Interaction between Smad anchor for receptor activation and Smad3 is not essential for TGF-β/Smad3-mediated signaling
D Goto, H Nakajima, Y Mori, K Kurasawa… - Biochemical and …, 2001 - Elsevier
D Goto, H Nakajima, Y Mori, K Kurasawa, N Kitamura, I Iwamoto
Biochemical and biophysical research communications, 2001•ElsevierRegulation of subcellular localization of Smad proteins is supposed to be critical for the
effective initiation and maintenance of TGF-β 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-β/Smad2-mediated signaling. In
this study, we determined whether the interaction between SARA and Smad3 is essential for
TGF-β/Smad3-mediated signaling. We found that a mutant Smad3 (Smad3NS) that lacked …
effective initiation and maintenance of TGF-β 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-β/Smad2-mediated signaling. In
this study, we determined whether the interaction between SARA and Smad3 is essential for
TGF-β/Smad3-mediated signaling. We found that a mutant Smad3 (Smad3NS) that lacked …
Regulation of subcellular localization of Smad proteins is supposed to be critical for the effective initiation and maintenance of TGF-β 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-β/Smad2-mediated signaling. In this study, we determined whether the interaction between SARA and Smad3 is essential for TGF-β/Smad3-mediated signaling. We found that a mutant Smad3 (Smad3NS) that lacked the binding to SARA was phosphorylated by TGF-β 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-β-induced transcription. Therefore, these findings indicate that, in contrast to SARA/Smad2 interaction, SARA/Smad3 interaction is not essential for TGF-β/Smad3-mediated signaling.
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