Metabolic adaptation to the chronic loss of Ca2+ signaling induced by KO of IP3 receptors or the mitochondrial Ca2+ uniporter
Michael Young, Zachary T. Schug, David M. Booth, David I. Yule, Katsuhiko Mikoshiba, György Hajnóczky, Suresh K. Joseph
Abstract
R TKO and MCU KO human cancer cells, likely because of adequate basal glycolytic and TCA cycle flux. However, in MCU KO cells, the higher energy expenditure associated with increased proliferation and oxygen consumption makes these cells more prone to bioenergetic failure under conditions of metabolic stress.
Topics & Concepts
UniporterReceptorCell biologyMitochondrionAdaptation (eye)ChemistryCalcium signalingBiophysicsBiologyBiochemistryNeuroscienceCytosolEnzymeProtein Kinase Regulation and GTPase SignalingMitochondrial Function and PathologyEndoplasmic Reticulum Stress and Disease