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.
Keywords: Bioinformatics; Eva1a; Neuronal differentiation; Quantitative proteomics.
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