Clusterin, a novel modulator of TGF-beta signaling, is involved in Smad2/3 stability
- Authors
- Lee, Kwan-Bok; Jeon, Jun-Ho; Choi, Inpyo; Kwon, O-Yu; Yu, Kweon; You, 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - ETC > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.