Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 1, Pages 93-98Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3974-09.2010
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Funding
- United States Public Health Service [DA00266, DA00074]
- American Heart Association Pre-doctoral Fellowship
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Death-associated protein kinase (DAPK) is a key player in multiple cell death signaling pathways. We report that DAPK is regulated by DANGER, a partial MAB-21 domain-containing protein. DANGER binds directly to DAPK and inhibits DAPK catalytic activity. DANGER-deficient mouse embryonic fibroblasts and neurons exhibit greater DAPK activity and increased sensitivity to cell death stimuli than do wild-type control cells. In addition, DANGER-deficient mice manifest more severe brain damage after acute excitotoxicity and transient cerebral ischemia than do control mice. Accordingly, DANGER may physiologically regulate the viability of neurons and represent a potential therapeutic target for stroke and neurodegenerative diseases.
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