RGD Reference Report - Expression of death-associated protein kinase and recruitment to the tumor necrosis factor signaling pathway following brief seizures. - Rat Genome Database

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Expression of death-associated protein kinase and recruitment to the tumor necrosis factor signaling pathway following brief seizures.

Authors: Henshall, DC  Araki, T  Schindler, CK  Shinoda, S  Lan, JQ  Simon, RP 
Citation: Henshall DC, etal., J Neurochem 2003 Sep;86(5):1260-70.
RGD ID: 1299334
Pubmed: PMID:12911633   (View Abstract at PubMed)

Death-associated protein (DAP) kinase is calcium-regulated and known to function downstream of death receptors, prompting us to examine its role in the mechanism of seizure-induced neuronal death. Brief seizures were focally evoked in rats, eliciting neuronal death within the CA3 subfield of the hippocampus, and to a lesser extent, cortex. Western blotting confirmed expression of DAP kinase within hippocampus and cortex at the predicted weight of approximately 160 kDa. Immunohistochemistry revealed seizures triggered a significant increase in numbers of DAP kinase-expressing cells within CA3 and cortex, without affecting cell counts within seizure-resistant CA2 or the dentate gyrus. Numbers of DAP kinase-expressing cells were increased in relation to specific patterns of injury-causing seizure activity, electrographically defined. Seizures caused an early increase in DAP kinase binding to actin, and association with calmodulin. Co-immunoprecipitation studies also revealed seizures triggered binding of DAP kinase to the tumor necrosis factor receptor 1 and the Fas-associated death domain protein, commensurate with caspase-8 proteolysis. In contrast, within surviving fields of the hippocampus, DAP kinase interacted with the molecular chaperone 14-3-3. These data suggest DAP kinase is involved in the molecular pathways activated during seizure-induced neuronal death.

Objects referenced in this article
Gene Dapk3 death-associated protein kinase 3 Rattus norvegicus

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