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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2006-4-25
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pubmed:abstractText |
The physiological function of cellular prion protein (PrPc) is not yet understood. Recent findings suggest that PrPc may have neuroprotective properties, and its absence increases susceptibility to neuronal injury. The purpose of this study was to elucidate the role of PrPc in ischemic brain injury in vivo.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1524-4628
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1296-300
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16574930-Animals,
pubmed-meshheading:16574930-Brain Ischemia,
pubmed-meshheading:16574930-Caspase 3,
pubmed-meshheading:16574930-Caspases,
pubmed-meshheading:16574930-Cell Death,
pubmed-meshheading:16574930-Enzyme Activation,
pubmed-meshheading:16574930-Gene Deletion,
pubmed-meshheading:16574930-Infarction, Middle Cerebral Artery,
pubmed-meshheading:16574930-Ischemic Attack, Transient,
pubmed-meshheading:16574930-Mice,
pubmed-meshheading:16574930-Mice, Knockout,
pubmed-meshheading:16574930-Mice, Transgenic,
pubmed-meshheading:16574930-Prions,
pubmed-meshheading:16574930-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:16574930-Signal Transduction
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pubmed:year |
2006
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pubmed:articleTitle |
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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pubmed:affiliation |
Department of Neurology, University of Goettingen Medical School, Germany. jweise@gwdg.de
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pubmed:publicationType |
Journal Article
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