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Detailed molecular characterization of a constitutively active bacterial NADPH oxidase (NOX) provides clues to the activation mechanism required to trigger electron transfer and reactive oxygen species (ROS) production in tightly regulated eukaryotic NOX.

Six-transmembrane epithelial antigen of the prostate isoform 1 (STEAP1) can establish a physiologically relevant electron transfer chain and STEAP2 can transfer electrons via a diffusible FAD mechanism.

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation of MYC signaling pathways.

Constraint-based modelling predicts C4 photosynthesis evolves under resource limitation from an ancestral ground state of C3 photosynthesis and attributes divergent metabolic routes in extant C4 subtypes to light.

Transgenic mice and cell models provide evidence of a pathophysiological mechanism that connects mtDNA damage to cardiac dysfunction via reduced NAD⁺ levels and loss of mitochondrial function and communication.

Animal models reveal that mitochondrial complex I is dispensable for homeostatic functions of the mouse liver.

Mechanistic insight into the chaperone-like activity of NMNAT to phosphorylated Tau reveals a connection between NAD⁺metabolism and Tau homeostasis.

The cryo-EM structure of a functional human NOX2-p22 complex in nanodisc in the resting state reveals the architecture of this key enzyme essential for innate immunity.

Mathematical analyses explore the impact of co-substrate cycling on the dynamics of cellular metabolism, and demonstrate that these dynamics can limit cellular fluxes and that co-substrate pool dynamics can be regulated to regulate fluxes.