Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

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.

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.

Biochemical and cellular analyses reveal the mechanism by which EROS regulates NOX2 and P2X7 abundance in mouse and human.

Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.

The chloroplast 2-cysteine peroxiredoxin is central player and missing link in the chloroplast thiol-disulfide redox regulatory network, and participates in oxidative inactivation of reductively activated enzymes in photosynthesis.

Reative oxygen species modulate microtubules and diaphragm function.

Mitochondrial metabolic fluxes display a subcellular spatial gradient within a single mouse oocyte, and the fluxes are not controlled by nutrient supply or energy demand of the cell, but by the intrinsic rates of mitochondrial respiration.

A phosphorylation circuitry balancing among kinase, transcription factor, transcription repressor, and phosphatase in response against host immunity during M. oryzae–rice interaction.

NETs induction, a central component of the innate immune response, utilises assorted signalling pathways as demonstrated through the analysis of healthy and patient neutrophils treated with five distinct stimuli.