When neurons are stimulated, calcium entry into mitochondria upregulates mitochondrial energy production, but glycolytic energy production in the cytosol is stimulated by elevated energy demand, not Ca²⁺ signaling.

Multi-omic analyses reveal a connection between the integrated stress response and the regulation of redox and amino acid metabolism when the TCA cycle is impaired.

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

The dual function of an ancient prokaryotic enzyme, which is linked to specific metabolite signals, may have been the evolutionary driving force behind its dual localization in eukaryotes.

Volatile anesthetics impair hepatic tricarboxylic acid cycle function in adult and neonatal mice, with citrate accumulation driving a neonate-specific inhibition of beta-oxidation and ketosis through their increased relative sensitivity to malonyl-CoA.

SDH-null cancer cells decrease mitochondrial complex I to drive rewired aspartate synthesis through reductive carboxylation and pyruvate carboxylase, supporting cell proliferation and tumor growth.

Metabolic defects following expression of Aβ1-42 in nematode neurons are partially caused by inactivation of alpha-ketoglutarate dehydrogenase and can be rescued by Metformin.

A deep-sea Planctomycetes bacterium performs a unique budding mode of division and recruits chronic phages for metabolizing nitrogen through the function of auxiliary metabolic genes.

Integrative multi-omics reveals global dysregulation in hepatic metabolism during prolonged sepsis.

The iron-sulfur cluster containing Ferredoxin 1 (FDX1), critical in steroidogenesis and TCA cycle, is required for mammalian embryonic development and maintenance of lipid homeostasis at cellular and organismal levels.