NDUFB7

Last update 08 May 2025

Basic Info

Synonyms

B18, Cell adhesion protein SQM1, CI-B18

+ [6]

Introduction

Accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), that is believed not to be involved in catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone.

100 Clinical Results associated with NDUFB7

100 Translational Medicine associated with NDUFB7

0 Patents (Medical) associated with NDUFB7

Literatures (Medical) associated with NDUFB7

01 Mar 2025·Anti-Cancer Drugs

Research on the mechanism of eugenol in the treatment of liver cancer based on network pharmacology, molecular docking technology, and in vitro experiments

Article

Author: Liu, Kaiping ; Zhu, Haitao ; Wang, Min ; Wang, Yunhao ; Jiang, Jiuliang ; Yu, Zhenyu

Eugenol, a phenolic natural product with diverse pharmacological activities, remains unexplored in liver cancer. Using network pharmacology, we investigated eugenol’s therapeutic mechanisms in liver cancer. We obtained eugenol’s molecular structure from PubChem and screened its targets using similarity ensemble approach in Swiss Target Predictiondatabases. Overlapping genes with liver cancer-related genes from GeneCards were identified. Protein–protein interaction networks, Gene Ontology annotations, and Kyoto Encyclopedia of Genes and Genomes pathway analyses were conducted. A target-pathway network revealed eugenol’s interaction with 122 liver cancer-related genes. Molecular docking confirmed eugenol’s high affinity for mitochondrial nicotinamide adenine dinucleotide, reduced form (NADH) dehydrogenase 1 (MT-ND1), AKT1, NDUFB7, and NADH dehydrogenase (complex I) subunit S3 (NDUFS3). Expression levels of these targets in normal liver and liver cancer tissues were examined using GEPIA2 and HPA databases. The CCK-8 assay and colony formation assay demonstrated that eugenol significantly inhibited the proliferation of hepatocellular carcinoma cells. Western blot analysis confirmed that eugenol upregulated MT-ND1 while downregulating the expression of targets such as AKT1, NDUFB7, and NDUFS3. Furthermore, it was found that eugenol could influence the expression of the AKT1 target through the AKT/p70 S6K pathway. This study provides new insights into the potential mechanisms of eugenol in liver cancer and offers novel perspectives for network-based liver cancer research.

01 Mar 2025·International Journal of Biological Macromolecules

Identification and validation of Atp5f1c in CD4+ T cell as a hub protein in Parkinson's disease

Article

Author: Tang, Xianjin ; Zhang, Feng ; Wang, Guoqing ; Li, Daidi ; Zhao, Yujia ; Wang, Yuanyuan

Parkinson's disease (PD) is an age-related and progressive neurodegenerative disease. Growing evidences indicate that CD4⁺ T cell dysfunction plays an essential role in the progress of PD. Here, in LPS-induced PD mice, we isolated midbrain CD4⁺ T cell and peripheral CD4⁺ T cell to perform proteomics, and then screened a total of 167 co-expression proteins via integrated bioinformatics analysis. In addition, the subcellular localization, GO analysis, KEGG pathways and protein-protein interaction of 167 co-expression proteins were assessed. Furthermore, GeneMANIA searched the hub proteins and their co-expression genes and found 13 overlapping hub proteins, including Ndufa3, Cox5b, Mrpl21, Ndufab1, Idh3g, Ndufb7, Cyc1, Cisd1, Atp5f1c, Sdhc, Ndufb9, Mtnd1 and Mrpl17. Next, GO analysis and KEGG analysis of the 13 overlapping hub proteins were also exhibited. Further analysis identified that 4 hub proteins (Idh3g, Cisd1, Atp5f1c and Mtnd1) were downregulated both in midbrain and peripheral CD4⁺ T cell from proteomics. Identification and rescue experiment analysis showed that only Atp5f1c was decreased in LPS- and 6-OHDA-induced PD mice and dopamine (DA) neuronal loss and ATP production decrease were disappeared after Atp5f1c over-expression/Atp5f1c reinfusion both in vivo and in vitro. In conclusion, Atp5f1c was verified as a potential CD4⁺ T cell-related hub protein for PD.

01 Aug 2024·Heliyon

MicroRNA-2861 regulates the proliferation and apoptosis of human retinal vascular endothelial cells treated with high glucose by targeting NDUFB7

Article

Author: Shi, Qiqin ; Liu, Zhuoran ; Wang, Ruobing ; Mao, Ke ; Wang, Qiangsheng

ObjectivesAlthough anti-VEGF and retinal laser photocoagulation are two therapeutic modalities that have been used in the clinical treatment of diabetic retinopathy (DR), it is unknown how these modalities target vascular endothelial function in DR.MethodsWe first downloaded and analyzed the differential genes in two DR-related datasets, GSE60436 and GSE53257. The differential gene expression was then verified using RT-qPCR, and the most upregulated gene, NDUFB7, was selected for subsequent experiments. Subsequently, the role of NDUFB7 silencing and enforced expression on the proliferation and apoptosis of HRVECs was explored using CCK-8 assay, EDU proliferation assay and apoptotic TUNEL staining. In addition, the upstream potential miRNAs of NDUFB7 were predicted online using the Targetscan website. RT-qPCR, Western blotting (WB), and dual luciferase gene reporter assay were used to confirm the targeting connection between miR-2861 and NDUFB7. Finally, miR-2861 expression after high glucose (HG) treatment and its effect on proliferation and apoptosis of HRVECs under HG were investigated.ResultsIn this study, we first downloaded and analyzed the differential genes in two DR-related datasets, GSE60436 and GSE53257. We found that TUFM, PRELID1, MRPL32, NDUFB7, MRPL4, MRPL40, HSD17B10 and SLC25A13 were upregulated in DR, and RT-qPCR showed that NDUFB7 was most upregulated. Subsequent CCK-8 assay, EDU proliferation assay and TUNEL staining showed that up-picked NDUFB7 promotes proliferation and inhibits apoptosis of HRVECs. In addition, the upstream potential miRNAs of NDUFB7 were predicted online using the Targetscan website. RT-qPCR, Western blotting (WB), and dual luciferase gene reporter assay confirmed the targeting connection between miR-2861 and NDUFB7. Finally, it was observed that miR-2861 can inhibit the proliferation and promote the apoptosis of HRVECs by targeting NDUFB7.ConclusionsOur findings showed that upregulated NDUFB7 in DR promotes proliferation and inhibits apoptosis of HRVECs, and miR-2861 can rescue the pathogenic effect of NDUFB7 upregulation by targeting NDUFB7.

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NDUFB7

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