Ttrap is a novel component of the non-canonical TRAF6-TAK1 TGF-β signaling pathway

György Várady, B. Sarkadi, K. Fátyol

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Transforming growth factor-β (TGF-β) principally relays its effects through the Smad pathway however, accumulating evidence indicate that alternative signaling routes are also employed by this pleiotropic cytokine. For instance recently, we have demonstrated that ligand occupied TGF-β receptors can directly trigger the TRAF6-TAK1 signaling module, resulting in MAP kinase activation. Here we report identification of the adaptor molecule TTRAP as a novel component of this non-canonical TGF-β pathway. We show that the protein associates with TGF-β receptors and components of the TRAF6-TAK1 signaling module, resulting in differential regulation of TGF-β activated p38 and NF-κB responses. Modulation of cellular TTRAP level affects cell viability in the presence of TGF-β, suggesting that the protein is an important component of the TGF-β induced apoptotic process.

Original languageEnglish
Article numbere25548
JournalPLoS One
Volume6
Issue number9
DOIs
Publication statusPublished - Sep 27 2011

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TNF Receptor-Associated Factor 6
transforming growth factors
Transforming Growth Factors
Growth Factor Receptors
receptors
mitogen-activated protein kinase
cell viability
Cell Survival
Proteins
cytokines
Phosphotransferases
proteins
Chemical activation
Cells
Modulation
Cytokines
Ligands
Molecules

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

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Ttrap is a novel component of the non-canonical TRAF6-TAK1 TGF-β signaling pathway. / Várady, György; Sarkadi, B.; Fátyol, K.

In: PLoS One, Vol. 6, No. 9, e25548, 27.09.2011.

Research output: Contribution to journalArticle

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