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FEBS Lett. 2012 Sep 21;586(19):3367-72. doi: 10.1016/j.febslet.2012.07.027. Epub 2012 Jul 20.

SARA is dispensable for functional TGF-β signaling.

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Department of Immunology, Institute for Cancer Research, Oslo University Hospital HF, Montebello, Oslo, Norway.


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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