Copyright
©The Author(s) 2021.
World J Psychiatr. Nov 19, 2021; 11(11): 1075-1094
Published online Nov 19, 2021. doi: 10.5498/wjp.v11.i11.1075
Published online Nov 19, 2021. doi: 10.5498/wjp.v11.i11.1075
Figure 5 ERVWE1 reduced NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2) expression by suppressing cytoplasmic polyadenylation element-binding protein 1 (CPEB1).
A: The mRNA levels of NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2) after overexpression of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in SH-SY5Y cells using quantitative polymerase chain reaction (qPCR); B: Western blots of NDUFV2 and GAPDH in SH-SY5Y cells; C: Represent the mRNA levels of NDUFV2 in SH-SY5Y cells after co-transfection with ERVWE1 and CPEB1 using qPCR; D: Western blots of ERVWE1, CPEB1, NDUFV2, and GAPDH in SH-SY5Y cells. Each bar represents the mean ± SD of three independent experiments. aP < 0.05; bP < 0.01; NS: Not significant.
- Citation: Xia YR, Wei XC, Li WS, Yan QJ, Wu XL, Yao W, Li XH, Zhu F. CPEB1, a novel risk gene in recent-onset schizophrenia, contributes to mitochondrial complex I defect caused by a defective provirus ERVWE1. World J Psychiatr 2021; 11(11): 1075-1094
- URL: https://www.wjgnet.com/2220-3206/full/v11/i11/1075.htm
- DOI: https://dx.doi.org/10.5498/wjp.v11.i11.1075