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 6 ERVWE1 contributed to complex I deficits through the cytoplasmic polyadenylation element-binding protein 1 (CPEB1)/ NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2) pseudogene (NDUFV2P1)/NDUFV2 signaling pathway.
A: Complex I activity in SH-SY5Y cells transfected with pCMV-ERVWE1 or control; B: Complex I activity in SH-SY5Y cells co-transfected with pCMV-ERVWE1 + shNDUFV2P1 or control; C: Complex I activity in SH-SY5Y cells co-transfected with pCMV-ERVWE1 + pcDNA3.1-CPEB1 or control. Each bar represents the mean ± SD of three independent experiments. aP < 0.05.
- 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