Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
33
pubmed:dateCreated
2004-7-22
pubmed:abstractText
Mbd4 (methyl-binding domain 4) has been shown to be mutated in a high percentage of mismatch repair (MMR)-deficient colorectal tumours that exhibit microsatellite instability (MSI). However, the significance of these mutations is still unclear as they are predominantly monoallelic and the majority occur at a poly-A tract. Apart from MMR-deficient tumours, no other reports of mutations of Mbd4 in human neoplasia are as yet published. To address the significance of loss of Mbd4 in the absence of MMR, we have crossed Mbd4-deficient mice to mice lacking DNA MMR. We show that, in the context of MMR deficiency, additional loss of Mbd4 does not alter spontaneous mutation frequency at the endogenous Dlb-1b locus, nor does it modify tumour onset, tumour spectrum or MSI compared to singly mutant Msh2 or Mlh1 mice. Taken together, these findings show that nullizygosity or heterozygosity for Mbd4 does not affect MMR-dependent tumorigenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-9232
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Nature Publishing Group
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5693-6
pubmed:dateRevised
2009-2-25
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
MBD4 deficiency does not increase mutation or accelerate tumorigenesis in mice lacking MMR.
pubmed:affiliation
School of Biosciences, University of Cardiff, Museum Avenue, PO Box 911, Cardiff CF10 3US, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't