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.
A phosphorylation circuitry balancing among kinase, transcription factor, transcription repressor, and phosphatase in response against host immunity during M. oryzae–rice interaction.
The conditional reduction of glutaminase in mouse dopamine neurons selectively attenuates glutamate cotransmission at phasic frequencies, revealing the role of dopamine neuron glutamate cotransmission in the attribution of motivational salience.
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.
Heterotrimeric G proteins are coupled to and regulate plant receptor signaling, which allows optimum immune activation and enhances the production of reactive oxygen species.
In the Drosophila hematopoietic microenvironment, a regulatory network involving Toll/NF-B, EGFR signaling and reactive oxygen species controls blood cell production in response to immune stress.
In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.
