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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA9hmdtwMhG3lJXXtdq5Z4A0BwI7eoIlJHfCqIQ3CqGAY#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RA9hmdtwMhG3lJXXtdq5Z4A0BwI7eoIlJHfCqIQ3CqGAY#_4 http://www.w3.org/ns/prov#value Intracellular [Ca2+] increases in ischemic areas (487), partly due to overactivation of NMDA receptors; MAP2 and alpha-spectrin (fodrin) are degraded in animal models of cerebral ischemia with the calpain-specific 150-kDa alpha-spectrin fragment appearing 5 (28) or 60 min (319) after ischemia in rat brains; rate of expansion of the area of spectrin degradation is reduced by synthetic calpain inhibitors, A275 and A295 (28). Calpastatin is degraded by calpain to a membrane-bound 50-kDa polypeptide in ischemic brain (41). 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