pubmed-article:17954608 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17954608 | lifeskim:mentions | umls-concept:C1366911 | lld:lifeskim |
pubmed-article:17954608 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:17954608 | lifeskim:mentions | umls-concept:C0021721 | lld:lifeskim |
pubmed-article:17954608 | lifeskim:mentions | umls-concept:C1426113 | lld:lifeskim |
pubmed-article:17954608 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:17954608 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:17954608 | pubmed:dateCreated | 2007-10-23 | lld:pubmed |
pubmed-article:17954608 | pubmed:abstractText | Cerebral cavernous malformation (CCM), a disease associated with defective endothelial junctions, result from autosomal dominant CCM1 mutations that cause loss of KRIT-1 protein function, though how the loss of KRIT-1 leads to CCM is obscure. KRIT-1 binds to Rap1, a guanosine triphosphatase that maintains the integrity of endothelial junctions. Here, we report that KRIT-1 protein is expressed in cultured arterial and venous endothelial cells and is present in cell-cell junctions. KRIT-1 colocalized and was physically associated with junctional proteins via its band 4.1/ezrin/radixin/moesin (FERM) domain. Rap1 activity regulated the junctional localization of KRIT-1 and its physical association with junction proteins. However, the association of the isolated KRIT-1 FERM domain was independent of Rap1. Small interfering RNA-mediated depletion of KRIT-1 blocked the ability of Rap1 to stabilize endothelial junctions associated with increased actin stress fibers. Thus, Rap1 increases KRIT-1 targeting to endothelial cell-cell junctions where it suppresses stress fibers and stabilizes junctional integrity. | lld:pubmed |
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pubmed-article:17954608 | pubmed:language | eng | lld:pubmed |
pubmed-article:17954608 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17954608 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17954608 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17954608 | pubmed:month | Oct | lld:pubmed |
pubmed-article:17954608 | pubmed:issn | 0021-9525 | lld:pubmed |
pubmed-article:17954608 | pubmed:author | pubmed-author:HanJaewonJ | lld:pubmed |
pubmed-article:17954608 | pubmed:author | pubmed-author:GladingAngela... | lld:pubmed |
pubmed-article:17954608 | pubmed:author | pubmed-author:GinsbergMark... | lld:pubmed |
pubmed-article:17954608 | pubmed:author | pubmed-author:StocktonRebec... | lld:pubmed |
pubmed-article:17954608 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17954608 | pubmed:day | 22 | lld:pubmed |
pubmed-article:17954608 | pubmed:volume | 179 | lld:pubmed |
pubmed-article:17954608 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17954608 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17954608 | pubmed:pagination | 247-54 | lld:pubmed |
pubmed-article:17954608 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17954608 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17954608 | pubmed:articleTitle | KRIT-1/CCM1 is a Rap1 effector that regulates endothelial cell cell junctions. | lld:pubmed |
pubmed-article:17954608 | pubmed:affiliation | Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. | lld:pubmed |
pubmed-article:17954608 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17954608 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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