| pubmed-article:6933469 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0018555 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0204727 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:6933469 | lifeskim:mentions | umls-concept:C1151778 | lld:lifeskim |
| pubmed-article:6933469 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:6933469 | pubmed:dateCreated | 1981-1-29 | lld:pubmed |
| pubmed-article:6933469 | pubmed:abstractText | Mutants of Chinese hamster ovary cells lacking dihydrofolate reductase (tetrahydrofolate dehydrogenase, 7,8-dihydrofolate:NADP+ oxidoreductase; EC 1.5.1.3) activity were isolated after mutagenesis and exposure to high-specific-activity [3H]deoxyuridine as a selective agent. Fully deficient mutants could not be isolated starting with wild-type cells, but could readily be selected from a putative heterozygote that contains half of the wild-type level of dihydrofolate reductase activity. The heterozygote itself was selected from wild-type cells by using [3H]deoxyuridine together with methotrexate to reduce intracellular dihydrofolate reductase activity. Fully deficient mutants require glycine, a purine, and thymidine for growth; this phenotype is recessive to wild type in cell hybrids. Revertants have been isolated, one of which produces a heat-labile dihydrofolate reductase activity. These mutants may be useful for metabolic studies relating to cancer chemotherapy and for fine-structure genetic mapping of mutations by using available molecular probes for this gene. | lld:pubmed |
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| pubmed-article:6933469 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:6933469 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:6933469 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6933469 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:6933469 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:6933469 | pubmed:author | pubmed-author:ChasinL ALA | lld:pubmed |
| pubmed-article:6933469 | pubmed:author | pubmed-author:UrlaubGG | lld:pubmed |
| pubmed-article:6933469 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6933469 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:6933469 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6933469 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6933469 | pubmed:pagination | 4216-20 | lld:pubmed |
| pubmed-article:6933469 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:6933469 | pubmed:year | 1980 | lld:pubmed |
| pubmed-article:6933469 | pubmed:articleTitle | Isolation of Chinese hamster cell mutants deficient in dihydrofolate reductase activity. | lld:pubmed |
| pubmed-article:6933469 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6933469 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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