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.

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.

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.

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

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

Glycolysis is locally enhanced and redirected in zebrafish to generate lactate, which functions as a signaling molecule to fully activate Fgf target genes required for proper sensory and neural development.

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.