Linked Life Data

10397247

Source:http://linkedlifedata.com/resource/pubmed/id/10397247

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1999-7-28
pubmed:abstractText
To explore further the possibility that some forms of mutated p53 may increase mutagenesis in a positive manner, a double p53 knockout cell line was created, using a promoterless gene targeting approach. The identity of these p53-null cells was confirmed by Southern blot and Western blot analyses. Radiation-induced toxicity and mutagenicity was then compared among p53-null cells, TK6 cells with wild-type p53, and WTK1 cells with a p53 point mutation in codon 237. At the autosomal, heterozygous thymidine kinase locus, p53-null cells had equivalent background mutation frequencies and were approximately equally mutable as TK6, whereas WTK1 was much more sensitive to spontaneously arising and X-ray-induced mutation. Thus, these results indicate that the lack of wild-type p53 did not lead to increased mutagenesis.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3073-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Radiation-induced mutations at the autosomal thymidine kinase locus are not elevated in p53-null cells.
pubmed:affiliation
Department of Radiation Oncology, Massachusetts General Hospital, Boston 02114, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.