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本文引用的文献

1
Chromosomal region maintenance 1 (CRM1)-dependent nuclear export of Smad ubiquitin regulatory factor 1 (Smurf1) is essential for negative regulation of transforming growth factor-beta signaling by Smad7.染色体区域维持蛋白1（CRM1）依赖的Smad泛素调节因子1（Smurf1）核输出对于Smad7对转化生长因子-β信号的负调控至关重要。
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Gene silencing in mammals by small interfering RNAs.小干扰RNA介导的哺乳动物基因沉默
Nat Rev Genet. 2002 Oct;3(10):737-47. doi: 10.1038/nrg908.
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Smad7 mediates transforming growth factor-beta-induced apoptosis in mesangial cells.Smad7介导转化生长因子-β诱导的系膜细胞凋亡。
Kidney Int. 2002 Oct;62(4):1178-86. doi: 10.1111/j.1523-1755.2002.kid583.x.
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Smurf1 regulates the inhibitory activity of Smad7 by targeting Smad7 to the plasma membrane.Smurf1通过将Smad7靶向质膜来调节Smad7的抑制活性。
J Biol Chem. 2002 Oct 18;277(42):39919-25. doi: 10.1074/jbc.M201901200. Epub 2002 Jul 31.
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The COP9 signalosome: at the interface between signal transduction and ubiquitin-dependent proteolysis.COP9信号体：位于信号转导与泛素依赖性蛋白水解的界面处。
J Cell Sci. 2002 Feb 1;115(Pt 3):467-73. doi: 10.1242/jcs.115.3.467.
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Jab1 antagonizes TGF-beta signaling by inducing Smad4 degradation.Jab1通过诱导Smad4降解来拮抗转化生长因子-β（TGF-β）信号传导。
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Jab1 interacts directly with HIF-1alpha and regulates its stability.Jab1与缺氧诱导因子-1α（HIF-1α）直接相互作用并调节其稳定性。
J Biol Chem. 2002 Jan 4;277(1):9-12. doi: 10.1074/jbc.C100442200. Epub 2001 Nov 13.
8
The cytoplasmic shuttling and subsequent degradation of p27Kip1 mediated by Jab1/CSN5 and the COP9 signalosome complex.由Jab1/CSN5和COP9信号体复合物介导的p27Kip1的胞质穿梭及随后的降解过程。
J Biol Chem. 2002 Jan 18;277(3):2302-10. doi: 10.1074/jbc.M104431200. Epub 2001 Nov 9.
9
Smad7 inhibits the survival nuclear factor kappaB and potentiates apoptosis in epithelial cells.Smad7抑制存活核因子κB并增强上皮细胞的凋亡。
Oncogene. 2001 Feb 15;20(7):879-84. doi: 10.1038/sj.onc.1204167.
10
Phosphorylation of Smad7 at Ser-249 does not interfere with its inhibitory role in transforming growth factor-beta-dependent signaling but affects Smad7-dependent transcriptional activation.Smad7在丝氨酸249位点的磷酸化并不干扰其在转化生长因子-β依赖性信号传导中的抑制作用，但会影响Smad7依赖性的转录激活。
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Jab1/CSN5是COP9信号体的一个组成部分，通过与Smad7结合并促进其降解来调节转化生长因子β信号通路。

Jab1/CSN5, a component of the COP9 signalosome, regulates transforming growth factor beta signaling by binding to Smad7 and promoting its degradation.

作者信息

Kim Byung-Chul, Lee Ho-Jae, Park Seok Hee, Lee Sae Ra, Karpova Tatiana S, McNally James G, Felici Angelina, Lee Dug Keun, Kim Seong-Jin

机构信息

Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-5055, USA.

出版信息

Mol Cell Biol. 2004 Mar;24(6):2251-62. doi: 10.1128/MCB.24.6.2251-2262.2004.

DOI:10.1128/MCB.24.6.2251-2262.2004
PMID:14993265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC355855/
Abstract

Smad7 inhibits responses mediated by transforming growth factor beta (TGF-beta) and acts in a negative-feedback loop to regulate the intensity or duration of the TGF-beta signal. However, the aberrant expression and continued presence of Smad7 may cause TGF-beta resistance. Here we report that Jab1/CSN5, which is a component of the COP9 signalosome complex, associates constitutively with Smad7 and that overexpression of Jab1/CSN5 causes the translocation of Smad7 from the nucleus to the cytoplasm, promoting its degradation. Overexpression of Jab1/CSN5 increases Smad2 phosphorylation and enhances TGF-beta-induced transcriptional activity. The inhibition of endogenous Jab1/CSN5 expression by small interfering RNA (siRNA) induces Smad7 expression. This study thus defines Jab1/CSN5 as an adapter that targets Smad7 for degradation, thus releasing Smad7-mediated suppression of TGF-beta signaling.

摘要

Smad7抑制由转化生长因子β（TGF-β）介导的反应，并在负反馈回路中发挥作用，以调节TGF-β信号的强度或持续时间。然而，Smad7的异常表达和持续存在可能导致TGF-β抵抗。在此我们报告，COP9信号体复合物的一个组分Jab1/CSN5与Smad7组成性结合，并且Jab1/CSN5的过表达导致Smad7从细胞核易位至细胞质，促进其降解。Jab1/CSN5的过表达增加Smad2磷酸化并增强TGF-β诱导的转录活性。小干扰RNA（siRNA）对内源性Jab1/CSN5表达的抑制诱导Smad7表达。因此，本研究将Jab1/CSN5定义为一种衔接蛋白，其靶向Smad7进行降解，从而解除Smad7介导的对TGF-β信号传导的抑制。