Cardiolipin, a critical determinant of mitochondrial carrier protein assembly and function.

Cardiolipin, a critical determinant of mitochondrial carrier protein assembly and function.
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DOI:
10.1016/j.bbamem.2009.04.020
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发表时间:
2009-10
影响因子:
3.4
通讯作者:
Claypool, Steven M.
Claypool, Steven M.
中科院分区:
生物学3区
文献类型:
--
作者:
Claypool, Steven M.

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磷脂作为膜蛋白结构和功能的决定因素的能力可能最好的例子是心磷脂(CL),线粒体的标志性磷脂。早期重建个体呼吸复合物和线粒体载体家族成员的努力,尤其是ADP/ATP载体(AAC),经常证明CL的重要性。在过去的十年中,CL在组织电子传递链的组分进入高阶组装(称为呼吸超配合物)中的重要性已经确立。氧化磷酸化所需的另一种蛋白质AAC受到的关注相对较少,这可能是因为AAC被认为是作为同型二聚体或单体单独发挥作用。然而,最近,AACs已被证明与呼吸超复合体、线粒体载体家族的其他成员和TIM23转座子相互作用。有趣的是,许多(如果不是全部的话)这些交互都依赖于CL。作为线粒体载体家族的范例,AAC的这些发现表明,这一重要蛋白质大群体的其他成员可能比预期的更具群居性。此外,有人提出AAC和线粒体载体家族的其他成员可能是涉及CL改变的病理状态的下游目标。
The ability of phospholipids to act as determinants of membrane protein structure and function is probably best exemplified by cardiolipin (CL), the signature phospholipid of mitochondria. Early efforts to reconstitute individual respiratory complexes and members of the mitochondrial carrier family, most notably the ADP/ATP carrier (AAC), often demonstrated the importance of CL. Over the past decade, the significance of CL in the organization of components of the electron transport chain into higher order assemblies, termed respiratory supercomplexes, has been established. Another protein required for oxidative phosphorylation, AAC, has received comparatively little attention likely stemming from the fact that AACs were thought to function in isolation as either homodimers or monomers. Recently however, AACs have been demonstrated to interact with the respiratory supercomplex, other members of the mitochondrial carrier family, and the TIM23 translocon. Interestingly, many if not all of these interactions depend on CL. As the paradigm for the mitochondrial carrier family, these discoveries with AAC suggest that other members of this large group of important proteins may be more gregarious than anticipated. Moreover, it is proposed that AAC and perhaps additional members of the mitochondrial carrier family might represent downstream targets of pathological states involving alterations in CL.
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