The regulation of TGF-β/SMAD signaling by protein deubiquitination

被引：87

作者：

Zhang, Juan ^{[1
,2
,3
]}

Zhang, Xiaofei ^{[2
,3
]}

Xie, Feng ^{[1
]}

Zhang, Zhengkui ^{[1
]}

van Dam, Hans ^{[2
,3
]}

Zhang, Long ^{[1
,2
,3
]}

Zhou, Fangfang ^{[2
,3
]}

机构：

[1] Zhejiang Univ, Inst Life Sci, Hangzhou 310058, Zhejiang, Peoples R China

[2] Leiden Univ, Med Ctr, Dept Mol Cell Biol, NL-2300 RC Leiden, Netherlands

[3] Leiden Univ, Med Ctr, Ctr Biomed Genet, NL-2300 RC Leiden, Netherlands

来源：

PROTEIN & CELL | 2014年 / 5卷 / 07期

关键词：

TGF-beta; T beta RI; SMAD; DUB; ubiquitin; deubiquitination; TRANSFORMING-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; UBIQUITIN LIGASE COMPLEX; TUMOR-SUPPRESSOR SMAD4; CANCER BONE METASTASIS; KAPPA-B ACTIVATION; II RECEPTOR GENE; FACTOR-BETA; NEGATIVE REGULATION; LINEAR UBIQUITINATION;

D O I：

10.1007/s13238-014-0058-8

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Transforming growth factor-beta (TGF-beta) members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-beta type II (T beta R II) and type I (T beta RI) and serine/threonine kinases receptors. Aberrant activation of TGF-beta signaling leads to diseases, including cancer. In advanced cancer, the TGF-beta/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-beta/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-beta signaling components by deubiquitinating enzymes (DUBs). In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-beta signaling pathway. The regulatory roles of these DUBs as a driving force for cancer progression as well as their underlying working mechanisms are also discussed.

引用

页码：503 / 517

页数：15

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