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白细胞介素-1β诱导人支气管上皮细胞中RANTES信使核糖核酸与核因子-κB DNA结合活性增加有关。

Inducibility of RANTES mRNA by IL-1beta in human bronchial epithelial cells is associated with increased NF-kappaB DNA binding activity.

作者信息

Manni A, Kleimberg J, Ackerman V, Bellini A, Patalano F, Mattoli S

机构信息

Institute of Experimental Medicine, Milan, Italy.

出版信息

Biochem Biophys Res Commun. 1996 Mar 7;220(1):120-4. doi: 10.1006/bbrc.1996.0367.

DOI:10.1006/bbrc.1996.0367
PMID:8602829
Abstract

RANTES is a member of a large supergene family of proinflammatory chemokines that seems to play an important role in inflammatory processes. It is produced by many cell types in response to specific stimuli and during inflammatory reactions, but the marked differences in the pattern of induced expression suggest that different control mechanisms regulate transcription of RANTES in various tissue types. This is supported by the presence of a large number of potential binding sites for transcriptional factors in the promoter region of the RANTES gene. Our data indicate that expression of RANTES mRNA induced by IL-1beta in human lung epithelial cells is associated with the activation of the transcriptional factor NF-kappaB.

摘要

调节激活正常T细胞表达和分泌的因子(RANTES)是促炎趋化因子大家族的成员之一,该家族似乎在炎症过程中发挥重要作用。它由许多细胞类型在特定刺激下以及炎症反应期间产生,但诱导表达模式的显著差异表明不同的控制机制调节RANTES在各种组织类型中的转录。RANTES基因启动子区域存在大量转录因子潜在结合位点支持了这一点。我们的数据表明,白细胞介素-1β(IL-1β)诱导人肺上皮细胞中RANTES mRNA的表达与转录因子核因子κB(NF-κB)的激活有关。

相似文献

1
Inducibility of RANTES mRNA by IL-1beta in human bronchial epithelial cells is associated with increased NF-kappaB DNA binding activity.白细胞介素-1β诱导人支气管上皮细胞中RANTES信使核糖核酸与核因子-κB DNA结合活性增加有关。
Biochem Biophys Res Commun. 1996 Mar 7;220(1):120-4. doi: 10.1006/bbrc.1996.0367.
2
Double-stranded RNA activates RANTES gene transcription through co-operation of nuclear factor-kappaB and interferon regulatory factors in human airway epithelial cells.双链RNA通过核因子-κB与干扰素调节因子的协同作用激活人气道上皮细胞中的RANTES基因转录。
Clin Exp Allergy. 2004 May;34(5):745-52. doi: 10.1111/j.1365-2222.2004.1941.x.
3
Tumour necrosis factor-alpha and interferon-gamma synergistically activate the RANTES promoter through nuclear factor kappaB and interferon regulatory factor 1 (IRF-1) transcription factors.肿瘤坏死因子-α和干扰素-γ通过核因子κB和干扰素调节因子1(IRF-1)转录因子协同激活RANTES启动子。
Biochem J. 2000 Aug 15;350 Pt 1(Pt 1):131-8.
4
Bile acids regulate RANTES gene expression through its cognate NF-kappaB binding sites.胆汁酸通过其同源的核因子κB结合位点调节调节激活正常T细胞表达和分泌因子(RANTES)基因的表达。
Biochem Biophys Res Commun. 2001 Nov 16;288(5):1095-101. doi: 10.1006/bbrc.2001.5893.
5
Nuclear factor-kappa B potently up-regulates the promoter activity of RANTES, a chemokine that blocks HIV infection.核因子-κB能有效上调调节激活正常T细胞表达和分泌的趋化因子(RANTES)的启动子活性,RANTES是一种可阻断HIV感染的趋化因子。
J Immunol. 1997 Apr 1;158(7):3483-91.
6
Regulation of RANTES/CCL5 expression in human astrocytes by interleukin-1 and interferon-beta.白细胞介素-1和干扰素-β对人星形胶质细胞中RANTES/CCL5表达的调控
J Neurochem. 2004 Jul;90(2):297-308. doi: 10.1111/j.1471-4159.2004.02487.x.
7
Activation of eotaxin gene transcription by NF-kappa B and STAT6 in human airway epithelial cells.人呼吸道上皮细胞中NF-κB和STAT6对嗜酸性粒细胞趋化因子基因转录的激活作用
J Immunol. 1999 Dec 15;163(12):6876-83.
8
Transforming growth factor beta 1(TGF-beta1) down-regulates TNFalpha-induced RANTES production in rheumatoid synovial fibroblasts through NF-kappaB-mediated transcriptional repression.转化生长因子β1(TGF-β1)通过核因子κB(NF-κB)介导的转录抑制作用下调类风湿性滑膜成纤维细胞中肿瘤坏死因子α(TNFα)诱导的调节激活正常T细胞表达和分泌的趋化因子(RANTES)的产生。
Immunol Lett. 2006 Jun 15;105(2):159-66. doi: 10.1016/j.imlet.2006.02.003. Epub 2006 Mar 3.
9
Role of the Rho GTPase in bradykinin-stimulated nuclear factor-kappaB activation and IL-1beta gene expression in cultured human epithelial cells.Rho GTP酶在缓激肽刺激的人培养上皮细胞核因子-κB激活及白细胞介素-1β基因表达中的作用
J Immunol. 1998 Mar 15;160(6):3038-45.
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Responses to the proinflammatory cytokines interleukin-1 and tumor necrosis factor alpha in cells derived from rheumatoid synovium and other joint tissues involve nuclear factor kappaB-mediated induction of the Ets transcription factor ESE-1.类风湿性滑膜和其他关节组织来源的细胞对促炎细胞因子白细胞介素-1和肿瘤坏死因子α的反应涉及核因子κB介导的Ets转录因子ESE-1的诱导。
Arthritis Rheum. 2003 May;48(5):1249-60. doi: 10.1002/art.10942.

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