NDUFS1

Last update 08 May 2025

Basic Info

Synonyms

CI-75k, CI-75kD, Complex I-75kD

+ [3]

Introduction

Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) which catalyzes electron transfer from NADH through the respiratory chain, using ubiquinone as an electron acceptor (PubMed:30879903, PubMed:31557978). Essential for catalysing the entry and efficient transfer of electrons within complex I (PubMed:31557978). Plays a key role in the assembly and stability of complex I and participates in the association of complex I with ubiquinol-cytochrome reductase complex (Complex III) to form supercomplexes (PubMed:30879903, PubMed:31557978).

100 Clinical Results associated with NDUFS1

100 Translational Medicine associated with NDUFS1

0 Patents (Medical) associated with NDUFS1

165

Literatures (Medical) associated with NDUFS1

01 Jun 2025·Toxicology

Bioinformatics identification of shared signaling pathways and core targets linking Benzo[a]pyrene exposure to HCC progression

Article

Author: Tang, Meng ; Liu, Guo-Yang ; Jiang, Li-He ; Li, Yong-Le ; Lan, Jing-Yi ; He, Rong

With the increasing prevalence of environmental pollutants, there is growing concern about the potential effects of these substances in major diseases such as liver cancer. Previous studies have suggested that various chemicals, such as benzo[a]pyrene(BaP), produced by burning carbon containing fuels, may negatively affect liver health, but the exact mechanisms remain unclear. This study aimed to explore the potential molecular mechanisms of BaP in the progression of liver cancer. Through an exhaustive study of databases such as ChEMBL, SwissTargetPrediction, STITCH and TCGA, we identified 169 potential targets that are closely related to BaP and liver cancer. Next, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses using the clusterProfiler package to study the biological functions and important pathways of potential targets induced by BaP, which showed that these targets were associated with mitochondrial function, cellular energy metabolism and REDOX reactions. The protein interaction (PPI) network was constructed using the STRING database and Cytoscape software to identify the core targets UBA52, NDUFS8, CYP1A2, NDUFS1 and CYP3A4. The interaction between BaP and these core proteins was further analyzed via molecular docking using the CB-Dock2 database, demonstrating high binding stability, which suggests their critical role in BaP-induced hepatocellular carcinoma (HCC) toxicity. Subsequently, we found significant differences in the expression of five core genes (UBA52, NDUFS8, CYP1A2, NDUFS1, CYP3A4) in HCC, and significant correlation between UBA52, NDUFS8 and CYP3A4 and survival of HCC patients. Single-cell sequencing analysis showed that the expression of UBA52 gene was particularly pronounced in the three immune cells.

01 Apr 2025·Journal of Orthopaedic Research

A Novel Disulfidptosis‐Related Risk Signature for Prognostic Prediction in Patients With Ewing Sarcoma

Article

Author: Che, Chunqing ; Song, Delei ; Yin, Xuqing ; Xue, Peng

ABSTRACTEwing sarcoma (ES) is a malignant bone tumor prevalent among children and adolescents. Disulfidptosis represents a novel form of cell death; however, the mechanism of disulfidptosis in ES remains unclear. Our aim is to explore the disulfidptosis‐related prognostic signature in ES. Utilizing transcriptomic and clinical data of ES, disulfidptosis‐related hub genes (DRHGs) were identified by differential gene expression analysis and Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression analysis. A disulfidptosis‐related risk score model (DRRS) was constructed based on these DRHGs. The performance of DRRS was assessed using survival analysis and receiver operating characteristic curve analysis. Immune cell infiltration in different risk subgroups and correlations between DRRS and antitumor reagents were also analyzed. In this study, we developed a disulfidptosis‐related prognostic feature based on LRPPRC (leucine rich pentatricopeptide repeat containing), IQGAP1 (IQ motif containing GTPase activating protein 1), NDUFS1 (NADH:ubiquinone oxidoreductase core subunit S1), and TLN1 (talin 1), which may serve as a predictive and independent risk factor for ES. ES patients in the high‐risk group exhibited a poorer prognosis, had a higher proportion of myeloid‐derived suppressor cells (MDSCs) and M2 type of tumor‐associated macrophages, and showed heightened sensitivity to some antitumor agents such as nilotinib and olaparib. This study is the first to construct a disulfidptosis‐related prognostic signature that may predict the prognosis and immune response in ES patients, thereby providing a new reference for understanding the mechanisms of ES and guiding immunotherapy.

01 Apr 2025·Journal of Hazardous Materials

F-53B disrupts energy metabolism by inhibiting the V-ATPase-AMPK axis in neuronal cells

Article

Author: Zhang, Yue ; Ding, Xueman ; Zhang, Jingjing ; Ma, Runjiang ; Qin, Wenqi ; Niu, Qiang ; Yan, Chulin ; Keerman, Mulatibieke ; Li, Tingting ; Wang, Chun ; Liu, Li

6:2 chloro-polyfluorooctane ether sulfonate (F-53B) is considered neurotoxic, but its mechanisms remain unclear. This study aimed to investigate the toxic effects of F-53B on neuronal cells, focusing on the role of the V-ATPase-AMPK axis in the mechanism of abnormal energy metabolism. Mouse astrocytes (C8-D1A) and human neuroblastoma cells (SH-SY5Y) exposed to F-53B were used as in vitro models. Our findings demonstrated that F-53B inhibited the expression of V-ATPase B2 and reduced V-ATPase activity, leading to an increase in lysosomal pH, decreased expression of TRPML1, and lysosomal Ca^2 + accumulation. In turn, led to reduced the expression of CaMKK2 and phosphorylated AMPK (p-AMPK). Ultimately, mitochondria were damaged, evidenced by increased mitochondrial reactive oxygen species, mitochondrial membrane potential, and impaired mitochondrial oxidative phosphorylation, as shown by reduced NDUFS1 expression and diminished respiratory chain complex I activity. F-53B reduced the expression of the key glycolytic protein PFKFB3. Notably, V-ATPase B2 overexpression indirectly activates AMPK. Furthermore, resveratrol, an AMPK agonist, alleviates mitochondrial dysfunction and increases ATP production by promoting the recovery of mitochondria and glycolytic pathways. These findings elucidate a novel mechanism by which F-53B induces neurotoxicity through the V-ATPase-AMPK axis, and indicate V-ATPase and AMPK as potential therapeutic targets.

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