Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-5-18
pubmed:abstractText
The discovery that Rett syndrome is caused by mutations that affect the methyl-CpG-binding protein MeCP2 provided a major breakthrough in understanding this severe neurodevelopmental disorder. Animal models and expression studies have contributed to defining the role of MeCP2 in development, highlighting its contribution to postnatal neuronal morphogenesis and function. Furthermore, in vitro assays and microrray studies have delineated the potential molecular mechanisms of MeCP2 function, and have indicated a role in the transcriptional silencing of specific target genes. As well as unravelling the mechanisms that underlie Rett syndrome, these studies provide more general insights into how DNA-methylation patterns are recognized and translated into biological outcomes.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1471-0056
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
415-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Molecular genetics of Rett syndrome: when DNA methylation goes unrecognized.
pubmed:affiliation
Institut Cochin, Départment de Génétique et Developpement, Paris, F-75014 France.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't