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Clusterin, a novel modulator of TGF-beta signaling, is involved in Smad2/3 stability

Authors
Lee, Kwan-BokJeon, Jun-HoChoi, InpyoKwon, O-YuYu, KweonYou, Kwan-Hee
Issue Date
22-Feb-2008
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
clusterin; TGF-beta; Smad2; Smad3
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.366, no.4, pp 905 - 909
Pages
5
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
366
Number
4
Start Page
905
End Page
909
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14322
DOI
10.1016/j.bbrc.2007.12.033
ISSN
0006-291X
1090-2104
Abstract
Clusterin (CLU) is known as a multifunctional protein involved in a variety of physiological processes including lipid transport, epithelial cell differentiation, tumorigenesis, and apoptosis. It is known that CLU interacts with TGF-beta type 11 receptor (T beta R11). However, the relationship of CLU and TGF-beta signaling is unclear. Here we present that CLU is a novel modulator of TGF-beta signaling by regulating Smad2/3 proteins. Overexpression of CLU enhanced TGF-beta-induced transcriptional activity and increased the amount of Smad2/3 proteins, while CLU siRNA repressed TGF-beta-induced transcriptional activity and decreased the amount of Smad2/3 proteins in Hep3B cells. We also found that CLU was involved in Smad2/3 stability at the protein level. These findings suggest that CLU regulates TGF-beta signaling pathway by modulating the stability of Smad2/3 proteins. (c) 2007 Elsevier Inc. All rights reserved.
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