Abstract:
:A large series of protein pathway components have been shown to be dysregulated in Down syndrome (DS) brain. No information about pathomechanisms linked to the trisomic state can be obtained from adult DS brain, however, as neurodegeneration occurs from the fourth decade. The aim of the study was to search for protein dysregulation in fetal DS brain before neurodegenerative changes are observed. Proteins were extracted from fetal DS and control frontal cortex, run on 2-DE, followed by quantification of protein spots with subsequent nano-ESI-LC-MS/MS analysis using an ion trap. Aberrant expression of proteins tropomodulin-2, tubulin alpha 1A chain, and alpha-internexin may indicate disturbed synaptic plasticity; fatty acid binding protein 7 suggests impaired maintenance of neuroepithelial cells; and creatine kinase B may reflect defective energy metabolism. RNA binding protein 4B derangement may represent impaired splicing, altered retrotransposon gag domain-containing protein 1 levels may be pointing to altered retrotransposition, and level changes of the potassium-chloride transporter solute carrier family 12 member 7 may lead to impaired ion fluxes with electrophysiological consequences. Taken together, aberrant protein levels from several pathways in fetal DS are challenging as well as fertilizing the area of research and providing the basis for additional neurochemical and functional studies.
journal_name
J Proteomicsjournal_title
Journal of proteomicsauthors
Sun Y,Dierssen M,Toran N,Pollak DD,Chen WQ,Lubec Gdoi
10.1016/j.jprot.2011.01.009subject
Has Abstractpub_date
2011-04-01 00:00:00pages
547-57issue
4eissn
1874-3919issn
1876-7737pii
S1874-3919(11)00026-1journal_volume
74pub_type
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journal_title:Journal of proteomics
pub_type: 杂志文章,评审
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pub_type: 临床试验,杂志文章
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pub_type: 杂志文章
doi:10.1016/j.jprot.2012.09.013
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journal_title:Journal of proteomics
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pub_type: 杂志文章,评审
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