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    Neuroscience. 2009 Jun 30;161(2):451-8. Epub 2009 Mar 26.

    Upregulation of beta-catenin expression in down syndrome model Ts65Dn mouse brain.

    Ramakrishna N, Meeker HC, Li S, Brown WT, Rao R, El Idrissi A.

    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

    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.

    PMID: 19328224 [PubMed - indexed for MEDLINE]

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