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Obach M Navarro-Sabaté A Caro J Kong X Duran J Gómez M Perales JC Ventura F Rosa JL Bartrons R 《The Journal of biological chemistry》2004,279(51):53562-53570
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Wu LY Wang Y Jin B Zhao T Wu HT Wu Y Fan M Wang XM Zhu LL 《Neurochemical research》2008,33(10):2118-2125
Nervous system development at early stage is in hypoxic environment. Very little is known about the role of hypoxia in neuronal
development. P19 embryonal carcinoma (EC) cells are a widely used model for studying early neuronal development. In this study
we investigated the roles of hypoxia in differentiation of dopaminergic neurons derived from P19 EC cells. Results demonstrate
that hypoxia increases the percentage of differentiated neurons, especially neurons of dopaminergic phenotype. To investigate
the potential mechanism involved in hypoxia promoted differentiation of dopaminergic neurons, we measured the expression of
hypoxia-inducible factor 1α (HIF-1α), based on its characteristic response to hypoxia. The result shows that HIF-1α mRNA level
in P19 EC cells increases after hypoxia treatment. It is known that HIF-1α regulates the expression of tyrosine hydroxylase
(TH) gene through binding to its promoter. Therefore, we propose that the underlying mechanism for hypoxia promoted differentiation
of dopaminergic neurons was mediated by HIF-1α up-regulation under hypoxia.
Yue Wang—Co-first author.
Special Issue in honor of Dr. Ji-Sheng Han. 相似文献
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Hypoxia-mediated down-regulation of Bid and Bax in tumors occurs via hypoxia-inducible factor 1-dependent and -independent mechanisms and contributes to drug resistance 总被引:19,自引:0,他引:19
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Erler JT Cawthorne CJ Williams KJ Koritzinsky M Wouters BG Wilson C Miller C Demonacos C Stratford IJ Dive C 《Molecular and cellular biology》2004,24(7):2875-2889
Solid tumors with disorganized, insufficient blood supply contain hypoxic cells that are resistant to radiotherapy and chemotherapy. Drug resistance, an obstacle to curative treatment of solid tumors, can occur via suppression of apoptosis, a process controlled by pro- and antiapoptotic members of the Bcl-2 protein family. Oxygen deprivation of human colon cancer cells in vitro provoked decreased mRNA and protein levels of proapoptotic Bid and Bad. Hypoxia-inducible factor 1 (HIF-1) was dispensable for the down-regulation of Bad but required for that of Bid, consistent with the binding of HIF-1alpha to a hypoxia-responsive element (positions -8484 to -8475) in the bid promoter. Oxygen deprivation resulted in proteosome-independent decreased expression of Bax in vitro, consistent with a reduction in global translation efficiency. The physiological relevance of Bid and Bax down-regulation was confirmed in tumors in vivo. Oxygen deprivation resulted in decreased drug-induced apoptosis and clonogenic resistance to agents with different mechanisms of action. The contribution of Bid and/or Bax down-regulation to drug responsiveness was demonstrated by the relative resistance of normoxic cells that had no or reduced expression of Bid and/or Bax and by the finding that forced expression of Bid in hypoxic cells resulted in increased sensitivity to the topoisomerase II inhibitor etoposide. 相似文献