Activation of TAK1 by Sef-S induces apoptosis in 293T cells.
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.
Mesh Terms:
Alternative Splicing, Animals, Apoptosis, Gene Expression Regulation, HEK293 Cells, Humans, Interleukin-17, MAP Kinase Kinase Kinases, Mice, NF-kappa B, NIH 3T3 Cells, Phosphorylation, Signal Transduction, Ubiquitination
Alternative Splicing, Animals, Apoptosis, Gene Expression Regulation, HEK293 Cells, Humans, Interleukin-17, MAP Kinase Kinase Kinases, Mice, NF-kappa B, NIH 3T3 Cells, Phosphorylation, Signal Transduction, Ubiquitination
Cell. Signal.
Date: Oct. 01, 2013
PubMed ID: 23770285
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