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- W2011492248 endingPage "458" @default.
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- W2011492248 abstract "Fifty years since Peter Mitchell proposed the theory of chemiosmosis, the transformation of cellular redox potential into ATP synthetic capacity is still a widely recognized function of mitochondria. Mitchell used the term ‘proticity’ to describe the force and flow of the proton circuit across the inner membrane. When the proton gradient is coupled to ATP synthase activity, the conversion of fuel to ATP is efficient. However, uncoupling proteins (UCPs) can cause proton leaks resulting in poor fuel conversion efficiency, and some UCPs might control mitochondrial reactive oxygen species (ROS) production. Once viewed as toxic metabolic waste, ROS are now implicated in cell signaling and regulation. Here, we discuss the role of mitochondrial proticity in the context of ROS production and signaling. Fifty years since Peter Mitchell proposed the theory of chemiosmosis, the transformation of cellular redox potential into ATP synthetic capacity is still a widely recognized function of mitochondria. Mitchell used the term ‘proticity’ to describe the force and flow of the proton circuit across the inner membrane. When the proton gradient is coupled to ATP synthase activity, the conversion of fuel to ATP is efficient. However, uncoupling proteins (UCPs) can cause proton leaks resulting in poor fuel conversion efficiency, and some UCPs might control mitochondrial reactive oxygen species (ROS) production. Once viewed as toxic metabolic waste, ROS are now implicated in cell signaling and regulation. Here, we discuss the role of mitochondrial proticity in the context of ROS production and signaling. also called ADP/ATP translocator, it is a member of the mitochondrial inner membrane anion carrier superfamily. Integral membrane protein required for the antiport of ADP3− and ATP4− (ADP3− import in exchange for ATP4− export). Also thought to play other roles in mitochondria including basal proton leak, MPTP structure, and maintenance of cristae integrity. also known as chemiosmosis. Electron transfer along the respiratory chain establishes an electrochemical proton gradient, referred to as protonmotive force (PMF) across the selectively permeable mitochondrial inner membrane. PMF is subsequently used to drive the activity of ATP synthase for ATP production. a post-translational modification involving the formation of a disulfide bond between glutathione and available/reactive cysteine thiols on proteins. composed of several mitochondrial proteins including ANT. MPTP is a nonselective pore that permeabilizes the mitochondrial inner membrane to molecules <1500 Da in size. Assembly and opening normally associated with various pathologies and cell death. a form of electricity generated by mitochondria characterized by the flow of protons, instead of electrons, in the proton circuit from high to low protic potential. The electrochemical potential across the mitochondrial inner membrane. Consists of a transmembrane difference in electric potential (Δψ) and a transmembrane difference in pH (ΔpH). Drives the translocation of several ions and metabolites across the membrane, including H+ via ATP synthase. highly reactive oxygen-containing molecules. ROS are generated spontaneously or by cellular enzymes. Although most ROS species carry unpaired electrons in their outer valence shells, exceptions include hydrogen peroxide. member of the mitochondrial inner membrane anion carrier superfamily. UCP can ‘leak’ protons down the electrochemical gradient (or PMF) from the mitochondrial intermembrane space into the mitochondrial matrix. UCP lowers PMF available for ATP synthase activity. Leak through the UCPs is controlled allosterically (e.g. by purine nucleotides and fatty acids), and at least some UCPs (e.g. UCP2 and UCP3) are controlled by post-translational modification (i.e. glutathionylation). Uncoupling serves a broad range of functions including thermoregulation (UCP1 in brown adipose tissue) and control of mitochondrial ROS production (UCPs 2–4)." @default.
- W2011492248 created "2016-06-24" @default.
- W2011492248 creator A5014760843 @default.
- W2011492248 creator A5061668188 @default.
- W2011492248 date "2012-09-01" @default.
- W2011492248 modified "2023-10-17" @default.
- W2011492248 title "Mitochondrial proticity and ROS signaling: lessons from the uncoupling proteins" @default.
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