Bves modulates tight junction associated signaling.
Bves modulates tight junction associated signaling.
复制标题
DOI:
10.1371/journal.pone.0014563
复制
发表时间:
2011-01-20
期刊:
影响因子:
3.7
通讯作者:
Chang MS
中科院分区:
文献类型:
--
作者:
Russ PK;Pino CJ;Williams CS;Bader DM;Haselton FR;Chang MS
Blood vessel epicardial substance (Bves) is a transmembrane adhesion protein that regulates tight junction (TJ) formation in a variety of epithelia. The role of TJs within epithelium extends beyond the mechanical properties. They have been shown to play a direct role in regulation of RhoA and ZONAB/DbpA, a y-box transcription factor. We hypothesize that Bves can modulate RhoA activation and ZONAB/DbpA activity through its regulatory effect on TJ formation. Immortalized human corneal epithelial (HCE) cells were stably transfected with Flag-tagged full length chicken Bves (w-Bves) or C-terminus truncated Bves (t-Bves). We found that stably transfected w-Bves and t-Bves were interacting with endogenous human Bves. However, interaction with t-Bves appeared to disrupt cell membrane localization of endogenous Bves and interaction with ZO-1. w-Bves cells exhibited increased TJ function reflected by increased trans-epithelial electrical resistance, while t-Bves cells lost TJ protein immunolocalization at cell-cell contacts and exhibited decreased trans-epithelial electrical resistance. In parental HCE and w-Bves cells ZONAB/DbpA and GEF-H1 were seen at cell borders in the same pattern as ZO-1. However, expression of t-Bves led to decreased membrane localization of both ZONAB/DbpA and GEF-H1. t-Bves cells had increased RhoA activity, as indicated by a significant 30% increase in FRET activity compared to parental HCE cells. ZONAB/DbpA transcriptional activity, assessed using a luciferase reporter probe, was increased in t-Bves cells. These studies demonstrate that Bves expression and localization can regulate RhoA and ZONAB/DbpA activity.
登录
查看更多内容
影响因子:
4.4
作者:
Russ PK;Kupperman AI;Presley SH;Haselton FR;Chang MS
通讯作者:
Chang MS
影响因子:
4.8
作者:
Knight, RF;Bader, DM;Backstrom, JR
通讯作者:
Backstrom, JR
影响因子:
3
作者:
Hamada, Kazuma;Shitara, Yoshihisa;Horie, Toshiharu
通讯作者:
Horie, Toshiharu
影响因子:
11.4
作者:
Balda, MS;Matter, K
通讯作者:
Matter, K
影响因子:
11.4
作者:
Frankel, P;Aronheim, A;Marshall, CJ
通讯作者:
Marshall, CJ