Signal transduction - Actin, cofilin and cognition

被引：31

作者：

Rosenblatt, J

Mitchison, TJ

机构：

[1] Univ Calif San Francisco, Dept Biochem, San Francisco, CA 94143 USA

[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

来源：

NATURE | 1998年 / 393卷 / 6687期

关键词：

D O I：

10.1038/31597

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Patients with Williams syndrome have defects in visuo-spatial cognition (a failure to integrate parts into a whole) that are linked to deletion of the gene that encodes LIM kinase-1 (LIMK-1). The reasons for this are becoming clearer with the identification of a molecular target for LIMK-1. It turns out that this enzyme phosphorylates cofilin, which is essential for the turnover of actin filaments. Such turnover may be implicated in axon guidance, and could explain why high levels of LIMK-1 are found in neurons.

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收藏

页码：739 / 740

页数：2

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