rdf:type |
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lifeskim:mentions |
|
pubmed:issue |
1
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pubmed:dateCreated |
2002-1-4
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pubmed:abstractText |
Emerging evidence has shown that tumor suppressor p53 expression is enhanced in response to brain ischemia/hypoxia and that p53 plays a critical role in the cell death pathway in such an acute neurological insult. However the mechanism remains unclear. Recently it was reported that Peg3/Pw1, originally identified as a paternally expressed gene, plays a pivotal role in the p53-mediated cell death pathway in mouse fibroblast cell lines. In this study, we found that Peg3/Pw1 expression is enhanced in peri-ischemic neurons in rat stroke model by in situ hybridization analysis, where p53 expression was also induced by immunohistochemical analysis. Moreover, we found that p53 was co-localized with Peg3/Pw1 in brain ischemia/hypoxia by double staining analysis. In human neuroblastoma-derived SK-N-SH cells, Peg3/Pw1 mRNA expression is enhanced remarkably at 24 h post-hypoxia, when p53 protein expression was also enhanced at high levels. Subcellular localization of Peg3/Pw1 was observed in the nucleus. Adenovirus-mediated high dose p53 overexpression induced Peg3/Pw1 mRNA expression. Overexpression of Peg3/Pw1 reduced cell viability under hypoxic conditions, whereas that of the C-terminal-deleted mutant and anti-sense Peg3/Pw1 inhibited hypoxia-induced cell death. These results suggest that Peg3/Pw1 is involved in the p53-mediated cell death pathway as a downstream effector of p53 in brain ischemia/hypoxia.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jan
|
pubmed:issn |
0021-9258
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pubmed:author |
pubmed-author:HoriOsamuO,
pubmed-author:KasaiKousukeK,
pubmed-author:MatsuokaNobuyaN,
pubmed-author:MiyakeShin-ichiS,
pubmed-author:OgawaSatoshiS,
pubmed-author:SugimotoHisashiH,
pubmed-author:TamataniMichioM,
pubmed-author:TaniguchiManabuM,
pubmed-author:TohyamaMasayaM,
pubmed-author:TojoNobuteruN,
pubmed-author:YamaguchiAtsushiA,
pubmed-author:YamashitaToshihideT
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pubmed:issnType |
Print
|
pubmed:day |
4
|
pubmed:volume |
277
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
623-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11679586-Animals,
pubmed-meshheading:11679586-Cell Death,
pubmed-meshheading:11679586-Cell Survival,
pubmed-meshheading:11679586-DNA-Binding Proteins,
pubmed-meshheading:11679586-Gene Expression Regulation,
pubmed-meshheading:11679586-Hypoxia-Ischemia, Brain,
pubmed-meshheading:11679586-Kruppel-Like Transcription Factors,
pubmed-meshheading:11679586-Protein Kinases,
pubmed-meshheading:11679586-Proteins,
pubmed-meshheading:11679586-RNA, Messenger,
pubmed-meshheading:11679586-Rats,
pubmed-meshheading:11679586-Rats, Sprague-Dawley,
pubmed-meshheading:11679586-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11679586-Transcription Factors,
pubmed-meshheading:11679586-Tumor Suppressor Protein p53
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pubmed:year |
2002
|
pubmed:articleTitle |
Peg3/Pw1 is involved in p53-mediated cell death pathway in brain ischemia/hypoxia.
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pubmed:affiliation |
Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. yama@anat2.med.osaka-u.ac.jp
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pubmed:publicationType |
Journal Article
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