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.

Acetate concentration, which is significantly increased in association with energy stresses such as those that occur with diabetes or starvation, is emerging as a novel 'ketone body' with potential as a parameter for evaluating the progression of energy stress.

First high-resolution structure of HGSNAT-acetyl-CoA complex, that describes the architecture of a novel transmembrane N-acetyltransferase fold and provides a molecular basis for MPS IIIC causing mutation induced destabilization of HGSNAT.

A novel neuroprotective pathway that enhances acetyl-CoA metabolism via inhibition of acetyl-CoA carboxylase 1 may prevent the contribution of the aging process in the brain to Alzheimer's disease.

A single mutation in acetyl-CoA carboxylase blocking AMPK regulation inhibits food intake in mice in response to cold exposure or fasting causing them to lose weight.

General stress response factors Msn2 and Msn4 activate glycolytic genes and promote acetyl-CoA accumulation to stimulate growth and proliferation of yeast cells under a nutrient-limiting condition, suggesting the unexpected interrelationship between carbohydrate metabolism and stress response.

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.

TIGAR deficiency in cholinergic neuron enhanced intracellular acetyl-CoA levels and pyruvate dehydrogenase flux into the TCA cycle that drives increased cholinergic tone with reduced heart rate and blood pressure and raised resistance against the paralytic curare and cold-induced hypothermia.

The genome of Thermovibrio ammonificans encodes ancestral pathways (e.g., hydrogen oxidation) and more recently acquired ones (e.g., nitrate reduction) and a hybrid pathway for CO₂ fixation.

The development and functionalities of invariant natural-killer T cells are dependent upon their cell-intrinsic ACC1-mediated de novo fatty acid synthesis, which greatly affect outcomes of allergic asthma.