The novel tyrosine kinase ZAK1 activates GSK3 to direct cell fate specification

被引：157

作者：

Kim, L ^{[1
]}

Liu, JC ^{[1
]}

Kimmel, AR ^{[1
]}

机构：

[1] NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA

来源：

CELL | 1999年 / 99卷 / 04期

关键词：

D O I：

10.1016/S0092-8674(00)81526-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

Inhibition of GSK3 by 7-TM Wnt/wg receptor signaling is critical for specifying embryonic cell fate patterns. In Dictyostelium, the 7-TM cAMP receptors regulate GSK3 by parallel, antagonistic pathways to establish a developmental body plan. We describe here a novel tyrosine kinase, ZAK1, downstream of 7-TM cAMP receptor signaling that is required for GSK3 activation during development, zak1-nulls have reduced GSK3 activity and are defective in GSK3-regulated developmental pathways. Moreover, recombinant ZAK1 phosphorylates and activates GSK3 in vitro. We propose that ZAK1 is a positive regulator of GSK3 activity required for cell pattern formation in Dictyostelium and speculate that similar mechanisms exist to antagonize Wnt/wg signaling for metazoan cell fate specification.

引用

页码：399 / 408

页数：10

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