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.

The shutoff of aerobic glycolysis in neuronal differentiation is essential for neuronal survival.

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.

Isotope tracing, mathematical modeling, and single-cell ATP analysis reveal changes in blood cell metabolism under various conditions, showing stressed hematopoietic stem cells support hematopoiesis through glycolytic ATP production via PFKFB3.

The functional link between glycolytic flux, cell signalling and mesoderm patterning is investigated in mouse embryo.

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.

Neuronal glycolysis to restore energy consumed by ion movements is activated by engagement of the Na⁺/K⁺ pump, either directly by Na⁺ influx or indirectly, when Ca²⁺ influx is converted to Na⁺ accumulation by Na⁺/Ca²⁺ exchange.

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.

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.

Aerobic glycolysis in rod photoreceptors of adult mice is regulated by allostery and FGF signaling and is required for maintaining outer segments.