Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.
At most physiological concentrations, the short-chain fatty acids propionate and butyrate affect histone acetylation by modifying and activating the acetyltransferase p300/CBP, rather than by inhibiting histone deacetylases.
The Acyl-CoA binding domain-containing 7 (Acbd7) gene is expressed in the hypothalamus, encodes a peptide that suppresses appetite, increases metabolic rate and interacts with the leptin-melanocortin system.
Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.
Mitochondria can trigger massive endocytosis by releasing coenzyme A into the cytoplasm and thereby promoting the addition of fatty acids to surface membrane proteins.
Gajanan S Patil, Priyadarshan Kinatukara ... Rajan Sankaranarayanan
The structural basis of how an enzyme differentiates chemically identical molecules unlike its homolog to channel fatty acids towards secondary metabolism is elucidated.
An acetyl-CoA-mediated metabolic and epigenetic network has been elucidated that stimulates histone acetylation and anti-oxidative stress gene expression for heart repair after myocardial infarction.
Kahlan E Newman, Sarah N Tindall ... Marjan W Van Der Woude
The modelled structure of a membrane protein supports the hypothesis that it has a new fold with a channel that allows a chemical group to cross the membrane to decorate surface structures.
