Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.

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Biallelic C1QBP Mutations Cause Severe Neonatal-, Childhood-, or Later-Onset Cardiomyopathy Associated with Combined Respiratory-Chain Deficiencies.Physiological and pathological gestational cardiac hypertrophy: what can we learn from rodents?

P2860

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P2860

Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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Cardiomyocyte-specific loss of ...... nd activates stress responses.

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P1476

Cardiomyocyte-specific loss of ...... nd activates stress responses.

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P2093

Daiki Setoyama

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Dongchon Kang

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Mikako Yagi

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Rie Amamoto

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Takeshi Uchiumi

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Yuichi Matsushima

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P2860

An arginine to glutamine mutation in residue 109 of human ornithine transcarbamylase completely abolishes enzymatic activity in Cos1 cells

Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32

Copper supplementation restores cytochrome c oxidase assembly defect in a mitochondrial disease model of COA6 deficiency

Crystal structure of human p32, a doughnut-shaped acidic mitochondrial matrix protein

Protective coupling of mitochondrial function and protein synthesis via the eIF2α kinase GCN-2

p32 protein, a splicing factor 2-associated protein, is localized in mitochondrial matrix and is functionally important in maintaining oxidative phosphorylation.

A Comprehensive Genomic Analysis Reveals the Genetic Landscape of Mitochondrial Respiratory Chain Complex Deficiencies

OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion

p32/gC1qR is indispensable for fetal development and mitochondrial translation: importance of its RNA-binding ability

Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1

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1173-1185

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scholarly article

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10.1093/CVR/CVX095

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113

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Toshiro Saito

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2017-05-11T00:00:00Z

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28498888

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Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.

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P2860

P2860

Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.

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P1433

P1476

P2093

P2860

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P356

P433

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P50

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P698

P356

P1433

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P2860

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P433

P478

P50

P577

P698