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  • Allosteric Regulation of NCLX by Mitochondrial Membrane Potential Links the Metabolic State and Ca2+ Signaling in Mitochondria.

Allosteric Regulation of NCLX by Mitochondrial Membrane Potential Links the Metabolic State and Ca2+ Signaling in Mitochondria.

Cell reports (2018-12-20)
Marko Kostic, Tomer Katoshevski, Israel Sekler
摘要

Calcium is a key regulator of mitochondrial function under both normal and pathological conditions. The mechanisms linking metabolic activity to mitochondrial Ca2+ signaling remain elusive, however. Here, by monitoring mitochondrial Ca2+ transients while manipulating mitochondrial membrane potential (ΔΨm), we found that mild fluctuations in ΔΨm, which do not affect Ca2+ influx, are sufficient to strongly regulate NCLX, the major efflux pathway of Ca2+ from the mitochondria. Phosphorylation of NCLX or expression of phosphomimicking mutant (S258D) rescued NCLX activity from ΔΨm-driven allosteric inhibition. By screening ΔΨm sensitivity of NCLX mutants, we also identified amino acid residues that, through functional interaction with Ser258, control NCLX regulation. Finally, we find that glucose-driven ΔΨm changes in pancreatic β-cells control mitochondrial Ca2+ signaling primarily via NCLX regulation. Our results identify a feedback control between metabolic activity and mitochondrial Ca2+ signaling and the "safety valve" NCLX phosphorylation that can rescue Ca2+ efflux in depolarized mitochondria.

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货号包装规格是否有货价格数量
100 mg
预计发货时间 2025年4月14日
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¥2,672.55
500 mg
预计发货时间 2025年4月14日
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¥9,224.47
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货号包装规格是否有货价格数量
100 mg
预计发货时间 2025年4月14日
详情...
¥2,672.55
500 mg
预计发货时间 2025年4月14日
详情...
¥9,224.47