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Cell Signal. 2013 Oct;25(10):2039-46. doi: 10.1016/j.cellsig.2013.06.006. Epub 2013 Jun 11.

Activation of TAK1 by Sef-S induces apoptosis in 293T cells.

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1
State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China.

Abstract

Sef (similar expression to fgf genes, also named IL-17RD) was identified as a negative regulator of fibroblast growth factor signaling. Sef-S, an alternative splice isoform of Sef, inhibits FGF-induced NIH3T3 cell proliferation. Here we report that Sef-S physically interacts with TAK1, induces Lys63-linked TAK1 polyubiquitination on lysine 209 and TAK1-mediated JNK and p38 activation. Co-overexpression of TAK1 WT, K34R, K150R, K158R mutants with Sef-S induces Lys63-linked TAK1 polyubiquitination whereas TAK1 K63R and K209R mutants fail. Furthermore, co-overexpression of Sef-S and TAK1 induce 293T cells apoptosis. These results reveal Sef-S actives Lys63-linked TAK1 polyubiquitination on lysine 209, induces TAK1-mediated JNK and p38 activation and also results apoptosis in 293T cells.

KEYWORDS:

Apoptosis; Erk1/2; FBS; FGF; IgG; JNK; MAPK; SPRED; Sef; Sprouty-related EVH1-domain containing; Ub; fetal bovine serum; fibroblast growth factor; immunoglobulin G; nubiquitination; p38; ubiquitin; wild type; wt

PMID:
23770285
DOI:
10.1016/j.cellsig.2013.06.006
[Indexed for MEDLINE]
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