pubmed-article:8552587 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8552587 | lifeskim:mentions | umls-concept:C0085080 | lld:lifeskim |
pubmed-article:8552587 | lifeskim:mentions | umls-concept:C0008633 | lld:lifeskim |
pubmed-article:8552587 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
pubmed-article:8552587 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:8552587 | lifeskim:mentions | umls-concept:C0524999 | lld:lifeskim |
pubmed-article:8552587 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:8552587 | pubmed:dateCreated | 1996-2-22 | lld:pubmed |
pubmed-article:8552587 | pubmed:abstractText | High-density mutational spectra have been established for exon 3 of the gene encoding adenine phosphoribosyltransferase (APRT) of the Chinese hamster ovary (CHO) cell line derivative D422 and closely related and/or modified lines by using the mutagen ethyl methanesulfonate (EMS). The total number of selectable sites (GC-->AT transitions yielding a selectable APRT- phenotype) was estimated at 31 based on our own accumulated data base of 136 sequenced exon 3 mutations and on literature reports. D422 and two other APRT hemizygous lines each yielded very similar spectra and showed two populations of mutable sites: (i) 24 "baseline" sites that followed the Poisson distribution and therefore were equally susceptible to mutation and (ii) two hotspots, one comprising a cluster at nucleotides 1293-1309 and the other at nucleotide 1365. Collectively, the latter sites were about 10-fold more frequently mutated than the others. CHO cells are mer- as they lack the repair enzyme O6-methylguanidine methyltransferase (EC 2.1.1.63). In modified repair-proficient CHO cells, the distribution of mutations among all of the 31 sites was random, with only 3 of the 19 GC-->AT transitions in the above hotspots. To determine whether the distribution was locus-dependent, two independent lines carrying single copies of transfected APRT genes were generated from a derivative of D422 carrying a deletion in the endogenous APRT gene. Nucleotides 1293-1309 were again no longer preferentially mutated, but the site at nucleotide 1365 was still a hotspot. We conclude that mutational spectra in mer- cells are at least in part locus dependent and that some sequences are particularly susceptible to EMS mutagenesis and perhaps also to methyltransferase repair. | lld:pubmed |
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pubmed-article:8552587 | pubmed:language | eng | lld:pubmed |
pubmed-article:8552587 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8552587 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8552587 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8552587 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8552587 | pubmed:month | Jan | lld:pubmed |
pubmed-article:8552587 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:8552587 | pubmed:author | pubmed-author:BradleyW EWE | lld:pubmed |
pubmed-article:8552587 | pubmed:author | pubmed-author:GRAYD SDS | lld:pubmed |
pubmed-article:8552587 | pubmed:author | pubmed-author:BelouchiAA | lld:pubmed |
pubmed-article:8552587 | pubmed:author | pubmed-author:OuimetMM | lld:pubmed |
pubmed-article:8552587 | pubmed:author | pubmed-author:GaudreaultNN | lld:pubmed |
pubmed-article:8552587 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8552587 | pubmed:day | 9 | lld:pubmed |
pubmed-article:8552587 | pubmed:volume | 93 | lld:pubmed |
pubmed-article:8552587 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8552587 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8552587 | pubmed:pagination | 121-5 | lld:pubmed |
pubmed-article:8552587 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8552587 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8552587 | pubmed:articleTitle | Influence of alkyltransferase activity and chromosomal locus on mutational hotspots in Chinese hamster ovary cells. | lld:pubmed |
pubmed-article:8552587 | pubmed:affiliation | Institut du cancer de Montréal, Centre de Recherche Louis-Charles Simard, Montréal, Canada. | lld:pubmed |
pubmed-article:8552587 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8552587 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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