Literature DB >> 17276978

TAK1 MAPK kinase kinase mediates transforming growth factor-beta signaling by targeting SnoN oncoprotein for degradation.

Taisuke Kajino1, Emily Omori, Shunsuke Ishii, Kunihiro Matsumoto, Jun Ninomiya-Tsuji.   

Abstract

Transforming growth factor-beta (TGF-beta) regulates a variety of physiologic processes through essential intracellular mediators Smads. The SnoN oncoprotein is an inhibitor of TGF-beta signaling. SnoN recruits transcriptional repressor complex to block Smad-dependent transcriptional activation of TGF-beta-responsive genes. Following TGF-beta stimulation, SnoN is rapidly degraded, thereby allowing the activation of TGF-beta target genes. Here, we report the role of TAK1 as a SnoN protein kinase. TAK1 interacted with and phosphorylated SnoN, and this phosphorylation regulated the stability of SnoN. Inactivation of TAK1 prevented TGF-beta-induced SnoN degradation and impaired induction of the TGF-beta-responsive genes. These data suggest that TAK1 modulates TGF-beta-dependent cellular responses by targeting SnoN for degradation.

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Year:  2007        PMID： 17276978      PMCID： PMC2175395          DOI： 10.1074/jbc.M700875200

Source DB:  PubMed          Journal:  J Biol Chem        ISSN： 0021-9258            Impact factor:   5.157


  29 in total

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