NDUFS1 (NADH:Ubiquinone Oxidoreductase Core Subunit S1)

Conclusion The TCGA-BRCA cohort analysis emphasizes a potential interplay of metabolic genes like NDUFS1, TRPM4, ARMCX5, SLCO6A1, and epigenetic axis genes like SETDB1 and USP37 in the oncogenesis and prognosis of breast carcinomas. These observations could open potential avenues for exploring novel therapeutics in aggressive breast carcinomas.

These findings unveil a new germline-driven mechanism of complex I loss and metabolic reprogramming in cancer, and provide further evidence of the strong selective pressure for complex I impairment in OCT. Germline mutations in complex I induce aerobic glycolysis in oncocytic carcinoma of the thyroid through somatic loss of heterozygosity.

Our study identifies OXSM as a key DRG hub gene in glioma, with elevated expression strongly correlating with poor patient prognosis. The observed relationship between OXSM expression and immune cell infiltration suggests its potential role in modulating the glioma microenvironment. These findings advance our understanding of glioma's molecular mechanisms and may inform the development of novel therapeutic strategies.

Finally, disruption of ETC supercomplexes with the small molecule drug MitoTam increased the therapeutic efficacy of mtROS inducing chemotherapeutics in both C92D Ndufs1-knockin or metastatic lung cancer cells. These findings provide new insights into how the ETC can initiate supercomplex transformation.

This study uncovered a strong association between disulfidptosis and CC and developed a predictive model to assess the risk in CC patients. These findings offer novel insights into identifying biomarkers and potential therapeutic targets for CC, paving the way for improved diagnostic and treatment strategies.

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.

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.

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.

These mutations are rs267606829 (FOXRED1), COSV53860306 (HK1), rs201634181 (NDUFS1), rs774052186 (DONSON), rs119103242 (PC), rs1436643226 (PC), and rs104894677 (ETFB). They could be further investigated as potential biomarkers for diagnosis, prognosis, and treatment of BC patients.

RuCN/N-CDs either induce overexpression of the β-sheet-rich protein NDUFS1 and affect its random coil structure or interact and stabilise its structure via hydrogen bonding between -NH2 groups from N-CDs with protein C=O groups and -OH groups of serine, threonine, and tyrosine residues. The N-CD nanocarrier tunes this drug's action by directing it toward a specific protein target, changing this drug's coordination ability and inducing changes in the protein's secondary structures and function.

This study underscores the significant role of DRGs in various biological processes within DLBCL. Assessing the risk scores of individual DRGs allows for more precise stratification of prognosis and treatment strategies for DLBCL patients, thereby enhancing the effectiveness of clinical practice.

CLDN8 is downregulated in KIRC and is considered a potential tumor suppressor. CLDN8 deficiency may promote the initiation and progression of KIRC, potentially in conjunction with metabolic dysfunction.