pubmed-article:11311137 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C2936239 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0006100 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0107053 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0443301 | lld:lifeskim |
pubmed-article:11311137 | lifeskim:mentions | umls-concept:C0599896 | lld:lifeskim |
pubmed-article:11311137 | pubmed:issue | Pt 3 | lld:pubmed |
pubmed-article:11311137 | pubmed:dateCreated | 2001-4-20 | lld:pubmed |
pubmed-article:11311137 | pubmed:abstractText | In this study, we analysed the agonist-promoted trafficking of human B(2) (B(2)R) and B(1) (B(1)R) bradykinin (BK) receptors using wild-type and green fluorescent protein (GFP)-tagged receptors in HEK293 cells. B(2)R was sequestered to a major extent upon exposure to BK, as determined by the loss of cell-surface B(2)R using radioligand binding and by imaging of B(2)R-GFP using laser-scanning confocal fluorescence microscopy. Concurrent BK sequestration was revealed by the appearance of acid-resistant specific BK receptor binding. The same techniques showed that B(1)R was sequestered to a considerably lesser extent upon binding of des-Arg(10)-kallidin. B(2)R sequestration was rapid (half-life approximately 5 min) and reached a steady-state level that was significantly lower than that of BK sequestration. B(2)R sequestration was minimally inhibited by K44A dynamin (22.4+/-3.7%), and was insensitive to arrestin-(319-418), which are dominant-negative mutants of dynamin I and beta-arrestin respectively. Furthermore, the B(2)R-mediated sequestration of BK was completely insensitive to both mutants, as was the association of BK with a caveolae-enriched fraction of the cells. On the other hand, agonist-promoted sequestration of the beta(2)-adrenergic receptor was dramatically inhibited by K44A dynamin (81.2+/-16.3%) and by arrestin-(319-418) (36.9+/-4.4%). Our results show that B(2)R is sequestered to a significantly greater extent than is B(1)R upon agonist treatment in HEK293 cells. Furthermore, B(2)R appears to be recycled in the process of sequestering BK, and this process occurs in a dynamin- and beta-arrestin-independent manner and, at least in part, involves caveolae. | lld:pubmed |
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pubmed-article:11311137 | pubmed:language | eng | lld:pubmed |
pubmed-article:11311137 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11311137 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11311137 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11311137 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11311137 | pubmed:month | May | lld:pubmed |
pubmed-article:11311137 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:11311137 | pubmed:author | pubmed-author:LambM EME | lld:pubmed |
pubmed-article:11311137 | pubmed:author | pubmed-author:Leeb-Lundberg... | lld:pubmed |
pubmed-article:11311137 | pubmed:author | pubmed-author:De WeerdW FWF | lld:pubmed |
pubmed-article:11311137 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11311137 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11311137 | pubmed:volume | 355 | lld:pubmed |
pubmed-article:11311137 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11311137 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11311137 | pubmed:pagination | 741-50 | lld:pubmed |
pubmed-article:11311137 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:11311137 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11311137 | pubmed:articleTitle | Agonist-promoted trafficking of human bradykinin receptors: arrestin- and dynamin-independent sequestration of the B2 receptor and bradykinin in HEK293 cells. | lld:pubmed |
pubmed-article:11311137 | pubmed:affiliation | Department of Biochemistry, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. | lld:pubmed |
pubmed-article:11311137 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11311137 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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