| pubmed-article:6646118 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0085080 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0019425 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0314649 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
| pubmed-article:6646118 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:6646118 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:6646118 | pubmed:dateCreated | 1984-1-7 | lld:pubmed |
| pubmed-article:6646118 | pubmed:abstractText | A two-step model to explain the high frequency of mutation at the diploid adenine phosphoribosyltransferase (aprt) locus in CHO cells has been proposed previously (Simon et al., Mol. Cell. Biol. 2:1126-1133, 1982). This model indicates that two distinct classes of aprt heterozygotes can be isolated. Class 1 heterozygotes, the most abundant class, were defined as those which arose spontaneously and were capable of undergoing mutation to the APRT- phenotype only at a low frequency (putative point mutation). Class 2 heterozygotes arose from a mutation and gave rise at a high frequency to APRT- cells. This high-frequency event has been identified as a deletion of the wild-type allele (A. E. Simon and M. W. Taylor, Proc. Natl. Acad. Sci. U.S.A. 80:810-814, 1983). In this paper we report further analysis of class 1 heterozygotes with respect to genetic structure, gene products, and karyotype. Our study indicated that class 1 heterozygotes contain two different types of mutants. About half have only one copy of the aprt gene and an unaltered karyotype, indicating that a deletion (similar to the high-frequency second-step event observed for class 2 heterozygotes) rather than a loss of the chromosome was responsible for the generation of the aprt+/- genotype. The remainder of the previously designated class 1 heterozygotes still contained two copies of the aprt gene (within the limits of the quantitation technique used) and arose presumably by a point mutation. One of this group, D423, was characterized with respect to aprt gene products and found to produce an electrophoretic variant in addition to the wild-type protein. APRT- mutants derived from D423 retained the same number of aprt gene copies as D423 and still synthesized a protein that comigrated with wild type, unlike APRT- mutants derived from class 2 heterozygotes. D423 and the other heterozygotes with two aprt genes therefore did not fit into either class 1 or 2 and are now designated class 3. The model we present suggests that only one of the two aprt alleles present in wild-type cells can undergo the deletion. | lld:pubmed |
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| pubmed-article:6646118 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6646118 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6646118 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:6646118 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6646118 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:6646118 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:6646118 | pubmed:author | pubmed-author:BradleyW EWE | lld:pubmed |
| pubmed-article:6646118 | pubmed:author | pubmed-author:TaylorM WMW | lld:pubmed |
| pubmed-article:6646118 | pubmed:author | pubmed-author:SimonA EAE | lld:pubmed |
| pubmed-article:6646118 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6646118 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:6646118 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6646118 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6646118 | pubmed:pagination | 1703-10 | lld:pubmed |
| pubmed-article:6646118 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:6646118 | pubmed:meshHeading | pubmed-meshheading:6646118-... | lld:pubmed |
| pubmed-article:6646118 | pubmed:year | 1983 | lld:pubmed |
| pubmed-article:6646118 | pubmed:articleTitle | Mechanism of mutation at the aprt locus in Chinese hamster ovary cells: analysis of heterozygotes and hemizygotes. | lld:pubmed |
| pubmed-article:6646118 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6646118 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:6646118 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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