RGD Reference Report - Peg3/Pw1 is involved in p53-mediated cell death pathway in brain ischemia/hypoxia. - Rat Genome Database

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Peg3/Pw1 is involved in p53-mediated cell death pathway in brain ischemia/hypoxia.

Authors: Yamaguchi, A  Taniguchi, M  Hori, O  Ogawa, S  Tojo, N  Matsuoka, N  Miyake, S  Kasai, K  Sugimoto, H  Tamatani, M  Yamashita, T  Tohyama, M 
Citation: Yamaguchi A, etal., J Biol Chem 2002 Jan 4;277(1):623-9.
RGD ID: 70309
Pubmed: PMID:11679586   (View Abstract at PubMed)
DOI: DOI:10.1074/jbc.M107435200   (Journal Full-text)

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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Gene Hspa5 heat shock protein family A (Hsp70) member 5 Rattus norvegicus

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