| pubmed-article:9188650 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C0034848 | lld:lifeskim |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C0699791 | lld:lifeskim |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C0149678 | lld:lifeskim |
| pubmed-article:9188650 | lifeskim:mentions | umls-concept:C0056184 | lld:lifeskim |
| pubmed-article:9188650 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:9188650 | pubmed:dateCreated | 1997-7-10 | lld:pubmed |
| pubmed-article:9188650 | pubmed:abstractText | Recombinant Epstein-Barr virus (EBV) with a selectable marker successfully infected the human gastric carcinoma cell lines AGS, MKN28, and MKN74. Following incubation in selective media, drug-resistant cell clones were isolated and proved to be infected with EBV. All gastric carcinoma cell clones were positive for EBNA 1 but negative for EBNA 2. LMP 1 expression was negative in most clones, but there were a few exceptions. Gastric carcinoma cells were negative for the EBV receptor CD21, and infection was not inhibited by pretreatment of cells with the anti-CD21 monoclonal antibody OKB7. The results indicate that gastric carcinoma cells are susceptible to EBV infection and that infection is mediated via a new receptor different from CD21. | lld:pubmed |
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| pubmed-article:9188650 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9188650 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9188650 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9188650 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9188650 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:9188650 | pubmed:author | pubmed-author:ImaiSS | lld:pubmed |
| pubmed-article:9188650 | pubmed:author | pubmed-author:ShimizuNN | lld:pubmed |
| pubmed-article:9188650 | pubmed:author | pubmed-author:TakadaKK | lld:pubmed |
| pubmed-article:9188650 | pubmed:author | pubmed-author:YoshiyamaHH | lld:pubmed |
| pubmed-article:9188650 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9188650 | pubmed:volume | 71 | lld:pubmed |
| pubmed-article:9188650 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9188650 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9188650 | pubmed:pagination | 5688-91 | lld:pubmed |
| pubmed-article:9188650 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9188650 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9188650 | pubmed:articleTitle | Epstein-Barr virus infection of human gastric carcinoma cells: implication of the existence of a new virus receptor different from CD21. | lld:pubmed |
| pubmed-article:9188650 | pubmed:affiliation | Department of Virology, Cancer Institute, Hokkaido University School of Medicine, Sapporo, Japan. | lld:pubmed |
| pubmed-article:9188650 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9188650 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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