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Proteomic analysis of anoxia tolerance in the developing zebrafish embryo

机译:蛋白质组学分析的缺氧耐受发展中斑马鱼胚胎

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摘要

While some species and tissue types are injured by oxygen eprivation, anoxia tolerant organisms display a protective response that has not been fully elucidated and is well-suited to genomic and proteomic analysis.However, such methodologies have focused on transcriptional responses, prolonged anoxia, or have used cultured cells or isolated tissues. In this study of intact zebrafish embryos, a species capable of N24 h survival in anoxia, we have utilized 2D difference in gel electrophoresis to identify changes in the proteomic profile caused by near-lethal anoxic durations as well as acute anoxia (1 h), a timeframe relevant to ischemic events in human disease when response mechanisms are largely limited to post-transcriptional and posttranslational processes. We observed a general stabilization of the proteome in anoxia. Proteins involved in oxidative phosphorylation, antioxidant defense, transcription, and translation changed over this time period. Among the largest proteomic alterations was that of muscle cofilin 2, implicating the regulation of the cytoskeleton and actin assembly in the adaptation to acute anoxia. These studies in an intact embryo highlight proteomic components of an adaptive response to anoxia in a model organism amenable to genetic analysis to permit further mechanistic insight into the phenomenon of anoxia tolerance.
机译:虽然一些物种和组织类型是受伤了氧气eprivation,缺氧宽容的有机体显示没有保护性反应充分阐明,是适合基因组和蛋白质组学分析。方法主要集中在转录反应,长时间的缺氧,或使用培养的细胞或孤立的组织。完整的斑马鱼胚胎,一个物种的能力N24 h在缺氧生存,我们利用2 d差异凝胶电泳鉴别蛋白质组剖面的变化所致近乎致命缺氧时间以及急性缺氧(1 h)与缺血性相关的时间表事件在人类疾病的反应机制在很大程度上局限于转录后和转译后的流程。稳定蛋白质组的缺氧。蛋白质参与氧化磷酸化,抗氧化防御、转录和翻译这段时间内改变。蛋白质组的改变是最大的肌肉cofilin 2,暗示的规定细胞骨架肌动蛋白组装的急性缺氧适应。完整的胚胎强调蛋白质组的组成部分一个向缺氧适应性反应模型允许有机体的遗传分析进一步的了解这一现象缺氧的宽容。

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