Figure 2. Proposed tight junction signaling pathways modulated by Bves.

Bves is a transmembrane adhesion molecule capable of complexing with ZO-1 through an unknown mechanism and modulating tight junction (TJ) formation. We hypothesize that Bves is capable of modulating TJ associated signaling through the regulation of TJ formation (left). TJs are signaling complexes that regulate RhoA activation by sequestering the small GTPase GEF-H1 within the TJ. ZONAB/Dbpa, a Y-box transcription factor, is also sequestered at the TJ by an interaction with ZO-1. We further hypothesize that overexpression of truncated Bves in epithelial cells results in disruption of tight junctions, increased RhoA activation by free GEF-H1, and increased ZONAB/Dbpa transcriptional activity in the nucleus.