Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice - Test2 - elhamkhani - TriplyDB

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

http://www.wikidata.org/entity/Q28272272

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Mitochondrial Quality Control in Cardiac Diseases Homozygous YME1L1 mutation causes mitochondriopathy with optic atrophy and mitochondrial network fragmentation Targeting mitochondrial dysfunction in the treatment of heart failure.Doxycycline protects against ROS-induced mitochondrial fragmentation and ISO-induced heart failure.Age-Associated Loss of OPA1 in Muscle Impacts Muscle Mass, Metabolic Homeostasis, Systemic Inflammation, and Epithelial Senescence.Azidothymidine-triphosphate impairs mitochondrial dynamics by disrupting the quality control system.The Mitochondrial m-AAA Protease Prevents Demyelination and Hair Greying.Mitochondrial fission/fusion and cardiomyopathy.A threshold of transmembrane potential is required for mitochondrial dynamic balance mediated by DRP1 and OMA1.Mitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It!Eicosapentaenoic acid protects cardiomyoblasts from lipotoxicity in an autophagy-dependent manner.Mitochondrial Function in Engineered Cardiac Tissues is Co-Regulated by Extracellular Matrix Elasticity and Tissue Alignment.Reciprocal Degradation of YME1L and OMA1 Adapts Mitochondrial Proteolytic Activity during Stress.Mitochondrial remodeling: Rearranging, recycling, and reprogramming.Mitochondrial Quality Control Proteases in Neuronal Welfare.Mouse models for mitochondrial diseases.Sarcoplasmic reticulum-mitochondria communication in cardiovascular pathophysiology.Obesity-induced cardiac lipid accumulation in adult mice is modulated by G protein-coupled receptor kinase 2 levels.Mitochondrial Membrane Dynamics and Inherited Optic Neuropathies.Adult-onset obesity is triggered by impaired mitochondrial gene expression.Early Right Ventricular Apical Pacing-Induced Gene Expression Alterations Are Associated with Deterioration of Left Ventricular Systolic Function.Lung ultrasound as a translational approach for non-invasive assessment of heart failure with reduced or preserved ejection fraction in mice.Mitophagy and mitochondrial biogenesis in atrial tissue of patients undergoing heart surgery with cardiopulmonary bypass.Mitochondrial fusion dynamics is robust in the heart and depends on calcium oscillations and contractile activity.Role of Cardiolipin in Mitochondrial Signaling Pathways Implications of mitochondrial network organization in mitochondrial stress signalling in NARP cybrid and Rho0 cells.Mitophagy as a Protective Mechanism against Myocardial Stress.The Mitochondrial Basis of Aging and Age-Related Disorders.Mitophagy and Mitochondrial Quality Control Mechanisms in the Heart.Barth syndrome cardiomyopathy.Prohibitin Signaling at the Kidney Filtration Barrier.The mitochondrial metallochaperone SCO1 maintains CTR1 at the plasma membrane to preserve copper homeostasis in the murine heart.Mitochondrial uncoupling proteins: subtle regulators of cellular redox signaling.Regulation of mitochondrial bioenergetics by the non-canonical roles of mitochondrial dynamics proteins in the heart.Metalloproteases of the Inner Mitochondrial Membrane.Mitochondrial diseases: the contribution of organelle stress responses to pathology.The ever-growing complexity of the mitochondrial fission machinery.Structure of the mitochondrial inner membrane AAA+ protease YME1 gives insight into substrate processing.Estrogen receptor alpha protects pancreatic beta cells from apoptosis by preserving mitochondrial function and suppressing endoplasmic reticulum stress.To be or not to be cell autonomous? Autophagy says both.

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P2860

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

http://www.wikidata.org/entity/Q28272272

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2015 nî lūn-bûn

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2015 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2015 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2015年の論文

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年學術文章

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name

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

@en

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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prefLabel

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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SCIENCE.AAD0116

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Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

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Jaime García-Prieto

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Michael J Baker

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Paule Benit

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Pierre Rustin

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Thomas Langer

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P2860

Inducible proteolytic inactivation of OPA1 mediated by the OMA1 protease in mammalian cells

LRPPRC is necessary for polyadenylation and coordination of translation of mitochondrial mRNAs

Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice

An actin-dependent step in mitochondrial fission mediated by the ER-associated formin INF2

TRIAP1/PRELI complexes prevent apoptosis by mediating intramitochondrial transport of phosphatidic acid

MTERF3 is a negative regulator of mammalian mtDNA transcription

Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis

OPA1 requires mitofusin 1 to promote mitochondrial fusion

Fission and selective fusion govern mitochondrial segregation and elimination by autophagy

Mitochondrial form and function

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