The use of genetically encoded redox sensors in phagocytized bacteria reveals that, among the toxic cocktail of oxidants released into the neutrophil's phagolysosome, HOCl is the main component responsible for the oxidative modification of bacterial protein thiols.

Heterotrimeric G proteins are coupled to and regulate plant receptor signaling, which allows optimum immune activation and enhances the production of reactive oxygen species.

Glutamate excitotoxicity induces a circuit-dependent ROS feedback loop to alter motor system integrity.

The ability of cells to transmit information encoded in signaling dynamics is fundamentally limited by the gene decoding step.

Structure-function analysis reveals an allosteric mechanism activating a plant immune receptor kinase complex.

Mitogen-activated protein kinase phosphatase 1 (DUSP1) deficiency causes early redox imbalance and increased inflammatory response in the cochlea, leading to cell loss and progressive neurosensory hearing loss.

Staphylococcus aureus NAD kinase promotes infection by protecting bacteria from host antimicrobial defenses and by supporting production of major virulence factors.

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

Electrophysiological analyses reveal interactions between gasotransmitter enzymes and their respective products that regulate hypoglossal motoneuron excitability and may drive changes in upper airway tone in obstructive sleep apnea and perturb behaviors such as vocalization and swallowing.