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Requirement of Pyk2 for the activation of the MAP kinase cascade induced by Ca 2+ (but not by PKC or G protein) in PC12 cells
Author(s) -
Barsacchi Rico,
Heider Harald,
Girault Jean-Antoine,
Meldolesi Jacopo
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01468-4
Subject(s) - ionomycin , protein kinase c , microbiology and biotechnology , cyclin dependent kinase 9 , map kinase kinase kinase , ask1 , mitogen activated protein kinase kinase , tyrosine kinase , map2k7 , kinase , mediator , chemistry , stimulation , biology , signal transduction , protein kinase a , cyclin dependent kinase 2 , endocrinology
The role of the Ca 2+ ‐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 [Ca 2+ ] i rise (following application of the Ca 2+ 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 Ca 2+ but has minor roles with the other types of stimulation.