 13-acetate ( PMA ) an |
| 93321228 | IL-2R ) . Analysis of intracellular Ca2+ mobilization suggested that the CD3 / | TcR | -dependent signal transduction was impaired in PMA / Bt2cAMP-treated cells. Rema |
| 93321228 | ment each other in regulating gene expression and, conversely, downregulate the | TcR | transduction mechanisms. |
| 98001571 | h either phorbol myristate acetate plus ionophore or antibodies against the CD3- | T-cell receptor | complex and simultaneously activated the binding of AP-1. Furthermore, PDTC dif |
| 99369970 | Cutting edge: | TCR | stimulation by antibody and bacterial superantigen induces Stat3 activation in |
| 99369970 | l superantigen induces Stat3 activation in human T cells. Recent data show that | TCR | / CD3 stimulation induces activation of Stat5 in murine T cells. Here, we show |
| 99369970 | sphorylation of Stat3 in human CD4+ T cells. Moreover, we provide evidence that | TCR | / CD3 and IL-2 induce Stat3 activation via distinct signaling pathways. |
| 99146379 | RFLAT-1 | : a new zinc finger transcription factor that activates RANTES gene expression i | |
| 99146379 | ied the first "late" T lymphocyte associated transcription factor and named it " | RANTES Factor of Late Activated T Lymphocytes-1 | " ( RFLAT-1 ) . RFLAT-1 is a novel, phosphorylated, zinc finger transcription fa |
| 99146379 | ription factor and named it "RANTES Factor of Late Activated T Lymphocytes-1" ( | RFLAT-1 | ) . RFLAT-1 is a novel, phosphorylated, zinc finger transcription factor that i |
| 99146379 | or and named it "RANTES Factor of Late Activated T Lymphocytes-1" ( RFLAT-1 ) . | RFLAT-1 | is a novel, phosphorylated, zinc finger transcription factor that is expressed |
| 99146379 | e Rel proteins play the dominant role in RANTES gene expression in fibroblasts, | RFLAT-1 | is a strong transactivator for RANTES in T cells. |
| 93321228 | erentiation. In this report, we show that upon the stimulation of both pathways | T lymphocytes | became refractory to activation via the CD3 / T cell receptor ( TcR ) complex. |
| 94107268 | llular proteins is a crucial event in the transduction of activation signals to | T-lymphocytes | . The regulatory role of protein tyrosine phosphatases ( PTPases ) in this proce |
| 94107268 | e c-fos gene and accumulation of its mRNA as well as several other hallmarks of | T-lymphocyte | activation such as surface expression of the CD69 antigen and the interleukin 2 |
| 94107268 | a crucial role in the negative regulation of signal transduction culminating in | T-lymphocyte | activation. Moreover, induction of tyrosine phosphorylation appears sufficient |
| 94209654 | ctivated after ligation of the CD3 and CD2 receptors in Jurkat and normal human | T lymphocytes | and in response to IL-6 and anti-IgM in the human B cell lines AF10 and Ramos, |
| 95166251 | e, transcripts of PEBP2 alpha A and mouse AML1 / PEBP2 alpha B were detected in | T lymphocytes | in the thymuses from day 16 embryos and newborns, as well as 4-week-old adult m |
| 95222739 | lymphomas and the transcriptional activity of the viral long terminal repeat in | T lymphocytes | . CBF consists of two subunits, a DNA binding subunit, CBF alpha, and a second s |
| 95222739 | subunits. They also provided support for the hypothesis that CBF is a factor in | T lymphocytes | that is responsible for recognition of the SL3 cores. We also examined whether |
| 96079922 | Prolactin and interleukin-2 receptors in | T lymphocytes | signal through a MGF-STAT5-like transcription factor. The cell surface receptor |
| 96079922 | interleukin-2 ( IL-2 ) are structurally distinct, but share regulatory tasks in | T lymphocytes | . They can stimulate proliferation and activate transcription of over-lapping se |
| 96195006 | P inducibility of transcriptional repressor ICER in developing and mature human | T lymphocytes | [published erratum appears in Proc Natl Acad Sci U S A 1996 Jul 23;93 ( 15 ) :8 |
| 96195006 | opment in the human thymus and is retained by the majority of mature peripheral | T lymphocytes | . Here we show that elevated cAMP levels in T cells correlate with the expressio |
| 96239534 | nd cell extracts derived from human T-cell leukemia virus type 1-infected human | T lymphocytes | support higher levels of 5S rRNA and tRNA gene transcription than chromatin or |
| 96239534 | 5S rRNA and tRNA gene transcription than chromatin or extracts from uninfected | T lymphocytes | . The viral protein Tax was likely responsible for this higher level of class II |
| 97207294 | ned immunodeficiency. Interleukin-4 ( IL-4 ) is an important cytokine for B and | T lymphocyte | function and mediates its effects via a receptor that contains gammac. B cells |
| 97307577 | Abnormal | T lymphocyte | development induced by targeted overexpression of Ikappa B alpha. A role in thy |
| 97307577 | ct in maturation resulted in a transgene dose-dependent reduction in peripheral | T lymphocytes | , with the CD8 lineage being more severely affected. These data provide direct e |
| 97307577 | dence for the involvement of NF-kappa B / Rel family proteins in late stages of | T lymphocyte | development, coincident with positive and negative selection. |
| 97468093 | ase C gamma 1 overexpression and activation induced by interferon beta in human | T lymphocytes | : an ISGF3-independent response. Interferons exert their antiviral, antiprolifer |
| 97468093 | of the hydrolytic activity of phospholipase C gamma 1 ( PLC gamma 1 ) in human | T lymphocytes | by IFN-beta. The increased level of PLC gamma 1 becomes evident after 90 min of |
| 97468093 | revent the association of ISGF3 components. These results suggest that in human | T lymphocytes | IFN-beta can activate other transcription factor ( s ) distinct from ISGF3 to r |
| 99146379 | a new zinc finger transcription factor that activates RANTES gene expression in | T lymphocytes | . RANTES ( Regulated upon Activation, Normal T cell Expressed and Secreted ) is |
| 99146379 | ry into immune cells. RANTES is expressed late ( 3-5 days ) after activation in | T lymphocytes | . Using expression cloning, we identified the first "late" T lymphocyte associat |
| 99146379 | tion in T lymphocytes. Using expression cloning, we identified the first "late" | T lymphocyte | associated transcription factor and named it "RANTES Factor of Late Activated T |
| 99168986 | he expression of IL-2Ralpha, c-myc, and pim-1 genes in anti-CD3-activated human | T lymphocytes | . The induction of these genes is associated with interleukin-2 ( IL-2 ) -induce |
| 99168986 | ociated with interleukin-2 ( IL-2 ) -induced T-cell proliferation. Treatment of | T lymphocytes | with IFN-alpha, IL-2, IL-12, and IL-15 upregulated IL-2Ralpha, c-myc, and pim-1 |
| 91190842 | y of 57- to 53-kD proteins that are abundantly expressed in mature and immature | T-cell lines | ( Jurkat, CCRF-CEM ) and not in mature B cells ( JY, Namalwa ) or nonlymphoid ( |
| 91190842 | Tandem copies of this enhancer functioned synergistically in mature ( Jurkat ) | T-cell lines | as well as resting and activated immature ( CCRF-CEM ) T-cell lines. Mutation o |
| 91190842 | ( Jurkat ) T-cell lines as well as resting and activated immature ( CCRF-CEM ) | T-cell lines | . Mutation of the TCF-1 alpha binding site diminished enhancer activity and disr |
| 92135145 | ed KBF1, are constitutively expressed and localized in the nucleus of the human | T-cell line | IARC 301.5. In order to define the roles of these two factors, which bind to th |
| 95036290 | I hypersensitive sites are associated with TAL-1 transcription in erythroid and | T-cell lines | . The tal-1 gene, frequently activated in human T-cell acute lymphoblastic leuke |
| 95036290 | gated tal-1 chromatin structure in erythroid / megakaryocytic cell lines and in | T-cell lines | either with or without tal-1 rearrangements. Tal-1 transcription was shown to b |
| 95036290 | -1 rearrangements. Tal-1 transcription was shown to be monoallelic in Jurkat, a | T-cell line | that expresses tal-1 in the absence of apparent genomic alteration of the locus |
| 95036290 | cell line. HS III was weak in HEL and Jurkat, and greatly enhanced in DU528, a | T-cell line | that bears a t ( 1;14 ) and initiates tal-1 transcription within exon 4. These |
| 96079922 | investigated the ability of PRL and IL-2 to activate Stat proteins in different | T cell lines | . The DNA binding specificities, the reactivities toward Stat-specific antisera, |
| 96079922 | a, and the mol wt of IL-2 -and PRL-induced DNA-binding proteins in Nb2 and C196 | T cell lines | were investigated. A comparison with the Stat proteins induced by interferon-ga |
| 96279111 | L-9 ) gene expression in a human T cell leukemia virus type I-transformed human | T cell line | , C5MJ2, were investigated. We demonstrated that IL-9 gene expression is control |
| 99369970 | erine phosphorylation of Stat3 ( but not Stat5 ) in allogen-specific human CD4+ | T cell lines | . In contrast, IL-2 induces a rapid and transient tyrosine and serine phosphoryl |
| 95127261 | uction through its specific receptor ( the AhR ) and not through effects on the | estrogen receptor | . Both TCDD and estradiol induce extrathymic T-cell differentiation in the liver |
| 98089072 | Estrogen receptor | diminishes DNA-binding activities of chicken GATA-1 and-binding proteins. The e | |
| 98089072 | r diminishes DNA-binding activities of chicken GATA-1 and-binding proteins. The | estrogen receptor | ( ER ) repressed erythroid differentiation and erythroid-specific gene expressi |
| 98089072 | ding activities of chicken GATA-1 and-binding proteins. The estrogen receptor ( | ER | ) repressed erythroid differentiation and erythroid-specific gene expression. I |
| 98089072 | rythroid-specific gene expression. In this study, we investigated the effect of | ER | alpha ( referred to throughout as ER ) on DNA-binding activities of transcripti |
| 98089072 | this study, we investigated the effect of ER alpha ( referred to throughout as | ER | ) on DNA-binding activities of transcription factors involved in regulating the |
| 98089072 | hift assays, we found that in the presence of rabbit reticulocyte lysate, human | ER | reduced the binding activities of chicken immature erythrocyte nuclear extracte |
| 98089072 | hancer. In contrast, the binding activities of NF1 and Sp1 were not affected by | ER | . Binding of ER to an estrogen response element was enhanced by addition of rabb |
| 98089072 | rast, the binding activities of NF1 and Sp1 were not affected by ER. Binding of | ER | to an estrogen response element was enhanced by addition of rabbit reticulocyte |
| 98089072 | d by addition of rabbit reticulocyte lysate. This lysate was also necessary for | ER | to diminish the DNA-binding activity of GATA-1. These results suggest that addi |
| 98089072 | TA-1. These results suggest that additional factor ( s ) are necessary for full | ER | function. Both GATA-1 and-binding proteins are critical for the developmentally |
| 98089072 | binding activities of GATA-1 and-binding proteins is the mechanism by which the | ER | inhibits regulation of these genes. |
| 99083144 | ell line, hER + IL-1beta-CAT+. This cell line stably transfected with the human | estrogen receptor | , and an IL-1beta promoter construct fused to the CAT reporter gene allows us to |
| 99083144 | ic response. The activity of the mycotoxins appeared to be mediated through the | estrogen receptor | , since both the antiestrogens H1285 and ICI 182,780 effectively inhibited their |
| 99394774 | Gender and vascular reactivity. | Estrogen receptors | are found on vascular endothelial and smooth muscle cells; their expression is |
| 99394774 | smooth muscle cells; their expression is influenced by exposure to the hormone. | Estrogen receptors | influence non-genomic events, which are rapid in onset and genomic events, whic |
| 99394774 | iate vascular responses, genomic sex may influence and / or limit expression of | estrogen receptors | and therefore actions of sex steroid hormones throughout the vasculature. |
| 94107268 | Induction of | tyrosine phosphorylation | and T-cell activation by vanadate peroxide, an inhibitor of protein tyrosine ph |
| 94107268 | tion by vanadate peroxide, an inhibitor of protein tyrosine phosphatases. Rapid | tyrosine phosphorylation | of key cellular proteins is a crucial event in the transduction of activation s |
| 94107268 | e kinases lck and fyn ( 4- and 3-fold respectively ) and a dramatic increase in | tyrosine phosphorylation | of cellular proteins, notably phospholipase C gamma 1. After this event, we obs |
| 94107268 | nts of Jurkat cells. In the CD45-negative variant, the effect of pervanadate on | tyrosine phosphorylation | was globally decreased and some phosphorylated substrates were specifically mis |
| 94107268 | nal transduction culminating in T-lymphocyte activation. Moreover, induction of | tyrosine phosphorylation | appears sufficient per se to initiate a complete activation programme. |
| 95332324 | Integrin-mediated | tyrosine phosphorylation | and cytokine message induction in monocytic cells. A possible signaling role fo |
| 95332324 | ctin or ligation of beta 1 integrins with antibodies causes a rapid and intense | tyrosine phosphorylation | of two sets of proteins of about 65-75 and 120-125 kDa. In addition, integrin l |
| 95332324 | osine kinase inhibitors genistein and herbimycin A block both integrin-mediated | tyrosine phosphorylation | and increases in IL-1 beta message levels, indicating a causal relationship bet |