线粒体中琥珀酸脱氢酶的调控 - Suppr

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超能文献

Control of succinate dehydrogenase in mitochondria.

作者信息

Gutman M, Kearney E B, Singer T P

出版信息

Biochemistry. 1971 Dec 7;10(25):4763-70. doi: 10.1021/bi00801a025.

DOI:10.1021/bi00801a025

PMID:5140191

Abstract

摘要

相似文献

Control of succinate dehydrogenase in mitochondria.线粒体中琥珀酸脱氢酶的调控

Biochemistry. 1971 Dec 7;10(25):4763-70. doi: 10.1021/bi00801a025.

Multiple control mechanisms for succinate dehydrogenase in mitochondria.线粒体中琥珀酸脱氢酶的多种调控机制。

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Inactivation of coupled respiration of mitochondria by inorganic arsenate and partial restoration by ATP.无机砷酸盐使线粒体偶联呼吸失活，ATP使其部分恢复。

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Correlation of the effects of citric acid cycle metabolites on succinate oxidation by rat liver mitochondria and submitochondrial particles.柠檬酸循环代谢物对大鼠肝脏线粒体和亚线粒体颗粒琥珀酸氧化作用的相关性

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Effects of certain iron-chelators and antibiotics on the interaction of succinate dehydrogenase and cytochrome b in ubiquinone-depleted submitochondrial particles.

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The inhibition by 2,4-dinitrophenol of the removal of oxaloacetate formed by the oxidation of succinate by rat-liver and -heart mitochondria.2,4-二硝基苯酚对大鼠肝脏和心脏线粒体氧化琥珀酸生成的草酰乙酸去除的抑制作用。

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Liver and skeletal muscle mitochondrial function following burn injury.烧伤后肝脏和骨骼肌的线粒体功能

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Control of beta-hydroxybutyrate and acetoacetate oxidation by inorganic phosphate and adenosine-5'-diphosphate in heart mitochondria.

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Avenaciolide inhibition of anion transport in mitochondria.燕麦酸内酯对线粒体阴离子转运的抑制作用。

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Phosphate acceptor specificity during oxidative phosphorylation in submitochondrial particles.亚线粒体颗粒氧化磷酸化过程中的磷酸受体特异性

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Brain Insulin Resistance: Focus on Insulin Receptor-Mitochondria Interactions.脑胰岛素抵抗：聚焦胰岛素受体与线粒体的相互作用。

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Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart.线粒体复合物II在脑和心脏中对草酰乙酸抑制作用的敏感性差异

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The 2-oxoacid dehydrogenase complexes in mitochondria can produce superoxide/hydrogen peroxide at much higher rates than complex I.线粒体中的 2-氧酸脱氢酶复合物可以比复合物 I 以更高的速率产生超氧阴离子/过氧化氢。

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Mitochondrial H2O2 as an enable signal for triggering autophosphorylation of insulin receptor in neurons.线粒体过氧化氢作为触发神经元中胰岛素受体自磷酸化的启动信号。

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Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel.复合物II抑制对衰老、疾病和线粒体ATP敏感性钾通道的生理影响。

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Mitochondrial complex II can generate reactive oxygen species at high rates in both the forward and reverse reactions.线粒体复合物 II 可以在正向和反向反应中以高速度产生活性氧物质。

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