TY - JOUR
T1 - Redox Regulation of Mitochondrial ATP Synthase
AU - Wang, Sheng Bing
AU - Murray, Christopher I.
AU - Chung, Heaseung S.
AU - Van Eyk, Jennifer E.
PY - 2013/1
Y1 - 2013/1
N2 - Reversible cysteine oxidative post-translational modifications (Ox-PTMs) represent an important mechanism to regulate protein structure and function. In mitochondria, redox reactions can modulate components of the electron transport chain (ETC), the F1F0-ATP synthase complex, and other matrix proteins/enzymes. Emerging evidence has linked Ox-PTMs to mitochondrial dysfunction and heart failure, highlighting some potential therapeutic avenues. Ox-PTMs can modify a variety of amino acid residues, including cysteine, and have the potential to modulate the function of a large number of proteins. Among this group, there is a selected subset of amino acid residues that can function as redox switches. These unique sites are proposed to monitor the cell's oxidative balance through their response to the various Ox-PTMs. In this review, the role of Ox-PTMs in the regulation of the F1F0-ATP synthase complex is discussed in the context of heart failure and its possible clinical treatment.
AB - Reversible cysteine oxidative post-translational modifications (Ox-PTMs) represent an important mechanism to regulate protein structure and function. In mitochondria, redox reactions can modulate components of the electron transport chain (ETC), the F1F0-ATP synthase complex, and other matrix proteins/enzymes. Emerging evidence has linked Ox-PTMs to mitochondrial dysfunction and heart failure, highlighting some potential therapeutic avenues. Ox-PTMs can modify a variety of amino acid residues, including cysteine, and have the potential to modulate the function of a large number of proteins. Among this group, there is a selected subset of amino acid residues that can function as redox switches. These unique sites are proposed to monitor the cell's oxidative balance through their response to the various Ox-PTMs. In this review, the role of Ox-PTMs in the regulation of the F1F0-ATP synthase complex is discussed in the context of heart failure and its possible clinical treatment.
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U2 - 10.1016/j.tcm.2012.08.005
DO - 10.1016/j.tcm.2012.08.005
M3 - Review article
C2 - 23312134
AN - SCOPUS:84872129139
SN - 1050-1738
VL - 23
SP - 14
JO - Trends in Cardiovascular Medicine
JF - Trends in Cardiovascular Medicine
IS - 1
ER -