Global up-regulation of chromosome 21 gene expression in the developing Down syndrome brain - PubMed (original) (raw)
Global up-regulation of chromosome 21 gene expression in the developing Down syndrome brain
Rong Mao et al. Genomics. 2003 May.
Abstract
Down syndrome (DS) results from complete or partial triplication of human chromosome 21. It is assumed that the neurological and other symptoms are caused by the overexpression of genes on chromosome 21, but this hypothesis has not yet been assessed on a chromosome-wide basis. Here we show that expression of genes localized to chromosome 21 is globally up-regulated in human fetal trisomy 21 cases, both in cerebral cortex extracts and in astrocytic cell lines cultured from cerebral cortex. This abnormal regulation of gene expression is specific to chromosome 21. Our data describe transcriptional changes that are specific to many genes assigned to chromosome 21 and do not directly measure the clinical phenotype of DS. However, it is possible that these gene expression changes ultimately relate to the phenotypic variability of DS.
Similar articles
- Gene expression analysis of cultured amniotic fluid cell with Down syndrome by DNA microarray.
Chung IH, Lee SH, Lee KW, Park SH, Cha KY, Kim NS, Yoo HS, Kim YS, Lee S. Chung IH, et al. J Korean Med Sci. 2005 Feb;20(1):82-7. doi: 10.3346/jkms.2005.20.1.82. J Korean Med Sci. 2005. PMID: 15716609 Free PMC article. - Altered gene expression in fetal Down syndrome brain as revealed by the gene hunting technique of subtractive hybridization.
Kitzmueller E, Labudova O, Rink H, Cairns N, Lubec G. Kitzmueller E, et al. J Neural Transm Suppl. 1999;57:99-124. doi: 10.1007/978-3-7091-6380-1_7. J Neural Transm Suppl. 1999. PMID: 10666671 - Primary and secondary transcriptional effects in the developing human Down syndrome brain and heart.
Mao R, Wang X, Spitznagel EL Jr, Frelin LP, Ting JC, Ding H, Kim JW, Ruczinski I, Downey TJ, Pevsner J. Mao R, et al. Genome Biol. 2005;6(13):R107. doi: 10.1186/gb-2005-6-13-r107. Epub 2005 Dec 16. Genome Biol. 2005. PMID: 16420667 Free PMC article. - Genetic mechanisms involved in the phenotype of Down syndrome.
Patterson D. Patterson D. Ment Retard Dev Disabil Res Rev. 2007;13(3):199-206. doi: 10.1002/mrdd.20162. Ment Retard Dev Disabil Res Rev. 2007. PMID: 17910086 Review. - Murine models for Down syndrome.
Dierssen M, Fillat C, Crnic L, Arbonés M, Flórez J, Estivill X. Dierssen M, et al. Physiol Behav. 2001 Aug;73(5):859-71. doi: 10.1016/s0031-9384(01)00523-6. Physiol Behav. 2001. PMID: 11566219 Review.
Cited by
- The cognitive phenotype of Down syndrome: insights from intracellular network analysis.
Ma'ayan A, Gardiner K, Iyengar R. Ma'ayan A, et al. NeuroRx. 2006 Jul;3(3):396-406. doi: 10.1016/j.nurx.2006.05.036. NeuroRx. 2006. PMID: 16815222 Free PMC article. Review. - Gene-dosage effects in Down syndrome and trisomic mouse models.
Gardiner K. Gardiner K. Genome Biol. 2004;5(10):244. doi: 10.1186/gb-2004-5-10-244. Epub 2004 Sep 30. Genome Biol. 2004. PMID: 15461808 Free PMC article. Review. - Human iPSC-derived Down syndrome astrocytes display genome-wide perturbations in gene expression, an altered adhesion profile, and increased cellular dynamics.
Ponroy Bally B, Farmer WT, Jones EV, Jessa S, Kacerovsky JB, Mayran A, Peng H, Lefebvre JL, Drouin J, Hayer A, Ernst C, Murai KK. Ponroy Bally B, et al. Hum Mol Genet. 2020 Mar 27;29(5):785-802. doi: 10.1093/hmg/ddaa003. Hum Mol Genet. 2020. PMID: 31943018 Free PMC article. - Targeting trisomic treatments: optimizing Dyrk1a inhibition to improve Down syndrome deficits.
Stringer M, Goodlett CR, Roper RJ. Stringer M, et al. Mol Genet Genomic Med. 2017 Sep 20;5(5):451-465. doi: 10.1002/mgg3.334. eCollection 2017 Sep. Mol Genet Genomic Med. 2017. PMID: 28944229 Free PMC article. Review. - DYRK1A enhances the mitogen-activated protein kinase cascade in PC12 cells by forming a complex with Ras, B-Raf, and MEK1.
Kelly PA, Rahmani Z. Kelly PA, et al. Mol Biol Cell. 2005 Aug;16(8):3562-73. doi: 10.1091/mbc.e04-12-1085. Epub 2005 May 25. Mol Biol Cell. 2005. PMID: 15917294 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical