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In this study, we found that loss of EVA1A could decrease neural differentiation in the brain of adult <jats:italic>Eva1a<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice. To determine the mechanism underlying this phenotype, we performed label\u2010free quantitative proteomics and bioinformatics analysis using the brains of <jats:italic>Eva1a<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and wild\u2010type mice. We identified 11 proteins that were up\u2010regulated and 17 that were down\u2010regulated in the brains of the knockout mice compared to the wild\u2010type 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\u00a0diseases, such as Alzheimer's disease and Huntington's disease, were strongly associated with <jats:italic>Eva1a<\/jats:italic> 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 <jats:italic>Eva1a<\/jats:italic> knockout mice. Our study provides valuable information on the molecular functions and regulatory network of the <jats:italic>Eva1a<\/jats:italic> gene, as well as new perspectives on the relationship between autography\u2010related proteins and neural differentiation.<\/jats:p>","DOI":"10.1002\/pmic.201600294","type":"journal-article","created":{"date-parts":[[2017,1,3]],"date-time":"2017-01-03T00:02:46Z","timestamp":1483401766000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Quantitative proteomics reveals EVA1A\u2010related proteins involved in neuronal differentiation"],"prefix":"10.1002","volume":"17","author":[{"given":"Lijun","family":"Zhong","sequence":"first","affiliation":[{"name":"Medical and Health Analytical Center Peking University Health Science Center  Beijing P.\u00a0R. 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