Inhibition of RhoA Signaling with Increased Bves in Trabecular Meshwork Cells | Zendy

Patricia K. Russ | Zendy; Asher I. Kupperman | Zendy; Sai-Han Presley | Zendy; Frederick R. Haselton | Zendy; Min S. Chang | Zendy

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Inhibition of RhoA Signaling with Increased Bves in Trabecular Meshwork Cells

Author(s) -

Patricia K. Russ,

Asher I. Kupperman,

Sai-Han Presley,

Frederick R. Haselton,

Min S. Chang

Publication year - 2010

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.09-3539

Subject(s) - rhoa , occludin , microbiology and biotechnology , trabecular meshwork , transfection , tight junction , chemistry , signal transduction , myosin light chain kinase , hek 293 cells , phosphorylation , biology , receptor , biochemistry , gene , neuroscience , glaucoma

Blood vessel epicardial substance (Bves) is a novel adhesion molecule that regulates tight junction (TJ) formation. TJs also modulate RhoA signaling, which has been implicated in outflow regulation. Given that Bves has been reported in multiple ocular tissues, the authors hypothesize that Bves plays a role in the regulation of RhoA signaling in trabecular meshwork (TM) cells.

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