| pubmed-article:8469973 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8469973 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
| pubmed-article:8469973 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:8469973 | lifeskim:mentions | umls-concept:C1158537 | lld:lifeskim |
| pubmed-article:8469973 | lifeskim:mentions | umls-concept:C1519877 | lld:lifeskim |
| pubmed-article:8469973 | pubmed:issue | 5105 | lld:pubmed |
| pubmed-article:8469973 | pubmed:dateCreated | 1993-5-10 | lld:pubmed |
| pubmed-article:8469973 | pubmed:abstractText | Cells maintain the integrity of their genome through an intricate network of repair systems that recognize and remove lesions from DNA. The only known site-directed recombination process in vertebrates is the V(D)J recombination of lymphocyte antigen receptor genes. A large panel of cell lines deficient in DNA repair were tested for the ability to perform V(D)J recombination after introduction of the RAG-1 and RAG-2 genes. Two mutants failed to generate normal V(D)J recombination, and further analysis provided evidence for two distinct nonlymphoid-specific genes that encode factors involved in both DNA repair and V(D)J recombination. | lld:pubmed |
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| pubmed-article:8469973 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8469973 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8469973 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8469973 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8469973 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8469973 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:YuHH | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:StamatoTT | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:JeggoP APA | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:RathbunGG | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:TaccioliG EGE | lld:pubmed |
| pubmed-article:8469973 | pubmed:author | pubmed-author:OltzEE | lld:pubmed |
| pubmed-article:8469973 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8469973 | pubmed:day | 9 | lld:pubmed |
| pubmed-article:8469973 | pubmed:volume | 260 | lld:pubmed |
| pubmed-article:8469973 | pubmed:geneSymbol | RAG-1 | lld:pubmed |
| pubmed-article:8469973 | pubmed:geneSymbol | RAG-2 | lld:pubmed |
| pubmed-article:8469973 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8469973 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8469973 | pubmed:pagination | 207-10 | lld:pubmed |
| pubmed-article:8469973 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:8469973 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8469973 | pubmed:articleTitle | Impairment of V(D)J recombination in double-strand break repair mutants. | lld:pubmed |
| pubmed-article:8469973 | pubmed:affiliation | Howard Hughes Medical Institute, Children's Hospital, Boston, MA. | lld:pubmed |
| pubmed-article:8469973 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8469973 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8469973 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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