Inhibition of RhoA Signaling with Increased Bves in Trabecular Meshwork Cells
Investigative Ophthalmology & Visual Science2010Vol. 51(1), pp. 223–223
Citations Over TimeTop 13% of 2010 papers
Abstract
Increased Bves in TM cells leads to increased TJ formation with decreased RhoA activation and decreased MLC-p. This is the first report of a regulatory pathway upstream of RhoA in TM cells. In TM tissue, RhoA has been implicated in outflow regulation; thus, Bves may be a key regulatory molecule in aqueous outflow.
Related Papers
- → Crosstalk of tight junction components with signaling pathways(2007)744 cited
- → Caveolin-1–dependent occludin endocytosis is required for TNF-induced tight junction regulation in vivo(2010)460 cited
- → The Epithelial Barrier Is Maintained by In Vivo Tight Junction Expansion During Pathologic Intestinal Epithelial Shedding(2011)275 cited
- → Regulation of myosin light chain phosphorylation in the trabecular meshwork: role in aqueous humour outflow facility(2004)146 cited
- → Rho GTP exchange factor ARHGEF11 regulates the integrity of epithelial junctions by connecting ZO-1 and RhoA-Myosin II signaling(2012)91 cited