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Regulation of TGF‐β signal transduction by mono‐ and deubiquitylation of Smads
Author(s) -
Dupont Sirio,
Inui Masafumi,
Newfeld Stuart J.
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.03.037
Subject(s) - smad , signal transduction , r smad , transforming growth factor , microbiology and biotechnology , receptor , ubiquitin , transduction (biophysics) , mechanism (biology) , biology , chemistry , genetics , biochemistry , tgf alpha , growth factor , gene , philosophy , epistemology
Polyubiquitylation leading to proteasomal degradation is a well‐established mechanism for regulating TGF‐β signal transduction components such as receptors and Smads. Recently, an equally important role was suggested for monoubiquitylation of both Smad4 and receptor‐associated Smads that regulates their function without protein degradation. Monoubiquitylation of Smads was discovered following the identification of deubiquitylases required for TGF‐β signaling, suggesting that continuous cycles of Smad mono‐ and deubiquitylation are required for proper TGF‐β signal transduction. Here we summarize and discuss recent work on Smad mono‐ and deubiquitylation.

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