Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 281, Issue 5, Pages 1100-1105Publisher
ACADEMIC PRESS INC
DOI: 10.1006/bbrc.2001.4489
Keywords
TGF-beta; SARA; Hgs; Smad2; Smad8; subcellular localization
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Regulation of subcellular localization of Smad proteins is supposed to be critical for the effective initiation and maintenance of TGF-beta signaling. Recently, Smad anchor for receptor activation (SARA) has been identified as a Smad2 binding protein. SARA regulates the subcellular localization of Smad2 and is required for TGF-beta /Smad2-mediated signaling. In this study, we determined whether the interaction between SARA and Smad3 is essential for TGF-beta /Smad3-mediated signaling. We found that a mutant Smad3 (Smad3NS) that lacked the binding to SARA, was phosphorylated by TGF-beta type I receptor at the similar level to that in wild-type Smad3 (Smad3WT). Smad3NS also formed complexes with Smad4 and translocalized into the nucleus. Moreover, Smad3NS and Smad3WT equally enhanced TGF-beta -induced transcription. Therefore, these findings indicate that, in contrast to SARA/Smad3 interaction, SARA/Smad3 interaction is not essential for TGF-beta /Smad3-mediated signaling. (C) 2001 Academic Press.
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