No role for RTK in GPCR activation of the Ras-MAPK pathway?

29 March 2001

Peter Lockyer

I would be interested in opinions about the recent work by the Schlessinger group (JBC, "in press", but full text available at this link) that shows by genetic manipulation that Pyk2, Src, and the EGFR are dispensable for GPCR-induced MAPK activation.

Clearly the results shows the importance of using a genetic approach to resolve a complex issue, and this highlights the context and cell type- specific nature of cell signalling. Does this mean that the these mechanisms are less important than previously thought? What are the dominant mechanisms then regulating GPCR-induced MAPK activation? And how might these knock-out cells be bypassing these routes?