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Exploiting the metabolic consequences of Akt activation in prostate cancer for therapeutic interventions that circumvent Akt inhibition therapy.

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

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

Mitochondrial fusion enables a metabolic transition during spermatogenesis.

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.

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.

Long-term exposure to recipient's alloantigens promotes major metabolic defects in T cells that are independent of PD-1-mediated regulation.

Skeletal muscle from world-class octogenarian athletes, representing a population with very high physical function in advanced age, exhibits greater mass and strength that is associated with overrepresentation of proteins involved in mitochondrial biology and more oxidatively competent muscle fibers.

Inducing the formation of mitochondrial respiratory chain supercomplexes in Drosophila melanogaster, where they are normally absent, does not have any noticeable impact in the function of the respiratory chain.

Zebrafish caudal fin amputation induces an increase in the glycolytic influx that leads to dedifferentiation of osteoblasts and their re-entry in the cell cycle, which is essential for blastema formation and bone regeneration.