Substrate phosphorylation in the protein kinase Cγ knockout mouse
Substrate phosphorylation in the protein kinase Cγ knockout mouse
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DOI：
10.1074/jbc.274.4.1873
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发表时间：
1999-01-22
影响因子：
4.8
通讯作者：
de Graan, PNE
中科院分区：
文献类型：
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作者：
Ramakers, GMJ;Gerendasy, DD;de Graan, PNE
The phosphorylation state of three identified neural-specific protein kinase C substrates (RC3, GAP-43/B-50, and MARCKS) was monitored in hippocampal slices of mice lacking the gamma-subtype of protein kinase C and wildtype controls by quantitative immunoprecipitation following P-32(i) labeling. Depolarization with potassium, activation of glutamate receptors with glutamate, or direct stimulation of protein kinase C: with a phorbol ester increased RC3 phosphorylation in wild-type animals but failed to affect RC3 phosphorylation in mice lacking the gamma-subtype of protein kinase C. Our results suggests the following biochemical pathway: activation of a postsynaptic (metabotropic) glutamate receptor stimulates the gamma-subtype of protein kinase C, which in turn phosphorylates RC3. The inability to increase RC3 phosphorylation in mice lacking the gamma-subtype of protein kinase C by membrane depolarization or glutamate receptor activation may contribute to the spatial learning deficits and impaired hippocampal LTP observed in these mice.
