SARA is dispensable for functional TGF‐β signaling
FEBS Letters2012Vol. 586(19), pp. 3367–3372
Citations Over TimeTop 19% of 2012 papers
Maren K. Bakkebø, Kanutte Huse, Vera Hilden, Lise Forfang, June H. Myklebust, Erlend B. Smeland, Morten P. Oksvold
Abstract
Smad anchor for receptor activation (SARA or ZFYVE9) has been proposed to mediate transforming growth factor β (TGF-β) signaling by direct interaction with the non-activated Smad proteins and the TGF-β receptors; however, these findings are controversial. We demonstrate no correlation between SARA expression and the levels of TGF-β-induced phosphorylation of Smads in various B-cell lymphomas. Moreover, knockdown of SARA in HeLa cells did not interfere with TGF-β-induced Smad activation, Smad nuclear translocation, or induction of TGF-β target genes. Various R-Smads and TGF-β receptors did not co-immunoprecipitate with SARA. Collectively, our results demonstrate that SARA is dispensable for functional TGF-β-mediated signaling.
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