细胞松弛素D破坏肌动蛋白微丝会导致p53激活。

Disruption of actin microfilaments by cytochalasin D leads to activation of p53.

作者信息

Rubtsova S N, Kondratov R V, Kopnin P B, Chumakov P M, Kopnin B P, Vasiliev J M

机构信息

Belozersky Institute of Physical and Chemical Biology, Moscow State University, Russia.

出版信息

FEBS Lett. 1998 Jul 3;430(3):353-7. doi: 10.1016/s0014-5793(98)00692-9.

DOI:10.1016/s0014-5793(98)00692-9

PMID:9688570

Abstract

Activation of p53 plays a central role in the cell's response to various stress signals. We investigated whether p53 is activated upon disruption of actin microfilaments, caused by cytochalasin D (CD). We show that treatment with CD leads to accumulation of p53 in the cells and activation of p53-dependent transcription. Treatment with CD led to arrest of G1-to-S transition in cells retaining wild-type p53, while cells with inactivated p53 showed partial rescue from it. CD also induces apoptosis in p53+/+, but not in p53-/- cells. The obtained data suggest that disruption of the actin microfilaments activates p53-dependent pathways.

摘要

p53的激活在细胞对各种应激信号的反应中起着核心作用。我们研究了细胞松弛素D（CD）导致肌动蛋白微丝破坏后p53是否被激活。我们发现，用CD处理会导致细胞中p53的积累以及p53依赖性转录的激活。用CD处理会导致保留野生型p53的细胞中G1期到S期的转换停滞，而p53失活的细胞则表现出部分恢复。CD还诱导p53+/+细胞凋亡，但不诱导p53-/-细胞凋亡。所获得的数据表明，肌动蛋白微丝的破坏激活了p53依赖性途径。