Open AccessFunctional Regulation of an Oxidative Stress Mediator, Rac1, in Diabetic Retinopathy
Author(s) -
Ghulam Mohammad,
Arul J. Duraisamy,
Anjaneyulu Kowluru,
Renu A. Kowluru
Publication year - 2019
Publication title -
molecular neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.569
H-Index - 111
eISSN - 1559-1182
pISSN - 0893-7648
DOI - 10.1007/s12035-019-01696-5
Subject(s) - rac1 , nadph oxidase , diabetic retinopathy , oxidative stress , retinal , biology , prenylation , microbiology and biotechnology , endocrinology , signal transduction , medicine , diabetes mellitus , chemistry , biochemistry , enzyme
Early activation of cytosolic NADPH oxidase-2 (Nox2) in diabetes increases retinal ROS production, damaging their mitochondria. The assembly of Nox2 holoenzyme requires activation of a small molecular weight G protein Rac1. Rac1 activation is regulated by guanine exchange factors and guanine nucleotide-dissociation inhibitors, and post-translational modifications assist in its association with exchange factors and dissociation inhibitors. The goal of this study is to investigate the mechanisms of Rac1 activation in the development of diabetic retinopathy.