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成功逃脱;蛋白激酶A对Ena/VASP的磷酸化促进丝状伪足的形成。

The great escape; phosphorylation of Ena/VASP by PKA promotes filopodial formation.

作者信息

Gomez Timothy M, Robles Estuardo

机构信息

Department of Anatomy, University of Wisconsin Medical School, Madison, WI 53706, USA.

出版信息

Neuron. 2004 Apr 8;42(1):1-3. doi: 10.1016/s0896-6273(04)00188-6.

DOI:10.1016/s0896-6273(04)00188-6
PMID:15066258
Abstract

The Ena/VASP family of proteins consists of adaptor molecules that localize to subcellular sites of actin polymerization. The role of Ena/VASP proteins in the regulation of cell motility and axon outgrowth has been controversial. Recently, these proteins have been proposed to function as "anticapping" factors, which may have differential effects on filopodial versus lammelipodial actin-based protrusions. A study by Lebrand et al. in this issue of Neuron supports this model and identifies PKA as a key regulator of Ena/VASP function downstream of the chemoattractant Netrin.

摘要

Ena/VASP蛋白家族由定位于肌动蛋白聚合亚细胞位点的衔接分子组成。Ena/VASP蛋白在细胞运动和轴突生长调节中的作用一直存在争议。最近,这些蛋白被认为起到“抗帽”因子的作用,这可能对丝状伪足与片状伪足的肌动蛋白依赖性突起产生不同影响。Lebrand等人在本期《神经元》杂志上发表的一项研究支持了这一模型,并确定蛋白激酶A(PKA)是趋化因子Netrin下游Ena/VASP功能的关键调节因子。

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