MCU gain- and loss-of-function models define the duality of mitochondrial calcium uptake in heart failure
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P. Jadiya | T. Luongo | J. Elrod | Joanne F. Garbincius | Alycia N. Hildebrand | Emma K Murray | A. Mangold | Jonathan P. Lambert | Emma K. Murray | Adam S. Mangold
[1] W. Koch,et al. Enhanced NCLX-dependent mitochondrial Ca2+ efflux attenuates pathological remodeling in heart failure. , 2022, Journal of molecular and cellular cardiology.
[2] Shangcheng Xu,et al. Elevated MCU Expression by CaMKIIδB Limits Pathological Cardiac Remodeling , 2022, Circulation.
[3] J. Elrod,et al. Mitochondrial calcium exchange in physiology and disease. , 2021, Physiological reviews.
[4] J. Elrod,et al. Is the Failing Heart Starved of Mitochondrial Calcium? , 2021, Circulation research.
[5] B. O’Rourke,et al. MCU Overexpression Rescues Inotropy and Reverses Heart Failure by Reducing SR Ca2+ Leak. , 2021, Circulation research.
[6] T. Luongo,et al. The debate continues - What is the role of MCU and mitochondrial calcium uptake in the heart? , 2020, Journal of molecular and cellular cardiology.
[7] E. Gao,et al. MCUB Regulates the Molecular Composition of the Mitochondrial Calcium Uniporter Channel to Limit Mitochondrial Calcium Overload During Stress. , 2019, Circulation.
[8] J. Kao,et al. Voltage-energized Calcium-sensitive ATP Production by Mitochondria , 2019, Nature Metabolism.
[9] X. Bai,et al. Structural Mechanism of EMRE-Dependent Gating of the Human Mitochondrial Calcium Uniporter , 2019, Cell.
[10] M. Salih,et al. Cardiac-Specific Cre Induces Age-Dependent Dilated Cardiomyopathy (DCM) in Mice , 2019, Molecules.
[11] J. Ge,et al. Mitochondrial calcium uniporter inhibition provides cardioprotection in pressure overload-induced heart failure through autophagy enhancement. , 2018, International journal of cardiology.
[12] D. Catalucci,et al. Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy , 2017, Proceedings of the National Academy of Sciences.
[13] S. Houser,et al. The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability , 2017, Nature.
[14] Julia C. Liu,et al. MICU1 Serves as a Molecular Gatekeeper to Prevent In Vivo Mitochondrial Calcium Overload. , 2016, Cell reports.
[15] S. Houser,et al. MCUR1 Is a Scaffold Factor for the MCU Complex Function and Promotes Mitochondrial Bioenergetics. , 2016, Cell reports.
[16] D. Bers,et al. Individual Cardiac Mitochondria Undergo Rare Transient Permeability Transition Pore Openings. , 2016, Circulation research.
[17] Qun Chen,et al. Activation of mitochondrial calpain and increased cardiac injury: beyond AIF release. , 2016, American journal of physiology. Heart and circulatory physiology.
[18] Ken-ichi Yoshida,et al. Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia-reperfusion. , 2015, International journal of cardiology.
[19] Julia C. Liu,et al. Assessment of cardiac function in mice lacking the mitochondrial calcium uniporter. , 2015, Journal of molecular and cellular cardiology.
[20] Jianyi(Jay) Zhang,et al. The Mitochondrial Calcium Uniporter Selectively Matches Metabolic Output to Acute Contractile Stress in the Heart. , 2015, Cell reports.
[21] S. Houser,et al. The Mitochondrial Calcium Uniporter Matches Energetic Supply with Cardiac Workload during Stress and Modulates Permeability Transition. , 2015, Cell reports.
[22] D. Hall,et al. The mitochondrial uniporter controls fight or flight heart rate increases , 2015, Nature Communications.
[23] T. Abraham,et al. Inhibiting Mitochondrial Na+/Ca2+ Exchange Prevents Sudden Death in a Guinea Pig Model of Heart Failure , 2014, Circulation research.
[24] R. Rizzuto,et al. MICU1 and MICU2 Finely Tune the Mitochondrial Ca2+ Uniporter by Exerting Opposite Effects on MCU Activity , 2014, Molecular cell.
[25] J. Cheung,et al. MICU1 motifs define mitochondrial calcium uniporter binding and activity. , 2013, Cell reports.
[26] S. Carr,et al. EMRE Is an Essential Component of the Mitochondrial Calcium Uniporter Complex , 2013, Science.
[27] S. Moro,et al. The mitochondrial calcium uniporter is a multimer that can include a dominant‐negative pore‐forming subunit , 2013, The EMBO journal.
[28] Sangita Choudhury,et al. Moderate and high amounts of tamoxifen in αMHC-MerCreMer mice induce a DNA damage response, leading to heart failure and death , 2013, Disease Models & Mechanisms.
[29] Steven P Jones,et al. Standardized bioenergetic profiling of adult mouse cardiomyocytes. , 2012, Physiological genomics.
[30] J. Kolesar,et al. MCUR1 is an essential component of mitochondrial Ca2+ uptake that regulates cellular metabolism , 2012, Nature Cell Biology.
[31] M. Birnbaum,et al. MICU1 Is an Essential Gatekeeper for MCU-Mediated Mitochondrial Ca2+ Uptake that Regulates Cell Survival , 2012, Cell.
[32] Klitos Konstantinidis,et al. Mechanisms of cell death in heart disease. , 2012, Arteriosclerosis, thrombosis, and vascular biology.
[33] V. Mootha,et al. Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter , 2011, Nature.
[34] J. Farber,et al. Cyclophilin D controls mitochondrial pore-dependent Ca(2+) exchange, metabolic flexibility, and propensity for heart failure in mice. , 2010, The Journal of clinical investigation.
[35] Y. Pinto,et al. Avoidance of Transient Cardiomyopathy in Cardiomyocyte-Targeted Tamoxifen-Induced MerCreMer Gene Deletion Models , 2009, Circulation research.
[36] B. O’Rourke,et al. Enhancing Mitochondrial Ca2+ Uptake in Myocytes From Failing Hearts Restores Energy Supply and Demand Matching , 2008, Circulation research.
[37] D. Michele,et al. Blebbistatin extends culture life of adult mouse cardiac myocytes and allows efficient and stable transgene expression. , 2008, American journal of physiology. Heart and circulatory physiology.
[38] L. Scorrano,et al. Organelle isolation: functional mitochondria from mouse liver, muscle and cultured filroblasts , 2007, Nature Protocols.
[39] R. Schnellmann,et al. Calpain 10: a mitochondrial calpain and its role in calcium-induced mitochondrial dysfunction. , 2006, American journal of physiology. Cell physiology.
[40] R. Schwartz,et al. Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte Viability , 2006, Circulation research.
[41] S. Korsmeyer,et al. Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[42] Jeffrey Robbins,et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death , 2005, Nature.
[43] 中川 崇. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. , 2005 .
[44] K. Mani,et al. Death begets failure in the heart. , 2005, The Journal of clinical investigation.
[45] M. Grounds,et al. Evans Blue Dye as an in vivo marker of myofibre damage: optimising parameters for detecting initial myofibre membrane permeability , 2002, Journal of anatomy.
[46] J. Molkentin,et al. Physiologic functions of cyclophilin D and the mitochondrial permeability transition pore. , 2013, Circulation journal : official journal of the Japanese Circulation Society.