Under hypoxic stress, when cellular demand for energy relies entirely on glycolysis, the machinery for glycolysis binds RNA and phase separates into G bodies, leading to enhanced glycolysis rates.
Activated Drosophila macrophages undergo transient metabolic remodeling towards Hypoxia inducible factor 1 α-driven aerobic glycolysis, a program that induces systemic metabolic changes and is crucial for resistance to infection.
A new computational model of the Warburg Effect reveals that the rate-limiting step of glycolysis is variable, identifies new control mechanisms, and could help to predict the responses to targeting glycolysis to treat cancer.
Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.
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.
When neurons are stimulated, calcium entry into mitochondria upregulates mitochondrial energy production, but glycolytic energy production in the cytosol is stimulated by elevated energy demand, not Ca2+ signaling.
Individual cells display heterogeneous fluctuations in metabolic activity, with amplitude and kinetics controlled by interlocking feedbacks between glycolysis and the Insulin/PI3K/Akt signaling pathway.
TRIM32-mediated glycolytic flux generates precursors that are utilized for biomass production in non-dividing muscle, brain and tumor cells, demonstrating a universal metabolic function for TRIM32 in cell growth.
