Linked Life Data

3018557

Source:http://linkedlifedata.com/resource/pubmed/id/3018557

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1986-10-22
pubmed:abstractText
We have demonstrated that X-rays induce mutations at 4 of 5 genetic loci. 2 of these loci, which code for a mRNA synthesis factor (resistance to 5,6-dichlororibofuranosylbenzimidazole) and tubulin (resistance to podophyllotoxin), are "small-marker" loci, in that they theoretically respond only to mutations which eliminate a toxin-binding site while leaving the major function of the protein intact. Thus mutations induced by X-rays in these two loci are most likely due to base-pair substitution-type alterations. X-Rays did not induce mutations in the Na+/K+ ATPase (resistance to ouabain), another small-marker locus. Two other loci, hypoxanthine guanine phosphoribosyl transferase (resistance to 6-thioguanine) and thymidine kinase (resistance to trifluorothymidine), are "whole-gene" targets in that they theoretically respond to a wide variety of mutagenic changes. X-Rays induced dose-dependent increases in mutant fraction at both of these loci. Ethyl methanesulfonate (EMS), an agent thought to produce mutations primarily through a base-pair substitution mechanism, induced mutations at all genetic loci tested. The pattern of mutations at the small-marker loci induced by EMS was different than that induced by X-rays, suggesting that the specificities of the mutagens and/or of the loci are different.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
X-rays mutate human lymphoblast cells at genetic loci that should respond only to point mutagens.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.