Guangjie Cheng

TL;DR: The cloning and tissue expression of three additional homologs of gp91phox, termed Nox3, Nox4 and Nox5, members of a growing family of gp 91phox homologicals are reported, which are predicted to encode proteins of around 65 kDa.

TL;DR: Overexpression of Nox4 provides a novel link between the IR and the generation of cellular reactive oxygen species that enhance insulin signal transduction, at least in part via the oxidative inhibition of cellular protein-tyrosine phosphatases (PTPases), including PTP1B, a PTPase that has been previously implicated in the regulation of insulin action.

TL;DR: Data indicate that smooth muscle-specific Nox1 overexpression augments the oxidative, pressor, and hypertrophic responses to Ang II, supporting the concept that medial Nox 1 participates in the development of cardiovascular pathologies.

TL;DR: High molecular weight homologues of gp91phox, the superoxide-generating subunit of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, have been identified in human and Caenorhabditis elegans and shown to catalyze the cross-linking of tyrosine residues involved in the stabilization of cuticular extracellular matrix.

TL;DR: The existence of homologs of gp91phox in noninflammatory tissues implies that the generation of reactive oxygen in these tissues is not an accident of respiration but is a deliberate biological strategy.