| pubmed-article:18641366 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C0300423 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C2699128 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C0023516 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C1332729 | lld:lifeskim |
| pubmed-article:18641366 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:18641366 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18641366 | pubmed:dateCreated | 2008-9-23 | lld:pubmed |
| pubmed-article:18641366 | pubmed:abstractText | Vascular endothelial-cadherin (VE-cad) is localized to adherens junctions at endothelial cell borders and forms a complex with alpha-, beta-, gamma-, and p120-catenins (p120). We previously showed that the VE-cad complex disassociates to form short-lived "gaps" during leukocyte transendothelial migration (TEM); however, whether these gaps are required for leukocyte TEM is not clear. Recently p120 has been shown to control VE-cad surface expression through endocytosis. We hypothesized that p120 regulates VE-cad surface expression, which would in turn have functional consequences for leukocyte transmigration. Here we show that endothelial cells transduced with an adenovirus expressing p120GFP fusion protein significantly increase VE-cad expression. Moreover, endothelial junctions with high p120GFP expression largely prevent VE-cad gap formation and neutrophil leukocyte TEM; if TEM occurs, the length of time required is prolonged. We find no evidence that VE-cad endocytosis plays a role in VE-cad gap formation and instead show that this process is regulated by changes in VE-cad phosphorylation. In fact, a nonphosphorylatable VE-cad mutant prevented TEM. In summary, our studies provide compelling evidence that VE-cad gap formation is required for leukocyte transmigration and identify p120 as a critical intracellular mediator of this process through its regulation of VE-cad expression at junctions. | lld:pubmed |
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| pubmed-article:18641366 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18641366 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18641366 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18641366 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18641366 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18641366 | pubmed:issn | 1528-0020 | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:GolanDavid... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:LuscinskasFra... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:MayadasTanya... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:SehrawatSeema... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:AlcaidePilarP | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:VincentPeterP | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:YaconoPatrick... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:NewtonGailG | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:AuerbachScott... | lld:pubmed |
| pubmed-article:18641366 | pubmed:author | pubmed-author:KowalczykAndr... | lld:pubmed |
| pubmed-article:18641366 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18641366 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18641366 | pubmed:volume | 112 | lld:pubmed |
| pubmed-article:18641366 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18641366 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18641366 | pubmed:pagination | 2770-9 | lld:pubmed |
| pubmed-article:18641366 | pubmed:dateRevised | 2010-12-3 | lld:pubmed |
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