PEA-15 mediates cytoplasmic sequestration of ERK MAP kinase
PEA-15 mediates cytoplasmic sequestration of ERK MAP kinase
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DOI：
10.1016/s1534-5807(01)00035-1
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发表时间：
2001-08-01
影响因子：
11.8
通讯作者：
Chneiweiss, H
中科院分区：
文献类型：
--
作者：
Formstecher, E;Ramos, JW;Chneiweiss, H
ERK 1/2 MAP激酶途径控制细胞生长和存活并调节整联蛋白功能。在这里，我们报告说，PEA-15，一种在多种细胞类型中表达的蛋白质，通过结合ERK并阻止其在细胞核中的定位来阻断ERK依赖的转录和增殖。PEA-15含有其在细胞质中锚ERK的能力所需的核输出序列。PEA-15的基因缺失导致ERK核定位增加，随之增加cFos转录和细胞增殖。因此，PEA-15可以通过调节ERK MAP激酶的亚细胞定位来重定向MAP激酶信号传导的生物学结果。
The ERK 1/2 MAP kinase pathway controls cell growth and survival and modulates integrin function. Here, we report that PEA-15, a protein variably expressed in multiple cell types, blocks ERK-dependent transcription and proliferation by binding ERKs and preventing their localization in the nucleus. PEA-15 contains a nuclear export sequence required for its capacity to anchor ERK in the cytoplasm. Genetic deletion of PEA-15 results in increased ERK nuclear localization with consequent increased cFos transcription and cell proliferation. Thus, PEA-15 can redirect the biological outcome of MAP kinase signaling by regulating the subcellular localization of ERK MAP kinase.