Deletion of cellular prion protein results in reduced Akt activation, enhanced postischemic caspase-3 activation, and exacerbation of ischemic brain injury

Stroke

Volumn 37, Issue 5, 2006, Pages 1296-1300

  Weise, Jens ^a   Sandau, Raoul ^a   Schwarting, Sönke ^a   Crome, Olaf ^a   Wrede, Arne ^a   Schulz Schaeffer, Walter ^a   Zerr, Inga ^a   Bähr, Mathias ^a  

^a UNIVERSITY MEDICAL CENTER GÖTTINGEN   (Germany)

Author keywords

Caspases; Cerebral ischemia; PrPc proteins; Signal transduction

Indexed keywords

CASPASE 3; PHOSPHATIDYLINOSITOL 3 KINASE; PRION PROTEIN; PROTEIN BAX; PROTEIN BCL 2; PROTEIN KINASE B;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BASAL GANGLION; BRAIN INFARCTION SIZE; BRAIN INJURY; BRAIN ISCHEMIA; CONTROLLED STUDY; DISEASE EXACERBATION; ENZYME ACTIVATION; GENE DELETION; IMMUNOHISTOCHEMISTRY; KNOCKOUT MOUSE; MOUSE; NEUROPROTECTION; NONHUMAN; PARIETAL LOBE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; SIGNAL TRANSDUCTION; WESTERN BLOTTING;

ANIMALS; BRAIN ISCHEMIA; CASPASE 3; CASPASES; CELL DEATH; ENZYME ACTIVATION; GENE DELETION; INFARCTION, MIDDLE CEREBRAL ARTERY; ISCHEMIC ATTACK, TRANSIENT; MICE; MICE, KNOCKOUT; MICE, TRANSGENIC; PRIONS; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION;

EID: 33646695909     PISSN: 00392499     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.STR.0000217262.03192.d4     Document Type: Article

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