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To complement mitochondrial complex I analysis, we measured NDUFS7, NDUFS8, NDUFV1, and NDUFV2 gene expression using qRT-PCR.
Acai freeze-dried hydroalcoholic extract modulated NDUFS7, NDUFS8, and NDUFV2 protein expression differently, as shown in Figure 4.
We measured NDUFS7, NDUFS8, NDUFV1, and NDUFV2 protein and gene expression at SH-SY5Y cell after rotenone and/or acai treatments.
3B) NADH dehydrogenase (NDUFV2), peroxiredoxin 6 (PRDX6), and Cypl7[alpha] were also significantly down-regulated.
DEGs in module up-2, such as ATP5D, UQCRC2, NDUFA2, NDUFB8, NDUFA7, COX4I1, NDUFA1, NDUFB1, NDUFS7, UQCR11, NDUFV1, NDUFV2, and NDUFS3, were enriched in the pathways of oxidative phosphorylation (P=3.31E-13), Parkinson's disease (P=3.81E-13), Alzheimer's disease (P=3.25E-11), and Huntington's disease (P=7.35E-11; Table 3).
Based on functional and pathway enrichment analyses of two upregulated modules, the identified DEGs (ATP5D, UQCRC2, NDUFA2, NDUFB8, NDUFA7, NDUFA1, NDUFB1, NDUFS7, UQCR11, NDUFV1, NDUFV2, and NDUFS3) were mainly related to mitochondrial ATP synthesis coupled electron transport, the respiratory electron transport chain, and mitochondrial electron transport.
DEGs such as NDUFA2, NDUFB8, NDUFA7, NDUFA1, NDUFB1, NDUFS7, NDUFV1, NDUFV2, and NDUFS3 jointly encode subunits of nicotinamide adenine dinucleotide (NADH):ubiquinone oxidoreductase (complex I) (23).
A study of postmortem prefrontal and parieto-occipital cortices of MD patients revealed downregulated mRNA and protein levels of Complex I subunits (NDUFV1, NDUFV2, and NADUFS1) .
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