| pubmed-article:8303278 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0071253 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C2936824 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0919338 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0005456 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C1149289 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0599896 | lld:lifeskim |
| pubmed-article:8303278 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:8303278 | pubmed:issue | 5147 | lld:pubmed |
| pubmed-article:8303278 | pubmed:dateCreated | 1994-3-10 | lld:pubmed |
| pubmed-article:8303278 | pubmed:abstractText | Human platelet-derived growth factor receptors (PDGFRs) expressed in human Hep G2 cells internalized and concentrated in a juxtanuclear region near the Golgi network within 10 minutes after the cells were treated with PDGF. A PDGFR mutant (F5) that lacks high-affinity binding sites for the Src homology 2 domain-containing proteins phosphatidylinositol-3 kinase (PI-3 kinase), Ras guanosine triphosphatase activating protein, phospholipase C-gamma, and a phosphotyrosine phosphatase (Syp) remained at the cell periphery. Restoration of the PI-3 kinase binding sites on F5 completely restored the ability of the receptor to concentrate intracellularly. A PDGFR mutant lacking only PI-3 kinase binding sites failed to concentrate intracellularly. Thus, PI-3 kinase binding sites appear both necessary and sufficient for the normal endocytic trafficking of the activated PDGFR. | lld:pubmed |
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| pubmed-article:8303278 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8303278 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8303278 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8303278 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8303278 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:8303278 | pubmed:author | pubmed-author:KRAS JSJ | lld:pubmed |
| pubmed-article:8303278 | pubmed:author | pubmed-author:JolyMM | lld:pubmed |
| pubmed-article:8303278 | pubmed:author | pubmed-author:KazlauskasAA | lld:pubmed |
| pubmed-article:8303278 | pubmed:author | pubmed-author:CorveraSS | lld:pubmed |
| pubmed-article:8303278 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8303278 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:8303278 | pubmed:volume | 263 | lld:pubmed |
| pubmed-article:8303278 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8303278 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8303278 | pubmed:pagination | 684-7 | lld:pubmed |
| pubmed-article:8303278 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:8303278 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8303278 | pubmed:articleTitle | Disruption of PDGF receptor trafficking by mutation of its PI-3 kinase binding sites. | lld:pubmed |
| pubmed-article:8303278 | pubmed:affiliation | Program in Molecular Medicine, University of Massachusetts Medical School, Worcester 01605. | lld:pubmed |
| pubmed-article:8303278 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8303278 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8303278 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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