[HTML][HTML] SARA is dispensable for functional TGF-β signaling

M Bakkebø, K Huse, VI Hilden, L Forfang, JH Myklebust… - FEBS letters, 2012 - Elsevier
M Bakkebø, K Huse, VI Hilden, L Forfang, JH Myklebust, EB Smeland, MP Oksvold
FEBS letters, 2012Elsevier
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 …
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.
Elsevier