| pubmed-article:6593710 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6593710 | lifeskim:mentions | umls-concept:C0023418 | lld:lifeskim |
| pubmed-article:6593710 | lifeskim:mentions | umls-concept:C0017428 | lld:lifeskim |
| pubmed-article:6593710 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
| pubmed-article:6593710 | lifeskim:mentions | umls-concept:C0009807 | lld:lifeskim |
| pubmed-article:6593710 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:6593710 | pubmed:dateCreated | 1984-12-7 | lld:pubmed |
| pubmed-article:6593710 | pubmed:abstractText | A TL+ leukemia of a (B6 X A)F1 hybrid mouse (H-2b/H-2a) was previously subjected to immunoselection against H-2a by passage in (B6 X A.SW)F1 mice (H-2b/H-2s). A variant leukemia line was obtained that serologically lacked not only the H-2a phenotype but also the TL phenotype determined by the linked cis Tlaa allele of strain A. The H-2b phenotype and the TL phenotype of the Tlab allele of the B6 strain, which is expressed only by leukemia cells, were retained by the variant. Southern blotting with an H-2 cDNA probe that identifies restriction fragment polymorphisms distinguishing alleles of the H-2 and Tla regions of the B6 and A strains indicates that both the H-2a and Tlaa alleles are missing from the genome of this H-2a:Tlaa negative variant. Since the variant has two apparently unaltered chromosomes 17, where the H-2:Tla complex is situated, and since the intensity of bands in Southern blotting is suggestive of H-2b homozygosity, it is considered that loss of the H-2a:Tlaa haplotype by the variant was accompanied by duplication of the H-2b:Tlab haplotype. The implied change from heterozygosity to homozygosity that the variant has undergone with respect to H-2:Tla was not paralleled by a similar change at the three other loci tested, since the variant retained heterozygosity for Pep-3 (chromosome 1), Gpi-1 (chromosome 7), and Es-1 (chromosome 8). | lld:pubmed |
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| pubmed-article:6593710 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6593710 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6593710 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:6593710 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:6593710 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6593710 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:6593710 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:ChagantiR SRS | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:SteinmetzMM | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:LitmanG WGW | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:BoyseE AEA | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:HoodLL | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:TICEG MGM | lld:pubmed |
| pubmed-article:6593710 | pubmed:author | pubmed-author:DoucetteL ALA | lld:pubmed |
| pubmed-article:6593710 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6593710 | pubmed:volume | 81 | lld:pubmed |
| pubmed-article:6593710 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6593710 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6593710 | pubmed:pagination | 6447-50 | lld:pubmed |
| pubmed-article:6593710 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:6593710 | pubmed:meshHeading | pubmed-meshheading:6593710-... | lld:pubmed |
| pubmed-article:6593710 | pubmed:year | 1984 | lld:pubmed |
| pubmed-article:6593710 | pubmed:articleTitle | Genomic constitution of an H-2:Tla variant leukemia. | lld:pubmed |
| pubmed-article:6593710 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6593710 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:6593710 | lld:pubmed |
