Absence (of the uniporter) makes the heart grow fonder: The cardiac response to injury adapts after prolonged EMRE inhibition

More than a decade after identifying the molecular components of the mitochondrial calcium uniporter, the main channel responsible for rapid mitochondrial Ca2+ uptake, questions remain regarding its modes of regulation during physiological and pathological stress. The uniporter complex comprises the pore-forming MCU subunit, targeting protein EMRE, gate-keeping proteins MICU 1, 2, and 3, and inhibitory subunit MCUB [1]. Maximal inhibition of rapid mitochondrial Ca2+ uptake can be obtained by genetic deletion of MCU, which prevents expression of the pore, or EMRE, which prevents accurate membrane targeting and assembly of MCU subunits into a channel.
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Source Type: research