| http://purl.uniprot.org/citations/15120593 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15120593 | http://www.w3.org/2000/01/rdf-schema#comment | "Accumulating evidence indicates that the mitochondrial cell-death pathway, which involves the release of cytochrome c from mitochondria, participates in neuronal cell death after transient cerebral ischemia. However, the upstream events, that induce cytochrome c release after transient global ischemia are not fully understood. Bad is a pro-apoptotic member of the bcl-2 gene family that promotes apoptosis by binding to and inhibiting functions of anti-apoptotic proteins Bcl-2 and Bcl-xL. We investigated the effects of transient (15 min) global ischemia on the intracellular localization of Bad and the interaction of Bad with calcineurin, Akt or Bcl-xL in the vulnerable CA1 and resistant CA3/dentate gyrus of the hippocampus. Immunoblotting analysis revealed that the amount of Bad in mitochondria significantly increased after ischemia. Co-immunoprecipitation studies showed decreased interactions of Bad with Akt and calcineurin in the cytosol and increased binding with Bcl-xL in the mitochondrial fraction of hippocampal CA1, but not in the CA3/dentate gyrus region. Further, we examined the effect of recombinant Bad on the cytochrome c release from isolated mitochondria. Treatment with both recombinant Bad and calcium, but not with recombinant Bad alone, induced cytochrome c release. These results suggest that changes in localization and complex formation by Bad are, at least in part, involved in the vulnerability of cells after transient global ischemia."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.brainres.2004.03.003"xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/author | "Abe T."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/author | "Nakano M."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/author | "Furuya M."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/author | "Takeo S."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/author | "Takagi N."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/name | "Brain Res"xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/pages | "159-168"xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/title | "Altered Bad localization and interaction between Bad and Bcl-xL in the hippocampus after transient global ischemia."xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://purl.uniprot.org/core/volume | "1009"xsd:string |
| http://purl.uniprot.org/citations/15120593 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15120593 |
| http://purl.uniprot.org/citations/15120593 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15120593 |
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