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细胞色素c氧化酶的内在解偶联可能导致母系遗传的线粒体疾病MELAS和LHON。

Intrinsic uncoupling of cytochrome c oxidase may cause the maternally inherited mitochondrial diseases MELAS and LHON.

作者信息

Mather M W, Rottenberg H

机构信息

Department of Pathology and Laboratory Medicine, MCP/Hahnemann School of Medicine, Allegheny University of the Health Sciences, Philadelphia, PA 19102, USA.

出版信息

FEBS Lett. 1998 Aug 14;433(1-2):93-7. doi: 10.1016/s0014-5793(98)00891-6.

Abstract

Mutations in the human mtDNA gene encoding subunit III of cytochrome c oxidase (CO) have been reported to cause MELAS and LHON. Poracoccus denitrificans cells expressing substitutions homologous to these MELAS- and LHON-causing mutations had lower growth yield than wild type cells and lower efficiency of proton pumping by CO (e.g. lower H+/e ratio and lower deltapsi), but had similar CO activity. These results indicate that both substitutions (F263L > A212T) cause intrinsic uncoupling, which may be the direct cause of the diseases. These results also suggest that subunit III is involved in proton pumping.

摘要

据报道,人类线粒体DNA(mtDNA)中编码细胞色素c氧化酶(CO)亚基III的基因突变会导致线粒体脑肌病伴乳酸血症和卒中样发作(MELAS)以及Leber遗传性视神经病变(LHON)。表达与这些导致MELAS和LHON的突变同源替代的反硝化副球菌细胞,其生长产量低于野生型细胞,且CO质子泵浦效率较低(例如,H⁺/e比率较低和膜电位较低),但CO活性相似。这些结果表明,这两种替代(F263L>A212T)都会导致内在解偶联,这可能是疾病的直接原因。这些结果还表明,亚基III参与质子泵浦。

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