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Sirtuin 3 (SIRT3) Protein Regulates Long-chain Acyl-CoA Dehydrogenase by Deacetylating Conserved Lysines Near the Active Site
TLDR
The results suggest that acetylation/deacetylation at Lys-318/Lys-322 is a mode of regulating fatty acid oxidation and the same mechanism may regulate other acyl-CoA dehydrogenases.
SIRT3 and SIRT5 Regulate the Enzyme Activity and Cardiolipin Binding of Very Long-Chain Acyl-CoA Dehydrogenase
TLDR
SIRT3 and SIRT5 promote fatty acid oxidation by converging upon VLCAD to promote its activity and membrane localization by exploiting a novel mechanism that is predicted to extrapolate to other metabolic proteins that localize to the inner mitochondrial membrane.
Lysine desuccinylase SIRT5 binds to cardiolipin and regulates the electron transport chain
TLDR
The findings suggest that SIRT5 is targeted to protein complexes on the inner mitochondrial membrane via affinity for cardiolipin to promote respiratory chain function.
Coordinated Activities of Multiple Myc-dependent and Myc-independent Biosynthetic Pathways in Hepatoblastoma*♦
TLDR
The results indicate that the role of Myc in HB pathogenesis is to impose mutually dependent changes in gene expression and metabolic reprogramming that are unattainable in non-transformed cells and that cooperate to maximize tumor growth.
Sirtuin 5 Regulates Proximal Tubule Fatty Acid Oxidation to Protect against AKI.
TLDR
These findings indicate that Sirt5 regulates the balance of mitochondrial versus peroxisomal fatty acid oxidation in proximal tubular epithelial cells to protect against injury in AKI.
Effects of labor on placental fatty acid β oxidation
TLDR
Term human placentas express all the enzymes required to oxidize FA, at a rate 20-fold lower than liver, suggesting that FA Oxidation is not likely an important placental energy source during labor.
Long-chain Acylcarnitines Reduce Lung Function by Inhibiting Pulmonary Surfactant*
TLDR
It is demonstrated that long-chain acylcarnitines, a class of lipids secreted by mitochondria when metabolism is inhibited, accumulate at the air-fluid interface in LCAD−/− lungs and contribute to reduced lung function in FAO-deficient mice.
Long-chain Acyl-CoA Dehydrogenase Deficiency as a Cause of Pulmonary Surfactant Dysfunction*
TLDR
The fatty acid oxidation pathway and LCAD in particular are identified as factors contributing to the pathophysiology of pulmonary disease and unexplained sudden infant death.
Aspirin increases mitochondrial fatty acid oxidation.
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