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

被引：94

作者：

Ohkawara, B

Shiratake, K

Hyodo-Miura, J

Matsuo, R

Ueno, N

Matsumoto, K

Shibuya, H ^{[1
]}

机构：

[1] Tokyo Med & Dent Univ, Dept Mol & Cell Biol, Med Res Inst, Tokyo 1010062, Japan

[2] Tokyo Med & Dent Univ, Dept Mol & Cell Biol, Sch Biomed Sci, Tokyo 1010062, Japan

[3] JST, CREST, Tokyo 1010062, Japan

[4] Natl Inst Basic Biol, Div Morphogenesis, Dept Dev Biol, Okazaki, Aichi 4448585, Japan

[5] Nagoya Univ, Grad Sch Sci, Dept Mol Biol, Nagoya, Aichi 4648602, Japan

[6] CREST, JST, Chikusa Ku, Nagoya, Aichi 4648602, Japan

[7] Tokyo Med & Dent Univ, Ctr Excellence Program Res Mol Destruct & Reconst, Tokyo 1010062, Japan

来源：

GENES & DEVELOPMENT | 2004年 / 18卷 / 04期

关键词：

TAK1; NLK; STAT3; TGF-beta signal; mesoderm induction;

D O I：

10.1101/gad.1166904

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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 for 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.

引用

页码：381 / 386

页数：6

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