Abstract:
: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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Barsacchi R,Heider H,Girault J,Meldolesi Jdoi
10.1016/s0014-5793(99)01468-4keywords:
subject
Has Abstractpub_date
1999-11-19 00:00:00pages
273-6issue
3eissn
0014-5793issn
1873-3468pii
S0014579399014684journal_volume
461pub_type
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