Lower mitochondrial coenzyme Q was a consistent feature across multiple in vitro and in vivo models of insulin resistance and was sufficient to cause insulin resistance through increased mitochondrial oxidants.
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.
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.
TET methylcytosine oxidases cooperate with B lineage-specific transcription factors to promote immunoglobulin gene rearrangement by depositing 5hmC, facilitating DNA demethylation and increasing chromatin accessibility at enhancers.
Analysis of aging yeast cells using the in-vivo roGFP2-based probe reveals redox-dependent heterogeneity, reflected in a bi-modal distribution of the oxidation status, differential growth and replication, as well as distinct proteomic and transcriptomic profiles.
An in vivo disulfide crosslinking assay shows preferential disassembly of nucleosomes with two H2A.Z histones by transcription machinery in yeast and conjugation to one or two ubiquitin moieties in human cells.
An integrative genome-wide approach supports a direct and collaborative role of ETS and AP-1 transcription factors in maintaining endothelial cell-specific and anti-inflammatory gene expression programs.
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.