PEA-15 Mediates Cytoplasmic Sequestration of ERK MAP Kinase

Etienne Formstecher, Joe W. Ramos, Mireille Fauquet, David A. Calderwood, Jyh Cheng Hsieh, Brigitte Canton, Xuan Thao Nguyen, Jean Vianney Barnier, Jacques Camonis, Mark H. Ginsberg, Hervé Chneiweiss

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)239-250
Number of pages12
JournalDevelopmental Cell
Volume1
Issue number2
DOIs
Publication statusPublished - 1 Jan 2001
Externally publishedYes

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