A Drosophila tumor model reveals how the activation of an oncogenic pathway can lead to both tumor growth and a reprogramming of metabolism known as the Warberg effect.

Mannose phosphate isomerase is a metabolic enzyme regulating cell survival in both embryonic and cancer cells.

In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

Genetic tools help to dissect the relationship between aerobic glycolysis and anabolic metabolism in the retinas of mice.

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.

Metabolic switches between oxidative phosphorylation and aerobic glycolysis plus glutaminolysis direct T cell function by altering the flux of glucose and glutamine to N-glycosylation.

Mitochondrial dysfunction in neural stem cells and brain tumour cells decreases proliferation and affects the generation of neuronal diversity and tumour heterogeneity.

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