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出 处:《高技术通讯》2006年第4期403-407,共5页Chinese High Technology Letters
摘 要:通过不同缺氧程度小白鼠模型,同时利用心肌组织的核DNA片段的基因体外表达和mRNA体外翻译,观察到了心肌缺氧信息获得、传导和储存的分子机理。观察结果表明:心肌等胞质中氧代谢相关的已有基因的开关蛋白质复合体等参与了人工轻度快速缺氧信息的获得;心肌等胞质中已有n mRNA链状复合体中mRNA迅速翻译出蛋白质,心肌等组织可传导较严重快速缺氧信息;心肌等细胞核内已有氧代谢相关的活性核基因迅速表达出自己编码的蛋白质,心肌等以储存较长时间严重缺氧信息。昆明种小白鼠在中国西藏拉萨郊区自然缺氧条件下饲喂30天,长期缺氧信息的储存分子机制与上述小白鼠较长时间严重缺氧模型类似,同时原有的和新形成的细胞的核DNA片段上的氧代谢等相关的核基因分别表达出较多蛋白质,并引起小白鼠的耳朵和尾巴增长等体型的明显变化。Molecular mechanism of obtaining, transferring and storing cardiac hypoxia information in mice was observed by using cardiac nuclear DNA fragment in vitro transcription and translation through mouse models with different extent of hypoxia. Switch protein complexes were involved in obtaining artificial slight speedy hypoxia information in cardiac cytoplasm. In cardiac cytoplasm, existing n mRNA chain complex's mRNAs quiekly translated proteins and the body can transfer speedy and comparatively serious hypoxia information. In cardiac nucleus, existing oxygen metabolism-associated active genes quickly expressed switch proteins, therefore, the body can store long serious hypoxia information. Kunming mice lived for 30 days under natural hypoxia in Tibet, China. The molecular mechanisn; for storing long hypoxia information was similar to the longer serious hypoxia model. Meanwhile, existing and newly formed oxygen metabolism-related nuclear genes expressed more proteins respectively and caused obvious changes, such as longer mouse ears and tails.
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