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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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羰基氰化物 4-(三氟甲氧基)苯腙, ≥98% (TLC), powder
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单克隆抗 β-肌动蛋白抗体 小鼠抗, clone AC-74, purified immunoglobulin, buffered aqueous solution
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货号包装规格是否有货价格数量
250 μg
预计发货时间 2026年4月28日
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¥1,081.44
1 mg
预计发货时间 2026年4月28日
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¥2,890.31
Sigma-Aldrich
白蛋白,牛血清,组分V,不含脂肪酸,不含核酸酶和蛋白酶, BSA Fatty Acid-free is designed for use in serological testing, RIA, and hormone response studies. Suitable for use in Molecular Biology applications, such as Northern and Southern blots.
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货号包装规格是否有货价格数量
250 μg
预计发货时间 2026年4月28日
详情...
¥1,081.44
1 mg
预计发货时间 2026年4月28日
详情...
¥2,890.31