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Human T-cell leukemia virus type I Tax-protein-mediated activation of NF-kappa B from p100 (NF-kappa B2)-inhibited cytoplasmic reservoirs. 总被引:8,自引:0,他引:8 下载免费PDF全文
T Kanno G Franzoso U Siebenlist 《Proceedings of the National Academy of Sciences of the United States of America》1994,91(26):12634-12638
The human T-cell leukemia virus type I Tax protein transforms T cells through induced expression of many cellular genes, including those encoding the growth-related proteins interleukin 2 and the alpha chain of its receptor. Induction of these genes is mediated, at least in part, through Tax-dependent posttranslational activation of NF-kappa B, typically heterodimers of p50 (NF-kappa B1) and p65 (RelA). The preexisting NF-kappa B proteins are retained in the cytoplasm of cells by association with inhibitory ankyrin-motif-containing I kappa B proteins, primarily I kappa B-alpha but also including the precursor proteins p105 (NF-kappa B1) and p100 (NF-kappa B2). Here we demonstrate the existence of a previously undescribed multimeric cytoplasmic complex in which NF-kappa B dimers are associated with the p100 inhibitor in a manner dependent on the precursor protein's ankyrin domain. We also demonstrate an antagonistic effect of the Tax protein on the cytoplasmic sequestration function of p100; this in turn leads to nuclear translocation of NF-kappa B dimers liberated from multimeric complexes. Tax may exert these effects through the physical association with p100. Tax also relieves the p100-mediated inhibition of DNA binding by p50-p65 heterodimers in vitro. The results demonstrate a mechanism by which Tax may activate NF-kappa B in T cells. 相似文献
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Multiple mechanisms are implicated in the regulation of NF-kappa B activity during human cytomegalovirus infection. 总被引:9,自引:0,他引:9 下载免费PDF全文
T F Kowalik B Wing J S Haskill J C Azizkhan A S Baldwin Jr E S Huang 《Proceedings of the National Academy of Sciences of the United States of America》1993,90(3):1107-1111
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The 65-kDa subunit of human NF-kappa B functions as a potent transcriptional activator and a target for v-Rel-mediated repression. 总被引:28,自引:1,他引:28 下载免费PDF全文
D W Ballard E P Dixon N J Peffer H Bogerd S Doerre B Stein W C Greene 《Proceedings of the National Academy of Sciences of the United States of America》1992,89(5):1875-1879
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Asbestos induces nuclear factor kappa B (NF-kappa B) DNA-binding activity and NF-kappa B-dependent gene expression in tracheal epithelial cells. 总被引:7,自引:0,他引:7 下载免费PDF全文
Y M Janssen A Barchowsky M Treadwell K E Driscoll B T Mossman 《Proceedings of the National Academy of Sciences of the United States of America》1995,92(18):8458-8462
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Autoregulation of the NF-kappa B transactivator RelA
(p65) by multiple cytoplasmic inhibitors containing ankyrin
motifs. 总被引:22,自引:5,他引:22 下载免费PDF全文
S C Sun P A Ganchi C Béraud D W Ballard W C Greene 《Proceedings of the National Academy of Sciences of the United States of America》1994,91(4):1346-1350
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Stimulation of a human T-cell clone with anti-CD3 or tumor necrosis factor induces NF-kappa B translocation but not human immunodeficiency virus 1 enhancer-dependent transcription 总被引:17,自引:0,他引:17 下载免费PDF全文
U Hazan D Thomas J Alcami F Bachelerie N Israel H Yssel J L Virelizier F Arenzana-Seisdedos 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(20):7861-7865
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The ankyrin repeat domains of the NF-kappa B precursor p105 and the protooncogene bcl-3 act as specific inhibitors of NF-kappa B DNA binding. 总被引:38,自引:1,他引:37 下载免费PDF全文
E N Hatada A Nieters F G Wulczyn M Naumann R Meyer G Nucifora T W McKeithan C Scheidereit 《Proceedings of the National Academy of Sciences of the United States of America》1992,89(6):2489-2493
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Gene deletion of NF-kappa B p50 does not alter the hepatic inflammatory response to ischemia/reperfusion 总被引:8,自引:0,他引:8
BACKGROUND/AIMS: Nuclear factor kappa B (NF-kappa B) is a primary regulator of gene expression and is activated during hepatic ischemia/reperfusion injury. The objective of the present study was to determine whether activation of NF-kappa B is causally related to the induction of the acute inflammatory response induced by hepatic ischemia/reperfusion. METHODS: Wild-type (p50(+/+)) and NF-kappa B p50-deficient (p50(-/-)) mice underwent hepatic ischemia/reperfusion. NF-kappa B activation was determined by electrophoretic mobility shift assay. Hepatic neutrophil accumulation was measured by liver myeloperoxidase content. Hepatocellular injury was assessed by serum level of alanine aminotransferase and liver histology. RESULTS: In p50(+/+) mice, ischemia/reperfusion induced marked activation of NF-kappa B consisting of p50/p65 heterodimers. In contrast, NF-kappa B activation in livers from p50(-/-) mice was abrogated, but p65 was observed in nuclear extracts. Despite amelioration of NF-kappa B activation there was no significant difference between p50(+/+) and p50(-/-) mice in expression of TNF alpha and MIP-2, liver accumulation of neutrophils or hepatocellular injury. CONCLUSIONS: Gene deletion of NF-kappa B p50 does not alter the hepatic inflammatory response to ischemia/reperfusion. Despite abrogation of DNA-binding by the NF-kappa B p50/p65 complex, p65 was still observed in nuclear extracts suggesting that there may be functional redundancy amongst members of the Rel protein family in order to preserve the inflammatory response. 相似文献
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Failure of TLR4-driven NF-kappa B activation to stimulate virus replication in models of HIV type 1 activation 总被引:1,自引:0,他引:1
Nordone SK Ignacio GA Su L Sempowski GD Golenbock DT Li L Dean GA 《AIDS research and human retroviruses》2007,23(11):1387-1395
The interaction of HIV-1 with Toll-like receptors (TLR) on host target cells is incompletely understood. Data from several in vivo and in vitro model systems suggest that TLR2, TLR4, and TLR9 remain functional and if stimulated, cause an upregulation of viral replication. In the present studies employing two different chronically HIV-1-infected cell lines and highly purified TLR agonists, we found ligation of TLR2 and TLR9, but not TLR4, resulted in significant upregulation of HIV-1 production. This result was not due to a lack of TLR4 expression or impaired NF-kappa B activation. Using HEK293 cells transfected with individual TLRs and an HIV-1 LTR reporter confirmed that TLR4 signaling does not directly activate the HIV-1 LTR. Finally, ultrapurified LPS did not enhance production of IL-1 beta or IL-6 in chronically infected U1 cells, whereas significant cytokine production was observed in uninfected U937 cells. These results confirm the biological activity of ultrapurified LPS and raise the possibility that TLR4 signaling pathways may be altered during chronic HIV-1 infection. Collectively, these studies suggest that although several TLR can upregulate NF-kappaB in HIV-1-infected cells, upregulation of NF-kappaB alone is insufficient to activate the viral LTR. Further dissection of the TLR signaling pathways is necessary to determine how TLR stimulation leads to LTR activation and whether HIV-1 infection can alter signaling through TLR4. 相似文献
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Antisense inhibition of the p65 subunit of NF-kappa B blocks tumorigenicity and causes tumor regression. 总被引:18,自引:4,他引:18 下载免费PDF全文
K A Higgins J R Perez T A Coleman K Dorshkind W A McComas U M Sarmiento C A Rosen R Narayanan 《Proceedings of the National Academy of Sciences of the United States of America》1993,90(21):9901-9905