| pubmed-article:7569935 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C0019629 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C0439857 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C1417898 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C1864009 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C1149098 | lld:lifeskim |
| pubmed-article:7569935 | lifeskim:mentions | umls-concept:C0034115 | lld:lifeskim |
| pubmed-article:7569935 | pubmed:issue | 5233 | lld:pubmed |
| pubmed-article:7569935 | pubmed:dateCreated | 1995-11-7 | lld:pubmed |
| pubmed-article:7569935 | pubmed:abstractText | Major histocompatibility complex (MHC) class I molecules bind peptides that are delivered from the cytosol into the endoplasmic reticulum by the MHC-encoded transporter associated with antigen processing (TAP). Peptide capture by immature heterodimers of class I heavy chains and beta 2-microglobulin may be facilitated by their physical association with TAP. A genetic defect in a human mutant cell line causes the complete failure of diverse class I heterodimers to associate with TAP. This deficiency impairs the ability of the class I heterodimers to efficiently capture peptides and results from loss of function of an unidentified gene or genes linked to the MHC. | lld:pubmed |
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| pubmed-article:7569935 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7569935 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7569935 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7569935 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:7569935 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:7569935 | pubmed:author | pubmed-author:SpierWW | lld:pubmed |
| pubmed-article:7569935 | pubmed:author | pubmed-author:GeraghtyD EDE | lld:pubmed |
| pubmed-article:7569935 | pubmed:author | pubmed-author:AthwalR SRS | lld:pubmed |
| pubmed-article:7569935 | pubmed:author | pubmed-author:AndrolewiczM... | lld:pubmed |
| pubmed-article:7569935 | pubmed:author | pubmed-author:GrandeaA... | lld:pubmed |
| pubmed-article:7569935 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7569935 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:7569935 | pubmed:volume | 270 | lld:pubmed |
| pubmed-article:7569935 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7569935 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7569935 | pubmed:pagination | 105-8 | lld:pubmed |
| pubmed-article:7569935 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:7569935 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7569935 | pubmed:articleTitle | Dependence of peptide binding by MHC class I molecules on their interaction with TAP. | lld:pubmed |
| pubmed-article:7569935 | pubmed:affiliation | Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA. | lld:pubmed |
| pubmed-article:7569935 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7569935 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7569935 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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