Oligomycin Sensitivity Conferring Protein of Mitochondrial ATP Synthase:  Deletions in the N-Terminal End Cause Defects in Interactions with F1, while Deletions in the C-Terminal End Cause Defects in Interactions with Fo†

Biochemistry ◽  
1996 ◽  
Vol 35 (37) ◽  
pp. 12094-12103 ◽  
Author(s):  
Saroj Joshi ◽  
Gong-Jie Cao ◽  
Cheryl Nath ◽  
Jyotsna Shah
Keyword(s):  
Atp Synthase ◽  
Mitochondrial Atp Synthase ◽  
Oligomycin Sensitivity Conferring Protein

scholarly journals The Oligomycin-Sensitivity Conferring Protein of Mitochondrial ATP Synthase: Emerging New Roles in Mitochondrial Pathophysiology

2014 ◽  
Vol 15 (5) ◽  
pp. 7513-7536 ◽  
Author(s):  
Manuela Antoniel ◽  
Valentina Giorgio ◽  
Federico Fogolari ◽  
Gary Glick ◽  
Paolo Bernardi ◽  
...  
Keyword(s):  
Atp Synthase ◽  
Mitochondrial Atp Synthase ◽  
Oligomycin Sensitivity Conferring Protein

scholarly journals The ATP Synthase Deficiency in Human Diseases

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 325
Author(s):  
Chiara Galber ◽  
Stefania Carissimi ◽  
Alessandra Baracca ◽  
Valentina Giorgio
Keyword(s):  
Oxidative Phosphorylation ◽  
Atp Synthase ◽  
Mitochondrial Protein ◽  
High Energy ◽  
Neurocognitive Disorders ◽  
Human Diseases ◽  
Age Related ◽  
Muscle Tissues ◽  
Mitochondrial Atp Synthase ◽  
Genes Encoding

Human diseases range from gene-associated to gene-non-associated disorders, including age-related diseases, neurodegenerative, neuromuscular, cardiovascular, diabetic diseases, neurocognitive disorders and cancer. Mitochondria participate to the cascades of pathogenic events leading to the onset and progression of these diseases independently of their association to mutations of genes encoding mitochondrial protein. Under physiological conditions, the mitochondrial ATP synthase provides the most energy of the cell via the oxidative phosphorylation. Alterations of oxidative phosphorylation mainly affect the tissues characterized by a high-energy metabolism, such as nervous, cardiac and skeletal muscle tissues. In this review, we focus on human diseases caused by altered expressions of ATP synthase genes of both mitochondrial and nuclear origin. Moreover, we describe the contribution of ATP synthase to the pathophysiological mechanisms of other human diseases such as cardiovascular, neurodegenerative diseases or neurocognitive disorders.

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