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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.

Author information

1
Department of Immunology, Institute for Cancer Research, Oslo University Hospital HF, Montebello, Oslo, Norway.

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.

PMID:
22819827
DOI:
10.1016/j.febslet.2012.07.027
[Indexed for MEDLINE]
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