title: Quantitative proteomics reveals EVA1A-related proteins involved in neuronal differentiation.
abstract: EVA1A is an autophagy-related protein, which plays an important role in embryonic neurogenesis. In this study, we found that loss of EVA1A could decrease neural differentiation in the brain of adult Eva1a-/-mice. To determine the mechanism underlying this phenotype, we performed label-free quantitative proteomics and bioinformatics analysis using the brains of Eva1a-/-and wild-type mice. We identified 11 proteins that were up-regulated and 17 that were down-regulated in the brains of the knockout mice compared to the wild-type counterparts. Bioinformatics analysis indicated that biological processes, including ATP synthesis, oxidative phosphorylation, and the TCA cycle, are involved in the EVA1A regulatory network. In addition, gene set enrichment analysis showed that neurodegenerative diseases, such as Alzheimer's disease and Huntington's disease, were strongly associated with Eva1a knockout. Western blot experiments showed changes in the expression of nicotinamide nucleotide transhydrogenase, an important mitochondrial enzyme involved in the TCA cycle, in the brains of Eva1a knockout mice. Our study provides valuable information on the molecular functions and regulatory network of the Eva1a gene, as well as new perspectives on the relationship between autography-related proteins and neural differentiation.
authors.affiliation: Medical and Health Analytical Center, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Zhong
authors.affiliation: Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Juntuo
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Medical and Health Analytical Center, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Xi
authors.initials: X
authors.lastname: Chen
authors.affiliation: Medical and Health Analytical Center, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Jiao
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, P. R. China.|Peking University Center for Human Disease Genomics, Beijing, P. R. China.
authors.forename: Yingyu
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, P. R. China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Bai
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D015153:Blotting, Western; D001921:Brain / Q000378:metabolism; D002454:Cell Differentiation / Q000235:genetics*; D063990:Gene Ontology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D024101:Mitochondrial Proteins / Q000378:metabolism; D061087:NADP Transhydrogenase, AB-Specific / Q000378:metabolism; D009474:Neurons / Q000166:cytology* / Q000502:physiology; D009713:Nucleotidyltransferases / Q000378:metabolism; D060066:Protein Interaction Maps; D040901:Proteomics / Q000379:methods
chemical_list: D051017:Apoptosis Regulatory Proteins; C000623320:Eva1a protein, mouse; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D061087:NADP Transhydrogenase, AB-Specific; C556048:Nnt protein, mouse; D009713:Nucleotidyltransferases; C000623321:Ugp2 protein, mouse
keywords: Bioinformatics; Eva1a; Neuronal differentiation; Quantitative proteomics