Solute Carrier Family SLC41, what do we really know about it?
Solute Carrier Family SLC41, what do we really know about it?
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DOI：
10.1002/wmts.95
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Kolisek, Martin
中科院分区：
文献类型：
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作者：
Fleig, Andrea;Schweigel-Rontgen, Monika;Kolisek, Martin
溶质载体的第41家族（SLC 41）包括三个成员A1、A2和A3，其与细菌Mg 2+通道MgtE远距离同源。SLC 41 A1最近被表征为Na+/Mg 2+交换器（NME;主要的细胞Mg 2+流出系统）。关于SLC 41 A2和SLC 41 A3的确切功能知之甚少，尽管这些蛋白质也与人（动物）细胞中的Mg 2+转运有关。与SLC 41 A1相比，SLC 41 A2和SLC 41 A3的分子生物学（包括膜拓扑结构、细胞定位、转录组学和蛋白质组学）仅得到很少的探索。关于SLC 41 A1的功能、功能调节、参与细胞信号传导、复合物形成能力、结合伴侣谱和参与人类疾病的病理生理学的数据显著更多。最近的三个观察结果，即在SLC 41 A1中鉴定出作为肾单位沉积样表型基础的无效突变c.698G>T，认识到SLC 41 A1和帕金森病之间的推定联系，以及观察到近55%的先兆子痫胎盘样品过表达SLC 41 A1，标志着该蛋白质作为这些疾病的可能治疗靶点。SLC 41 A3基因敲除小鼠发生异常运动协调的发现进一步证实了Mg 2+转运蛋白的SLC 41家族在人类疾病的病理生理学中的潜在作用。
The 41st family of solute carriers (SLC41) comprises three members A1, A2 and A3, which are distantly homologous to bacterial Mg2+ channel MgtE. SLC41A1 was recently characterized as being an Na+/Mg2+ exchanger (NME; a predominant cellular Mg2+ efflux system). Little is known about the exact function of SLC41A2 and SLC41A3, although, these proteins have also been linked to Mg2+ transport in human (animal) cells. The molecular biology (including membrane topology, cellular localization, transcriptomics and proteomics) of SLC41A2 and SLC41A3 compared with SLC41A1 has only been poorly explored. Significantly more data with regard to function, functional regulation, involvement in cellular signalling, complex-forming ability, spectrum of binding partners and involvement in the pathophysiology of human diseases are available for SLC41A1. Three recent observations namely the identification of the null mutation, c.698G>T, in SLC41A1 underlying the nephronophthisis-like phenotype, the recognition of a putative link between SLC41A1 and Parkinson’s disease, and the observation that nearly 55% of preeclamptic placental samples overexpress SLC41A1, marks the protein as a possible therapeutic target of these diseases. A potential role of the SLC41 family of Mg2+ transporters in the pathophysiology of human diseases is further substantiated by the finding that SLC41A3 knockout mice develop abnormal locomotor coordination.