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• W1915067981 startingPage "180" @default.
• W1915067981 abstract "Recent studies indicate that stimulation of NMDA receptors in cultured hippocampal cells activates MAP kinase. Although the pathway whereby MAP kinase is activated has been been characterized, little is known about the mechanisms that shut off MAP kinase. In the course of analyzing several immediate-early genes identified previously by differential screen as inducible by seizure activity, we found that one of them, BAD2, encodes dual purpose, threonine/tyrosine phosphates with specific activity directed against MAP kinase (MKP-1). In situ hybridization of BAD2 demonstrates that stimuli that produce seizure, kindling, and long-term potentiation cause a rapid increase in BAD2 mRNA (within 0.5-1 hr after stimulation) that has, in each case, a distinctive pattern of expression in the brain. In these regions, the induction of a MAP kinase-specific phosphatase may provide a negative feedback control associated with long-term synaptic changes." @default.
• W1915067981 created "2016-06-24" @default.
• W1915067981 creator A5034071817 @default.
• W1915067981 creator A5037969896 @default.
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• W1915067981 date "1994-01-01" @default.
• W1915067981 modified "2023-10-16" @default.
• W1915067981 title "Temporal and spatial regulation of the expression of BAD2, a MAP kinase phosphatase, during seizure, kindling, and long-term potentiation." @default.
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• W1915067981 doi "https://doi.org/10.1101/lm.1.3.180" @default.
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