共查询到20条相似文献,搜索用时 15 毫秒
1.
Intracellular thiols regulate activation of nuclear factor kappa B and transcription of human immunodeficiency virus. 总被引:69,自引:17,他引:52 下载免费PDF全文
F J Staal M Roederer L A Herzenberg L A Herzenberg 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(24):9943-9947
2.
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
3.
Cloning of the DNA-binding subunit of human nuclear factor kappa B: the level of its mRNA is strongly regulated by phorbol ester or tumor necrosis factor alpha. 总被引:55,自引:7,他引:55 下载免费PDF全文
R Meyer E N Hatada H P Hohmann M Haiker C Bartsch U R?thlisberger H W Lahm E J Schlaeger A P van Loon C Scheidereit 《Proceedings of the National Academy of Sciences of the United States of America》1991,88(3):966-970
The DNA binding subunit of nuclear factor kappa B (NF-kappa B), a B-cell protein that interacts with the immunoglobulin kappa light-chain gene enhancer, has been purified from nuclei of human HL-60 cells stimulated with tumor necrosis factor alpha (TNF alpha), and internal peptide sequences were obtained. Overlapping cDNA clones were isolated and sequenced. The encoded open reading frame of about 105 kDa contained at its N-terminal half all six tryptic peptide sequences, suggesting that the 51-kDa NF-kappa B protein is processed from a 105-kDa precursor. An in vitro synthesized protein containing most of the N-terminal half of the open reading frame bound specifically to an NF-kappa B binding site. This region also showed high homology to a domain shared by the Drosophila dorsal gene and the avian and mammalian rel (proto)oncogene products. The level of the 3.8-kilobase mRNA was strongly increased after stimulation with TNF alpha or phorbol ester. Thus, both factors not only activate NF-kappa B protein, as described previously, but also induce expression of the gene encoding the DNA-binding subunit of NF-kappa B. 相似文献
4.
Repeated B motifs in the human immunodeficiency virus type I long terminal repeat enhancer region do not exhibit cooperative factor binding. 总被引:10,自引:2,他引:8 下载免费PDF全文
R B Gaynor M D Kuwabara F K Wu J A Garcia D Harrich M Briskin R Wall D S Sigman 《Proceedings of the National Academy of Sciences of the United States of America》1988,85(24):9406-9410
5.
6.
Separation of oxidant-initiated and redox-regulated steps in the NF-kappa B signal transduction pathway. 总被引:9,自引:2,他引:7 下载免费PDF全文
M T Anderson F J Staal C Gitler L A Herzenberg L A Herzenberg 《Proceedings of the National Academy of Sciences of the United States of America》1994,91(24):11527-11531
Studies presented here show that overall NF-kappa B signal transduction begins with a parallel series of stimuli-specific pathways through which cytokines (tumor necrosis factor alpha), oxidants (hydrogen peroxide and mitomycin C), and phorbol ester (phorbol 12-myristate 13-acetate) individually initiate signaling. These initial pathways culminate in a common pathway through which all of the stimulating agents ultimately signal NF-kappa B activation. We distinguish the stimuli-specific pathways by showing that the oxidative stimuli trigger NF-kappa B activation in only one of two human T-cell lines (Wurzburg but not Jurkat), whereas tumor necrosis factor alpha and phorbol 12-myristate 13-acetate readily stimulate in both lines. We propose the common pathway as the simplest way of accounting for the common requirements and properties of the signaling pathway. We include a redox-regulatory mechanism(s) in this common pathway to account for the previously demonstrated redox regulation of NF-kappa B activation in Jurkat cells (in which oxidants don't activate NF-kappa B); we put tyrosine phosphorylation in the common pathway by showing that kinase activity (inhibitable by herbimycin A and tyrphostin 47) is required for NF-kappa B activation by all stimuli tested in both cell lines. Since internal sites of oxidant production have been shown to play a key role in the cytokine-stimulated activation of NF-kappa B, and since tyrosine kinase and phosphatase activities are known to be altered by oxidants, these findings suggest that intracellular redox status controls NF-kappa B activation by regulating tyrosine phosphorylation event(s) within the common step of the NF-kappa B signal transduction pathway. 相似文献
7.
8.
9.
10.
11.
Identification and purification of a human immunoglobulin-enhancer-binding protein (NF-kappa B) that activates transcription from a human immunodeficiency virus type 1 promoter in vitro 总被引:63,自引:12,他引:63 下载免费PDF全文
K Kawakami C Scheidereit R G Roeder 《Proceedings of the National Academy of Sciences of the United States of America》1988,85(13):4700-4704
12.
13.
Tumor necrosis factor alpha activates human immunodeficiency virus type 1 through induction of nuclear factor binding to the NF-kappa B sites in the long terminal repeat. 总被引:88,自引:16,他引:72 下载免费PDF全文
E J Duh W J Maury T M Folks A S Fauci A B Rabson 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(15):5974-5978
14.
A platelet-activating factor antagonist, RP 55778, inhibits cytokine-dependent induction of human immunodeficiency virus expression in chronically infected promonocytic cells. 总被引:2,自引:1,他引:1 下载免费PDF全文
D Weissman G Poli A Bousseau A S Fauci 《Proceedings of the National Academy of Sciences of the United States of America》1993,90(6):2537-2541
15.
Involvement of protein kinase C in superoxide anion-induced activation of nuclear factor-kappa B in human endothelial cells 总被引:17,自引:0,他引:17
OBJECTIVE: Nuclear factor-kappa B (NF-kappa B) plays an important role in the regulation of redox-sensitive genes which are related to the pathogenesis of various vascular diseases. Although oxygen free-radicals are known to activate NF-kappa B, the signaling pathway of oxygen free radical-induced NF-kappa B activation remains largely unclear. Thus, this study was performed to examine the possible involvement of protein kinase C (PKC) in the oxygen free radical-induced NF-kappa B activation in human umbilical vein endothelial cells (HUVECs). METHODS: Superoxide anion was generated by xanthine and xanthine oxidase. An electrophoretic mobility shift assay (EMSA) was performed using a kappa B-motif oligonucleotide and nuclear extracts from HUVECs. Immunoblot analysis using an antibody against I kappa B alpha, phosphorylated by I kappa B alpha kinase, or myristoylated alanine-rich C kinase substrate (MARCKS) phosphorylated by protein kinase C was carried out. An NF-kappa B luciferase reporter gene assay was also performed. RESULTS: The treatment of the cells with superoxide anion for 60 min increased the NF-kappa B/DNA binding activity. Immunoblot analysis showed that superoxide anion induced phosphorylation of I kappa B alpha within 10 min. Furthermore, phosphorylation of MARCKS occurred more rapidly than phosphorylation of I kappa B alpha. Pretreatment of the cells with calphostin C (100-400 nmol/l) and chelerythrine chloride (5-10 mumol/l), inhibitors of PKC, abolished the superoxide anion-induced NF-kappa B activation. Down-regulation of endogenous PKC by long-term exposure to phorbol 12-myristate 13-acetate decreased the superoxide anion-induced NF-kappa B activation to a basal level. Superoxide anion induced the luciferase reporter gene and this induction was completely inhibited by calphostin C (200 nmol/l) and 4,5-dihydroxy-1,3-benzene disulfonic acid (tiron). CONCLUSION: These results suggest that PKC is involved in the activation of NF-kappa B by superoxide anion in human endothelial cells. 相似文献
16.
17.
Coordinate viral induction of tumor necrosis factor alpha and interferon beta in human B cells and monocytes. 总被引:15,自引:4,他引:11
A E Goldfeld T Maniatis 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(5):1490-1494
Human tumor necrosis factor alpha (TNF-alpha) gene expression can be induced primarily in cells of the monocyte/macrophage lineage by a variety of inducers, including lipopolysaccharide, phorbol esters such as phorbol 12-myristate 13-acetate, and virus or synthetic double-stranded RNA [poly(I).poly(C)]. In this paper we show that the TNF-alpha gene also responds to virus and phorbol 12-myristate 13-acetate in B lymphocytes and that virus is the most potent inducer of TNF-alpha mRNA in both monocyte and B-cell lines. In addition, we show that viral infection coinduces the expression of TNF-alpha and interferon beta mRNA and that viral induction of both genes is blocked by the kinase inhibitor 2-aminopurine. Inhibition of protein synthesis with cycloheximide had no effect on mRNA expression of the genes in one of three cell lines tested (U937) but blocked the viral induction of both genes in another (Namalwa). Thus, the regulatory factors required for mRNA induction of both genes are present prior to the addition of virus in U937 but not in Namalwa cells. However, in a third cell line (JY), cycloheximide blocked viral induction of the interferon beta gene but not the TNF-alpha gene. Taken together, these observations suggest that viral induction of TNF-alpha and interferon beta gene expression may involve overlapping pathways with both common and distinct regulatory factors. 相似文献
18.
Regulation of human retroviral latency by the NF-kappa B/I kappa B family: inhibition of human immunodeficiency virus replication by I kappa B through a Rev-dependent mechanism. 总被引:5,自引:0,他引:5 下载免费PDF全文
B Y Wu C Woffendin C S Duckett T Ohno G J Nabel 《Proceedings of the National Academy of Sciences of the United States of America》1995,92(5):1480-1484
19.
The same target sequences are differentially important for activation of the interleukin 2 receptor alpha-chain gene in two distinct T-cell lines. 总被引:7,自引:1,他引:7 下载免费PDF全文
M B Toledano D G Roman N F Halden B B Lin W J Leonard 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(5):1830-1834
20.
Cytokine-stimulated human immunodeficiency virus replication is inhibited by N-acetyl-L-cysteine. 总被引:25,自引:12,他引:25 下载免费PDF全文
M Roederer F J Staal P A Raju S W Ela L A Herzenberg L A Herzenberg 《Proceedings of the National Academy of Sciences of the United States of America》1990,87(12):4884-4888
We show that the stimulation of human immunodeficiency virus (HIV) brought about by tumor necrosis factor alpha and phorbol 12-myristate 13-acetate can be inhibited by adding N-acetyl-L-cysteine (NAC). NAC, which replenishes intracellular glutathione, effectively inhibits the tumor necrosis factor alpha- or phorbol ester-stimulated replication of HIV in acutely infected cell cultures. NAC also inhibits the cytokine-enhanced HIV long terminal repeat-directed expression of beta-galactosidase in in vitro HIV model systems. These results show that intracellular thiol levels influence HIV production. Furthermore, because NAC reverses tumor necrosis factor alpha toxicity both in cells and in animals and is a well-known drug that can be administered orally without known toxicity in humans, these results suggest that NAC is a possible therapeutic agent in AIDS. 相似文献