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.

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.

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

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

ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.

Exosomes from cancer-associated fibroblasts enhance the "Warburg effect" in tumors and contain de novo metabolites that can contribute to the entire compendia of central carbon metabolism within cancer cells.