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An imprinted PEG1/MEST antisense expressed predominantly in human testis and in mature spermatozoa 总被引:10,自引:0,他引:10
Li T Vu TH Lee KO Yang Y Nguyen CV Bui HQ Zeng ZL Nguyen BT Hu JF Murphy SK Jirtle RL Hoffman AR 《The Journal of biological chemistry》2002,277(16):13518-13527
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Atsushi Yamaguchi Manabu Taniguchi Osamu Hori Satoshi Ogawa Nobuteru Tojo Nobuya Matsuoka Shin-ichi Miyake Kousuke Kasai Hisashi Sugimoto Michio Tamatani Toshihide Yamashita Masaya Tohyama 《The Journal of biological chemistry》2002,277(1):623-629
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. 相似文献
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