The role of the Ca2+-activated tyrosine kinase, Pyk2, in the pleiotropic coupling of nerve cell stimulation to the MAP kinase cascade still remains undefined. Using a panel of PC12 clones, one of which was defective in Pyk2, we demonstrate (1) that the MAP kinase response induced by a [Ca2+](i) rise (following application of the Ca2+ ionophore, ionomycin) is inappreciable in the defective clone and is re-established after Pyk2 transfection; and (2) that the responses to both protein kinase C and P(2y2) receptor activation occur normally even in the defective cells. We conclude that Pyk2 is the key mediator in the pathway activated by Ca2+ but has minor roles with the other types of stimulation. Copyright (C) 1999 Federation of European Biochemical Societies.
- Mitogen-activated protein kinase
- P(2y2) receptor
- Signal transduction
ASJC Scopus subject areas
- Molecular Biology