Crosstalk between cAMP and MAP kinase signaling in the regulation of cell proliferation

Philip J.S. Stork, John M. Schmitt

Research output: Contribution to journalReview article

688 Scopus citations

Abstract

Hormonal stimulation of cyclic adenosine monophosphate (cAMP) and the cAMP-dependent protein kinase PKA regulates cell growth by multiple mechanisms. A hallmark of cAMP is its ability to stimulate cell growth in many cell types while inhibiting cell growth in others. In this review, the cell type-specific effects of cAMP on the mitogen-activated protein (MAP) kinase (also called extracellular signal-regulated kinase, or ERK) cascade and cell proliferation are examined. Two basic themes are discussed. First, the capacity of cAMP for either positive or negative regulation of the ERK cascade accounts for many of the cell type-specific actions of cAMP on cell proliferation. Second, there are several specific mechanisms involved in the inhibition or activation of ERKs by cAMP. Emerging new data suggest that one of these mechanisms might involve the activation of the GTPase Rap1, which can activate or inhibit ERK signaling in a cell-specific manner.

Original languageEnglish (US)
Pages (from-to)258-266
Number of pages9
JournalTrends in Cell Biology
Volume12
Issue number6
DOIs
StatePublished - Jun 1 2002

ASJC Scopus subject areas

  • Cell Biology

Fingerprint Dive into the research topics of 'Crosstalk between cAMP and MAP kinase signaling in the regulation of cell proliferation'. Together they form a unique fingerprint.

  • Cite this