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Mitochondrial Ca2+ homeostasis is crucial for balancing cell survival and death. The recent discovery of the molecular identity of the mitochondrial Ca2+ uniporter pore (MCU) opens new possibilities for applying genetic approaches to study mitochondrial Ca2+ regulation in various cell types, including cardiac myocytes. Basal tyrosine phosphorylation of MCU was reported from mass spectroscopy of human and mouse tissues, but the signaling pathways that regulate mitochondrial Ca2+ entry through posttranslational modifications of MCU are completely unknown. Therefore, we investigated α1-adrenergic-mediated signal transduction of MCU posttranslational modification and function in cardiac cells.

antioxidants and redox signaling

Adrenergic Signaling Regulates Mitochondrial Ca<sup>2+</sup> Uptake Through Pyk2-Dependent Tyrosine Phosphorylation of the Mitochondrial Ca<sup>2+</sup> Uniporter

Adrenergic Signaling Regulates Mitochondrial Ca2+ Uptake Through Pyk2-Dependent Tyrosine Phosphorylation of the Mitochondrial Ca2+ Uniporter

Adrenergic Signaling Regulates Mitochondrial Ca²⁺ Uptake Through Pyk2-Dependent Tyrosine Phosphorylation of the Mitochondrial Ca²⁺ Uniporter