Linked Life Data

19328224

Source:http://linkedlifedata.com/resource/pubmed/id/19328224

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-6-1
pubmed:abstractText
Trisomy of human chromosome 21 (Hsa 21) causes the pathological characteristics of Down syndrome (DS). Little is known about the mechanisms by which trisomy 21 affects the expression of genes on other chromosomes. Using a mouse model of DS, the Ts65Dn mouse, we have performed mRNA and protein measurements to identify genes on chromosomes not syntenic with Hsa 21 whose expression is affected by the presence of three copies of genes between loci Mrpl39 and Znf295 on mouse chromosome 16 (Mmu 16). We report the upregulation of beta-catenin, located on mouse chromosome 9 (Mmu 9) in Ts65Dn brain. Using immunocytochemistry on Ts65Dn and control mouse brain tissue, we observed a striking increase in beta-catenin expression specifically in the endothelial cells lining the cerebral blood vessels of the Ts65Dn mice. Since beta-catenin is involved in cell-cell adhesion, upregulation of this protein in DS may alter adherens protein interactions that are involved in the normal functions of endothelial cells. Elevated beta-catenin might be responsible for altered endothelial cell function/s leading to the impairment of brachial flow velocity observed in DS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1873-7544
pubmed:author
pubmed:issnType
Electronic
pubmed:day
30
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
451-8
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Upregulation of beta-catenin expression in down syndrome model Ts65Dn mouse brain.
pubmed:affiliation
Molecular Biology Department, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA. narayan.ramakrishna@gmail.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't