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March 31, 2006Stroke

Deletion of Cellular Prion Protein Results in Reduced Akt Activation, Enhanced Postischemic Caspase-3 Activation, and Exacerbation of Ischemic Brain Injury

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Authors

JWJens WeiseVolkswagen Group (Germany)RSRaoul SandauS.P.E.C.I.E.S.SSSönke SchwartingUniversity of Augsburg

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Weise et al. (2006) studied this question.

synapsesocial.com/papers/6a0065a72ff633f36577ebf9https://doi.org/10.1161/01.str.0000217262.03192.d4
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1PrPC Directly Interacts with Proteins Involved in Signaling Pathways2001 · 227 citations
  2. 2Expression of Prion Protein Increases Cellular Copper Binding and Antioxidant Enzyme Activities but Not Copper Delivery2003 · 197 citations
  3. 3Evidence of Phosphorylation of Akt and Neuronal Survival after Transient Focal Cerebral Ischemia in Mice2001 · 285 citations
  4. 4Ablation of the prion protein (PrP) gene in mice prevents scrapie and facilitates production of anti-PrP antibodies.1993 · 471 citations