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cAMP regulates the functional activity, coupling efficiency and structural organization of mammalian FOF1 ATP synthase.

Authors: De Rasmo, Domenico  Micelli, Loris  Santeramo, Arcangela  Signorile, Anna  Lattanzio, Paolo  Papa, Sergio 
Citation: De Rasmo D, etal., Biochim Biophys Acta. 2016 Apr;1857(4):350-8. doi: 10.1016/j.bbabio.2016.01.006. Epub 2016 Jan 13.
Pubmed: (View Article at PubMed) PMID:26775111
DOI: Full-text: DOI:10.1016/j.bbabio.2016.01.006

The present study shows that in isolated mitochondria and myoblast cultures depletion of cAMP, induced by sAC inhibition, depresses both ATP synthesis and hydrolysis by the FOF1 ATP synthase (complex V) of the oxidative phosphorylation system (OXPHOS). These effects are accompanied by the decrease of the respiratory membrane potential, decreased level of FOF1 connecting subunits and depressed oligomerization of the complex. All these effects of sAC inhibition are prevented by the addition of the membrane-permeant 8-Br-cAMP. These results show, for the first time, that cAMP promotes ATP production by complex V and prevents, at the same time, its detour to a mitochondrial membrane leak conductance, which is involved in cell death.

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CRRD Object Information
CRRD ID: 13830872
Created: 2018-12-07
Species: All species
Last Modified: 2018-12-07
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.