The basal proton conductance of mitochondria depends on adenine nucleotide translocase content

The basal proton conductance of mitochondria depends on adenine nucleotide translocase content
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DOI:
10.1042/bj20050890
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发表时间:
2005-12-01
影响因子:
4.1
通讯作者:
Cornwall, EJ
Cornwall, EJ
中科院分区:
生物学3区
文献类型:
--
作者:
Brand, MD;Pakay, JL;Cornwall, EJ

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线粒体的基础质子电导引起轻度解偶联,可能是代谢率的重要贡献者。质子传导途径的分子性质是未知的。我们发现,从小鼠肌肉线粒体的质子传导,其中亚型I的腺嘌呤核苷酸移位酶已被消融是野生型对照的一半。由果蝇线粒体中的应激敏感B基因编码的腺嘌呤核苷酸移位酶的过表达增加质子传导性,而低表达降低质子传导性,即使载体被完全抑制。我们的结论是,一半到三分之二的线粒体的基础质子传导是由腺嘌呤核苷酸载体催化,独立于其ATP/ADP交换或脂肪酸依赖的质子泄漏功能。
The basal proton conductance of mitochondria causes mild uncoupling and may be an important contributor to metabolic rate. The molecular nature of the proton-conductance pathway is unknown. We show that the proton Conductance of muscle mitochondria from mice in which isoform I of the adenine nucleotide translocase has been ablated is half that of wild-type controls. Overexpression of the adenine nucleotide translocase encoded by the stress-sensitive B gene in Drosophila mitochondria increases proton conductance, and underexpression decreases it, even when the carrier is fully inhibited Using carboxyatractylate. We conclude that half to two-thirds of the basal proton conductance of mitochondria is catalysed by the adenine nucleotide carrier, independently of its ATP/ADP exchange or fatty-acid-dependent proton-leak functions.