|1.||Dong, Cheng: 5 articles (02/2015 - 01/2005)|
|2.||Vilgrain, Isabelle: 5 articles (08/2014 - 07/2011)|
|3.||Bouillet, Laurence: 5 articles (08/2014 - 07/2011)|
|4.||Dejana, Elisabetta: 5 articles (01/2014 - 05/2002)|
|5.||Seftor, Richard E B: 5 articles (05/2012 - 05/2003)|
|6.||Hendrix, Mary J C: 5 articles (05/2012 - 05/2003)|
|7.||Seftor, Elisabeth A: 5 articles (05/2012 - 05/2003)|
|8.||May, Chad: 5 articles (01/2010 - 06/2005)|
|9.||Bohlen, Peter: 5 articles (11/2005 - 05/2002)|
|10.||Sun, Baocun: 4 articles (04/2015 - 09/2007)|
12/30/2012 - "This effect correlated with a marked decrease of VE-Cadherin expression in endothelium of 3-OH-GA-treated tumors. "
10/01/2007 - "In this study, we report a loss of VE-cadherin in tumor-associated EC. "
09/01/2015 - "Subsequently, selective ablation of human GSC-derived VE-cadherin-expressing cells attenuated vascular formation in mouse intracranial tumors, thereby significantly prolonging mouse survival. "
07/01/2015 - "Expression of VE-cadherin by tumor cells (6% of cases, mainly ACA) as well as decreased MVD in the tumor centers was independently associated with poor prognosis in the entire cohort. "
04/10/2015 - "These data suggest that AM blockade selectively induces regression of unstable tumor neovessels, through disruption of VE-cadherin signalling. "
09/01/2011 - "The results confirm our hypotheses and indicate that (β15-66)(2) and (β15-44)(2) , which exhibited much higher affinity for VE-cadherin, are highly effective in suppressing inflammation by inhibiting leukocyte transmigration."
03/10/2014 - "These studies identify a unique role of Gα13 binding to VE-cadherin in mediating VE-cadherin internalization and endothelial barrier disruption and inflammation."
06/01/2010 - "The results of this study describe the spatial organization of the tonsil lymphatic vasculature, discontinuous expression of CD31 and VE-cadherin in human lymphatic capillaries, and a change in lymphatic vessel morphology in response to inflammation."
07/01/2015 - "Taken together, formation of sVE-cadherin is associated and contributes to inflammation-induced breakdown of endothelial barrier functions by inhibition of VE-cadherin binding. "
07/01/2015 - "Inhibition of the VE-cadherin-cleaving disintegrin and metalloproteinase ADAM10 using GI254023X attenuated inflammation-induced formation of sVE-cadherin and endothelial barrier disruption, suggesting ADAM10-mediated shedding as a mechanism underlying sVE-cadherin release. "
|3.||Brain Ischemia (Cerebral Ischemia)
01/01/2012 - "Recombinant human angiopoietin-1 ameliorates the expressions of ZO-1, occludin, VE-cadherin, and PKCα signaling after focal cerebral ischemia/reperfusion in rats."
10/01/2013 - "In our mouse model of cerebral ischemia, administration of rt-PA (10 mg/kg, i.v.) 6h after ischemia aggravated the post-ischemic degradation of ZO-1, claudin-5 and VE-cadherin, increased the hemorrhagic transformations (assessed by brain hemoglobin content and magnetic resonance imaging). "
03/01/2013 - "This study was performed to determine whether recombinant human angiopoietin-1 (rhAng-1) decreases the permeability of the blood-brain barrier (BBB) in focal cerebral ischemia and reperfusion rats, whether RhAng-1 opens the BBB by affecting tight junction associated proteins zonnula occludin-1 (ZO-1), occludin and adherens junction protein vascular endothelial (VE)-cadherin. "
01/01/2012 - "This study was performed to determine whether recombinant human angiopoietin-1 (Ang-1) decreases the permeability of the blood-brain barrier (BBB) in focal cerebral ischemia and reperfusion rats, whether Ang-1 opens the BBB by affecting tight junction associated proteins zonula occluden-1 (ZO-1), occludin and adherens junction protein vascular endothelial (VE)-cadherin, and whether the protein kinase C (PKC)α/myosin light chain (MLC) signaling pathway involves in it. "
06/01/2011 - "It is concluded that the lentiviral vector pLB-VEC carrying human VE-cadherin gene is successfully constructed; VE-cadherin gene is expressed in Sup-B15 cells via lentiviral vector transfection, which provides an optional tool for further study on the mechanism of VE-cadherin controlling leukemia development."
01/01/2010 - "Consistent with a role for VE-cadherin in modulation of leukemia cell viability, lentiviral-mediated expression of VE-cadherin in Ph- ALL cells resulted in increased resistance to treatment-induced apoptosis. "
01/08/2013 - "In the setting of Hh inhibition, induction of either Notch signaling or overexpression of Stem cell leukemia (Scl)/T-cell acute lymphocytic leukemia protein 1 rescued hemogenic vascular-endothelial cadherin(+) cells and hematopoietic progenitor formation. "
12/01/2014 - "Herein, we investigated the protective effects of the stromal cell-mediated VE-cadherin-β-catenin signal on Ph+ leukemia cells during imatinib treatment. "
12/01/2014 - "We found stromal cells could desensitize imatinib and up-regulate VE-cadherin expression on Ph+ leukemia cells (K562 and SUP-B15 cells), which further stabilized and activated β-catenin. "
|5.||Melanoma (Melanoma, Malignant)
05/01/2003 - "Based on the recent characterization of vasculogenic mimicry by aggressive melanoma cells, particularly their ability to express VE (vascular endothelial)-cadherin, TIE-1, and EphA2, current studies have focused on the molecular signals deposited by these cells as they remodel their microenvironment. "
12/20/2014 - "Here, we demonstrate that, in the metastatic Lu1205 melanoma cells, expression of the CD44 variant CD44v8-v10 induced junction disassembly and vascular endothelial (VE)-cadherin phosphorylation at Y658 and Y731. "
01/01/2014 - "Actinomyosin contraction, phosphorylation of VE-cadherin, and actin remodeling enable melanoma-induced endothelial cell-cell junction disassembly."
12/01/2012 - "VE-cadherin, the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation, is also overexpressed in melanoma. "
09/01/2012 - "Together, these data suggest that LH inhibits melanoma C8161 cell-dominant vasculogenic mimicry by reducing VE-cadherin gene expression and diminishing cell surface exposure of the protein."
|5.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|7.||Proteins (Proteins, Gene)
|8.||Messenger RNA (mRNA)
|9.||Biological Markers (Surrogate Marker)
|10.||Granulocyte Colony-Stimulating Factor (G-CSF)
|1.||Drug Therapy (Chemotherapy)
|3.||Heterologous Transplantation (Xenotransplantation)