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Cells 2014, 3(4), 981-993; doi:10.3390/cells3040981

Regulation of TGF-β Superfamily Signaling by SMAD Mono-Ubiquitination

1
Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China
2
Department of Molecular Cell Biology, Cancer Genomics Centre Netherlands and Centre for Biomedical Genetics, Leiden University Medical Center, Postbus 9600 2300 RC Leiden, The Netherlands
*
Authors to whom correspondence should be addressed.
Received: 19 March 2014 / Revised: 3 September 2014 / Accepted: 26 September 2014 / Published: 15 October 2014
(This article belongs to the Special Issue Protein Ubiquitination)
View Full-Text   |   Download PDF [2252 KB, uploaded 15 October 2014]   |  

Abstract

TGF-β(transforming growth factor-β) superfamily signaling mediators are important regulators of diverse physiological and pathological events. TGF-β signals are transduced by transmembrane type I and type II serine/threonine kinase receptors and their downstream effectors, the SMAD(drosophila mothers against decapentaplegic protein) proteins. Numerous studies have already demonstrated crucial regulatory roles for modification of TGF-β pathway components by poly-ubiquitination. Recently, several studies also uncovered mono-ubiquitination of SMADs as a mechanism for SMAD activation or inactivation. Mono-ubiquitination and subsequent deubiquitination of SMAD proteins accordingly play important roles in the control of TGF-β superfamily signaling. This review highlights the major pathways regulated by SMAD mono-ubiquitination. View Full-Text
Keywords: TGF-β; BMP; SMAD; Mono-ubiquitination TGF-β; BMP; SMAD; Mono-ubiquitination
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Xie, F.; Zhang, Z.; van Dam, H.; Zhang, L.; Zhou, F. Regulation of TGF-β Superfamily Signaling by SMAD Mono-Ubiquitination. Cells 2014, 3, 981-993.

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