Linked Life Data

10102049

Source:http://linkedlifedata.com/resource/pubmed/id/10102049

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
428
pubmed:dateCreated
1999-5-27
pubmed:abstractText
Determination of the mechanisms that lead to in utero overgrowth has proved elusive. Recently, however, our knowledge has significantly expanded as a result of the generation of experimental mouse models, engineered to disrupt the expression of one or more genes (knockout mice), and by detailed molecular and genetic analyses of infants and children with overgrowth syndromes. Studies of knockout mice have largely defined the essential roles of the insulin-like growth factors (IGF-I and IGF-II), insulin and their receptors in embryonic and fetal growth, and have provided compelling evidence that increased IGF-II gene expression and/or abundance can stimulate excessive fetal somatic growth. The IGF-II gene is usually expressed only by the paternally derived allele; however, when this imprinting is erased and IGF-II expression is biallelic, fetal overgrowth ensues. Such increased IGF-II expression would appear to explain the overgrowth in Beckwith-Wiedemann syndrome. Using the information gathered from knockout mice as a guide to human studies, detailed genetic investigations are likely to unravel the mechanisms behind other human overgrowth syndromes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0803-5326
pubmed:author
pubmed:issnType
Print
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Mechanisms of in utero overgrowth.
pubmed:affiliation
Department of Pediatrics, University of North Carolina-Chapel Hill 27599-7220, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review