Down syndrome (DS), the most common cause of genetic mental dysfunction, is caused by aberrant protein expression due to a trisomy of chromosome 21 (Ts21). A mouse model of Ts21, based on synteny of human chromosome 21 and murine chromosome 16, is used for studying the mechanisms involved in DS. In this study we measured protein expression in immortalized cell lines derived from normal and trisomy 16 (Ts16) fetal mouse cerebral cortex (CNh and CTb respectively). iTRAQ labeling and mass spectrometry were used to examine each cell line for significant up- or down-regulation of proteins. CTb cells showed increased expression of 71 proteins and decreased expression of 56 proteins when compared to the normal CNh control cells. Several of these differentially expressed proteins have previously been reported to show aberrant expression in DS and other neurological disorders such as Alzheimer’s disease, a condition closely associated with Down syndrome. Our results clearly demonstrate the aberrant expression of proteins with various cellular functions within the trisomy model and may lead to a deeper understanding of the proteins and mechanisms involved in the Down syndrome phenotype.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.