TGF-β-activated kinase 1 (Tak1) mediates agonist-induced Smad activation and linker region phosphorylation in embryonic craniofacial neural crest-derived cells.

ABSTRACT:

Background

The role of Smad-independent TGF-β signaling in craniofacial development is poorly elucidated.

Results

In craniofacial mesenchymal cells, Tak1 regulates both R-Smad C-terminal and linker region phosphorylation in TGF-β signaling.

Conclusion

Tak1 plays an irreplaceable role in craniofacial ecto-mesenchyme during embryogenesis.

Significance

Understanding the mechanisms of TGF-β signaling contributes to knowledge of pathogenetic mechanisms underlying common craniofacial birth defects. Although the importance of TGF-β superfamily signaling in craniofacial growth and patterning is well established, the precise details of its signaling mechanisms are still poorly understood. This is in part because of the concentration of studies on the role of the Smad-de

SUBMITTER: Yumoto K 

PROVIDER: S-EPMC3650384 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature