Abstract
Diverse ‘-omics’ technologies permit the comprehensive quantitative profiling of a variety of biological molecules. Comparative ‘-omics’ analyses, such as transcriptomics and proteomics, are powerful and useful tools for unraveling the molecular pathomechanisms of various diseases. As enhanced oxidative stress has been demonstrated in humans and mice with Down syndrome (DS), a redox proteomic analysis is useful for understanding how enhanced oxidative stress aggravates the state of individuals with oxidative stress-related disorders. In this review, ‘-omics’ analyses in humans with DS and mouse models of DS are summarized, and the molecular dissection of this syndrome is discussed.
Highlights
Understanding the changes in molecules provides important and valuable information for evaluating the molecular pathomechanisms of diseases
Most ‘-omics’ analyses assess the levels of target molecules, protein, transcripts, fatty acids, and various metabolites in organs, redox proteomics and phospho-proteomics indicate the degree of oxidative stress and activation of signal transduction or transcriptional factors, respectively
A number of comparative proteomics analyses using the brains from patients and mouse models have been performed
Summary
Understanding the changes in molecules provides important and valuable information for evaluating the molecular pathomechanisms of diseases. Brain Sci. 2017, 7, 44; doi:10.3390/brainsci7040044 www.mdpi.com/journal/brainsci carrying three copies of various segments of MMU16 syntenic to HSA21 have been recently established: Dp1Tyb, Dp2Tyb, Dp3Tyb, Dp4Tyb, Dp5Tyb, Dp6Tyb, and Dp9Tyb [7] (Figure 2). We discuss the changes in the molecules in brains from individuals with Down syndrome (DS) and DS mouse models according to ‘-omics’ analyses. Seven mouse models of DS carrying three copies of various segments of MMU16 syntenic to HSA21 have been recently established: Dp1Tyb, Dp2Tyb, Dp3Tyb, Dp4Tyb, Dp5Tyb, Dp6Tyb, and Dp9Tyb [7] (Figure 2). The numbers in brackets represent the number of protein-coding genes within each MMU16 region according to Ensembl release 87. Neu-associated kinase, Runx: runt-related transcription factor 1, Cbr: carbonyl reductase 1, Dscr: syndrome critical region gene 3, B3Galt: UDP-Gal:betaGlcNAc beta 1,3-galactosyltransferase, Down syndrome critical region gene 3, B3Galt: UDP-Gal:betaGlcNAc beta 1,3-galactosyltransferase, polypeptide 5, Mx2: MX dynamin-like GTPase 2, and Zbtb: zinc finger and BTB domain containing polypeptide 5, Mx2: MX dynamin-like GTPase 2, and Zbtb: zinc finger and BTB domain containing 21
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