Lack of maternal Heat Shock Factor 1 results in multiple cellular and developmental defects, including mitochondrial damage and altered redox homeostasis, and leads to reduced survival of mammalian oocytes and embryos.

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作者： Christiane,Bierkamp ^[1] ; Maëva,Luxey ; Aïcha,Metchat ; Christophe,Audouard ; Rémi,Dumollard ; Elisabeth,Christians

作者单位： Université Toulouse, UPS, UMR 5547, Centre de Biologie du Développement, IFR 109, CNRS, UPS, 118 route de Narbonne (Bat 4R3), 31062 Toulouse Cedex 09, France. bierkamp@cict.fr ^[1]

主题词动物(Animals);细胞凋亡(Apoptosis);半胱氨酸天冬氨酸蛋白酶3(Caspase 3);DNA结合蛋白质类(DNA-Binding Proteins);胚胎, 哺乳动物(Embryo, Mammalian);女(雌)性(Female);基因表达调控, 发育期(Gene Expression Regulation, Developmental);内环境稳定(Homeostasis);小鼠(Mice);小鼠, 基因敲除(Mice, Knockout);线粒体(Mitochondria);卵母细胞(Oocytes);氧化还原(Oxidation-Reduction);转录因子(Transcription Factors)

DOI 10.1016/j.ydbio.2009.12.037

PMID 20045681

发布时间 2017-11-16

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Developmental biology

2010年339卷2期

338-53页

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Lack of maternal Heat Shock Factor 1 results in multiple cellular and developmental defects, including mitochondrial damage and altered redox homeostasis, and leads to reduced survival of mammalian oocytes and embryos.

Developmental biology

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Developmental biology

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Lack of maternal Heat Shock Factor 1 results in multiple cellular and developmental defects, including mitochondrial damage and altered redox homeostasis, and leads to reduced survival of mammalian oocytes and embryos.

Developmental biology

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Developmental biology

相关期刊

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