Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 6
pubmed:dateCreated
2007-11-22
pubmed:abstractText
The correction of replication errors is an essential component of genetic stability. This is clearly demonstrated in humans by the observation that mutations in mismatch repair genes lead to HNPCC (hereditary non-polyposis colorectal cancer). This disease accounts for as many as 2-3% of colon cancers. Of these, most of them are in the two central components of mismatch repair, MLH1 (mutL homologue 1) and MSH2 (mutS homologue 2). MLH1 and MSH2 function as a complex with two other genes PMS2 and MSH6. Mismatch repair genes, and the mechanism that ensures that incorrectly paired bases are removed, are conserved from prokaryotes to human. Thus yeast can serve as a model organism for analysing mutations/polymorphisms found in human mismatch repair genes for their effect on post-replicative repair. To date, this has predominantly been accomplished by making the analogous mutations in yeast genes. However, this approach is only useful for the most highly conserved regions. Here, we discuss some of the benefits and technical difficulties involved in expressing human genes in yeast. Modelling human mismatch repair in yeast will allow the assessment of any functional effect of novel polymorphisms found in patients diagnosed with colon cancers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0300-5127
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1525-8
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Humanizing mismatch repair in yeast: towards effective identification of hereditary non-polyposis colorectal cancer alleles.
pubmed:affiliation
Department of Genetics, University of Leicester, Adrian Building, University Road, Leicester LE1 7RH, U.K.
pubmed:publicationType
Journal Article, Review