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XB-ART-3891
Genes Dev February 15, 2004; 18 (4): 381-6.

Role of the TAK1-NLK-STAT3 pathway in TGF-beta-mediated mesoderm induction.

Ohkawara B , Shirakabe K , Hyodo-Miura J , Matsuo R , Ueno N , Matsumoto K , Shibuya H .


Abstract
Transforming growth factor (TGF)-beta-activated kinase 1 (TAK1) and Nemo-like kinase (NLK) function in Xenopus, Drosophila, and Caenorhabditis elegans development. Here we report that serine phosphorylation of STAT3 induced by TAK1-NLK cascade is essential fo TGF-beta-mediated mesoderm induction in Xenopus embryo. Depletion of TAK1, NLK, or STAT3 blocks TGF-beta-mediated mesoderm induction. Coexpression of NLK and STAT3 induces mesoderm by a mechanism that requires serine phosphorylation of STAT3. Activin activates NLK, which in turn directly phosphorylates STAT3. Moreover, depletion of either TAK1 or NLK inhibits endogenous serine phosphorylation of STAT3. These results provide the first evidence that TAK1-NLK-STAT3 cascade participates in TGF-beta-mediated mesoderm induction.

PubMed ID: 15004007
PMC ID: PMC359392
Article link: Genes Dev


Species referenced: Xenopus laevis
Genes referenced: map3k7 nlk nlk.2 stat3.1 stat3.2 tgfb1
Morpholinos: map3k7 MO1 nlk.2 MO1 stat3.1 MO1

References [+] :
Agius, Endodermal Nodal-related signals and mesoderm induction in Xenopus. 2000, Pubmed, Xenbase