2 178

Cited 20 times in

DRAK2 participates in a negative feedback loop to control TGF-β/Smads signaling by binding to type I TGF-β receptor.

Authors
 Kyung-Min Yang  ;  Wonjoo Kim  ;  Eunjin Bae  ;  Jungsoo Gim  ;  Brian M. Weist  ;  Yunshin Jung  ;  Ja-Shil Hyun  ;  Jennifer B. Hernandez  ;  Sun-Hee Leem  ;  Taesung Park  ;  Joon Jeong  ;  Craig M. Walsh  ;  Seong-Jin Kim 
Citation
 CELL REPORTS, Vol.2(5) : 1286-1299, 2012 
Journal Title
 CELL REPORTS 
Issue Date
2012
Abstract
TGF-β1 is a multifunctional cytokine that mediates diverse biological processes. However, the mechanisms by which the intracellular signals of TGF-β1 are terminated are not well understood. Here, we demonstrate that DRAK2 serves as a TGF-β1-inducible antagonist of TGF-β signaling. TGF-β1 stimulation rapidly induces DRAK2 expression and enhances endogenous interaction of the type I TGF-β receptor with DRAK2, thereby blocking R-Smads recruitment. Depletion of DRAK2 expression markedly augmented the intensity and the extent of TGF-β1 responses. Furthermore, a high level of DRAK2 expression was observed in basal-like and HER2-enriched breast tumors and cell lines, and depletion of DRAK2 expression suppressed the tumorigenic ability of breast cancer cells. Thus, these studies define a function for DRAK2 as an intrinsic intracellular antagonist participating in the negative feedback loop to control TGF-β1 responses, and aberrant expression of DRAK2 increases tumorigenic potential, in part, through the inhibition of TGF-β1 tumor suppressor activity.
Full Text
http://www.sciencedirect.com/science/article/pii/S2211124712003324
DOI
10.1016/j.celrep.2012.09.028
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Jeong, Joon(정준) ORCID logo https://orcid.org/0000-0003-0397-0005
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/89907
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse

Links