Biochemical genetics of the mammalian oxidative phosphorylation system: Analysis of the difference in the sensitivity of various Chinese hamster cell lines to inhibitors of the mitochondrial ATP synthase complex

1983 ◽  
Vol 9 (5) ◽  
pp. 549-566 ◽  
Author(s):  
William A. Simmons ◽  
Gail A. M. Breen
Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 325
Author(s):  
Chiara Galber ◽  
Stefania Carissimi ◽  
Alessandra Baracca ◽  
Valentina Giorgio

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.


2018 ◽  
Vol 221 (4) ◽  
pp. 1776-1788 ◽  
Author(s):  
Sandra M. Kerbler ◽  
Nicolas L. Taylor ◽  
A. Harvey Millar

CYTOLOGIA ◽  
1981 ◽  
Vol 46 (4) ◽  
pp. 809-816 ◽  
Author(s):  
L. G. Weide ◽  
V. G. Dev ◽  
C. S. Rupert

2004 ◽  
Vol 1659 (2-3) ◽  
pp. 160-171 ◽  
Author(s):  
Immo E. Scheffler ◽  
Nagendra Yadava ◽  
Prasanth Potluri

1988 ◽  
Vol 174 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Vincenzo Giancotti ◽  
Bianca Pani ◽  
Paola D'Andrea ◽  
Peter Symmons

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