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Overriding MAP kinase

Transduction of extracellular signals that stimulate cell proliferation requires the small GTPase Ras. Precisely which Ras signalling pathways are involved remains obscure, however, given the numerous potential Ras effectors (e.g. Raf, PI3 kinase and phospholipase C) and doubts concerning the validity of the overexpression studies often used to define them. Chris Marshall and co-workers have now dissected mitogenic signalling through Ras by examining the requirement for ERK (part of the Ras-Raf-MEK-ERK MAP kinase cascade) signalling in cells lacking the tumour suppressor RB, using inhibitors of MEK to block ERK activation. Among their results is the observation that, unlike wild-type cells, RB^-/- mouse embryonic fibroblasts do not require significant ERK activation for exit from G0 phase and entry into S phase (see p. 4607). Since RB^-/- cells require Ras for exit from G0, this key finding indicates that although Ras/ERK signalling is required for the G1/S transition, an ERK-independent Ras mechanism drives exit from G0. It also demonstrates — for the first time — that loss of a tumour suppressor can alter cellular requirements for MAP kinase signalling.

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Loss of Rb overrides the requirement for ERK activity for cell proliferation

Giovanna M. D'Abaco, Steven Hooper, Hugh Paterson, and Christopher J. Marshall
JCS 2002 115: 4607-4616. [Abstract] [Full Text]  

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content