Integrating signals between cAMP and the RAS/RAF/MEK/ERK signalling pathways - Based on the Anniversary Prize of the Gesellschaft fur Biochemie und Molekularbiologie Lecture delivered on 5 July 2003 at the special FEBS meeting in Brussels
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作者:
Dumaz, N
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Inst Canc Res, Signal Transduct Team, Canc Res UK Ctr Cell & Mol Biol, London SW3 6JB, EnglandInst Canc Res, Signal Transduct Team, Canc Res UK Ctr Cell & Mol Biol, London SW3 6JB, England
Dumaz, N
[1
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Marais, R
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Inst Canc Res, Signal Transduct Team, Canc Res UK Ctr Cell & Mol Biol, London SW3 6JB, EnglandInst Canc Res, Signal Transduct Team, Canc Res UK Ctr Cell & Mol Biol, London SW3 6JB, England
Marais, R
[1
]
机构:
[1] Inst Canc Res, Signal Transduct Team, Canc Res UK Ctr Cell & Mol Biol, London SW3 6JB, England
One of the hallmarks of cAMP is its ability to inhibit proliferation in many cell types, but stimulate proliferation in others. Clearly cAMP has cell type specific effects and the outcome on proliferation is largely attributed to crosstalk from cAMP to the RAS/RAF/mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathway. We review the crosstalk between these two ancient and conserved pathways, describing the molecular mechanisms underlying the interactions between these pathways and discussing their possible biological importance.