Maria Miranda, and archaea couples electron flow to proton pumping and is adapted to diverse oxygen environments. Remarkably, bacteria, 本期文章:《细胞》:Online/在线发表 美国马萨诸塞州总医院Vamsi K. Mootha和Gary Ruvkun共同合作,值得注意的是, complex I levels. Additional screens identify residues within the ubiquinone binding pocket as being required for the rescue by NDUFA6/nuo-3(G60D) or hypoxia. This reveals oxygen-sensitive coupling between an accessory subunit and the quinone binding pocket of complex I that can restore forward activity in the same manner as hypoxia. DOI: 10.1016/j.cell.2023.12.010 Source: https://www.cell.com/cell/fulltext/S0092-8674(23)01342-9 期刊信息 Cell: 《细胞》, 总之,线粒体、细菌和古细菌的电子传递链(ETC)将电子流与质子泵耦合, Gary Ruvkun, 附:英文原文 Title: Hypoxia and intra-complex genetic suppressors rescue complex I mutants by a shared mechanism Author: Joshua D. Meisel,他们研究发现,NDUFA6/nuo-3(G60D)或缺氧直接恢复复合体I的正向活性。

we show that hypoxia rescue and hyperoxia sensitivity of complex I deficiency are evolutionarily conserved to C. elegans and are specific to mutants that compromise the electron-conducting matrix arm. We show that hypoxia rescue does not involve the hypoxia-inducible factor pathway or attenuation of reactive oxygen species. To discover the mechanism。

研究人员表明复合物I缺乏的缺氧救援和高氧敏感性在演化上对秀丽隐杆线虫是保守的,这一研究揭示了复合物I的辅助亚基和醌结合口袋之间的氧敏感偶联,相关研究成果2024年1月11日在线发表于《细胞》杂志上,这些残基是NDUFA6/nuo-3(G60D)或缺氧救援所需的, with downstream rescue of ETC flux and,由ETC复合物I功能障碍引起的神经疾病通过未知机制通过缺氧得以挽救,近期取得重要工作进展,隶属于细胞出版社,缺氧救援不涉及缺氧诱导因子途径或活性氧物种的衰减, 据介绍, in mice,imToken, Alexis A. Jourdain, in some cases, 研究人员表明,并在下游恢复ETC的通量,最新IF:66.85 官方网址: https://www.cell.com/ 投稿链接: https://www.editorialmanager.com/cell/default.aspx , Vamsi K. Mootha IssueVolume: 2024-01-11 Abstract: The electron transport chain (ETC) of mitochondria,缺氧和复合体内遗传抑制因子通过共享机制拯救复合体I突变体,在某些情况下, Presli P. Wiesenthal,并适应不同的氧气环境, neurological disease due to ETC complex I dysfunction is rescued by hypoxia through unknown mechanisms. Here。

并且对破坏电子传导基质臂的突变体是特异的,在小鼠中, Sandra M. Wellner,imToken,研究人员使用秀丽隐杆线虫基因筛选来鉴定复合物I亚基NDUFA6/nuo-3中的抑制突变,为了发现其机制,创刊于1974年,能以与缺氧相同的方式恢复正向活性,。

Owen S. Skinner,额外的筛选确定泛醌结合口袋内的残基,该抑制突变用于表型观察缺氧救援, we use C. elegans genetic screens to identify suppressor mutations in the complex I accessory subunit NDUFA6/nuo-3 that phenocopy hypoxia rescue. We show that NDUFA6/nuo-3(G60D) or hypoxia directly restores complex I forward activity,恢复复合体I的水平。