Ask about this productRelated genes to: NDUFB5 Blocking Peptide
- Gene:
- NDUFB5 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase subunit B5
- Previous symbol:
- -
- Synonyms:
- SGDH, CI-SGDH, MGC12314
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-09
- Date modifiied:
- 2016-10-05
Related products to: NDUFB5 Blocking Peptide
Related articles to: NDUFB5 Blocking Peptide
- Therapeutic resistance is a major cause of treatment failure in glioblastoma (GBM), highlighting the need for physiologically relevant models to identify actionable resistance mechanisms. While two-dimensional (2D) cultures are widely used for target discovery, they poorly represent the tumor microenvironment. In contrast, three-dimensional (3D) spheroid cultures better recapitulate spatial heterogeneity, hypoxic gradients, and stress-adaptive signaling observed in tumors. - Source: PubMed
Khotchawan WannawatRuengket PakornKheolamai PakpoomSathornsumetee SithSinthuvanich ChomdaoLorthongpanich ChanchaoIssaragrisil Surapol - Given the unclear pathogenesis and insidious progression of Alzheimer's disease (AD), the aim of the present study was to identify reliable diagnostic markers for AD detection using a combination of bioinformatics analysis, animal experiments and clinical patient validation. Gene expression profiles were retrieved from the GSE95587 dataset. Weighted gene co‑expression network analysis combined with four machine learning algorithms identified two signature genes: Serine/Arginine Rich Splicing Factor 1 (SRSF1) and NADH: Ubiquinone oxidoreductase subunit B5 (NDUFB5), and a diagnostic model with moderate efficiency in differentiating AD was established. The AD diagnostic signature genes (SRSF1 and NDUFB5) were associated with specific immune cell infiltration. SRSF1 was significantly enriched in the p38MAPK and AKT1/mTOR signalling pathways. Notably, in an Aβ‑induced mouse model, SRSF1 expression was upregulated in the hippocampus and cerebral cortex. Moreover, in patients with AD, SRSF1 mRNA levels in peripheral blood mononuclear cells showed a strong negative correlation with mini‑mental state examination and Montreal cognitive assessment scores and a positive correlation with clinical dementia rating scores, indicating a notable association between elevated SRSF1 expression and cognitive decline. Furthermore, SRSF1 levels were positively associated with plasma levels of p‑tau217, p‑tau181 and glial fibrillary acidic protein. These findings underscore the strong association between SRSF1 and AD pathology. The newly identified genes, particularly SRSF1, show potential as candidate biomarkers of AD progression and may provide insights into AD pathogenesis, but require further validation in a larger prospective cohort. - Source: PubMed
Publication date: 2026/04/17
Liu YanchenZhao YiYao YantingLiu DanSun YileiXu WeishiYu HongliChi Lijun - Intervertebral disc degeneration (IDD) is a common condition associated with aging and degeneration of the disc. Type 2 diabetes mellitus (T2DM) is linked to various musculoskeletal disorders, including IDD, but its molecular effects on IDD remain understudied. To explore the molecular differences in IDD between T2DM and non-T2DM patients, we conducted a quantitative proteomic analysis of nucleus pulposus (NP) tissues from patients with T2DM-IDD or non-T2DM-IDD individuals. We identified 3,720 proteins, with 221 significantly upregulated and 233 downregulated in T2DM-IDD. Multiple mitochondrial proteins were upregulated (NDUFV2, NDUFB5, NDUFA13, MPC2) indicating a potential increase in oxidative stress in the NP tissues from T2DM-IDD. Conversely, downregulated proteins such as versican (VCAN), an extracellular matrix proteoglycan, IL17B, a pro-inflammatory cytokine, and vascular endothelial growth factor A (VEGFA) indicate possible alterations in ECM composition and structure that impact the mechanical properties and integrity of the IVD as well as a reduced inflammatory response in NP tissues from non-T2DM-IDD. Additionally, T2DM-IDD showed enrichment in fatty acid metabolism pathways, while non-T2DM-IDD samples were enriched in epithelial mesenchymal transition and hypoxia pathways. Altogether, these results provide novel insights into the molecular mechanisms of T2DM-IDD and may guide future therapies. - Source: PubMed
Publication date: 2026/03/26
Moinuddin F MZhong JunAstudillo Potes Maria DDominari AsiminaDhar AshisPandey AkhileshBydon Mohamad - Alzheimer's disease (AD) is a neurodegenerative disorder marked by cognitive decline, memory impairment, and functional deterioration. Its complex pathogenesis involves factors such as amyloid plaques, tau tangles, neuroinflammation, and synaptic dysfunction, but the precise mechanisms remain unclear, hindering effective treatment. Genetic, environmental, and lifestyle factors contribute to AD risk, yet their interactions are poorly understood. Recent advances in transcriptomics and metabolomics have shed light on the molecular underpinnings of AD, with gene expression alterations and metabolic disruptions implicated in disease progression. These multi-omics disruptions highlight the need for integrative analytical approaches to better characterize AD-relevant biology and advance biomarker discovery. - Source: PubMed
Publication date: 2026/03/03
Choi Jerome JEngelman Corinne DLu Tianyuan - Alzheimer's disease (AD), a leading cause of dementia, is characterized by mitochondrial dysfunction, including impaired oxidative phosphorylation (OXPHOS), which drives neurodegeneration. This study aimed to identify OXPHOS-related AD biomarkers for early intervention. Integrated analysis of differentially expressed genes from AD temporal lobe and peripheral blood samples, using multivariate logistic regression and LASSO, identified ATP6V1E1 and NDUFB5 as key genes and potential AD risk factors. These genes exhibited strong diagnostic performance (AUC >0.7) and were validated in two independent cohorts. Further western blotting validation using an AD mouse model revealed that both genes were significantly downregulated in the hippocampus. Notably, their expression levels showed significant negative correlations with both Aβ and Tau pathology in AD mouse models. Single-cell RNA-seq analysis indicated their predominant expression in microglia, linking their expression to dysregulated immune cell infiltration. Furthermore, we observed a widespread downregulation of multiple mitochondrial complex I and V-ATPase subunits, indicating a systemic impairment in OXPHOS and lysosomal acidification in AD. This coordinated dysregulation underscores the synergistic dysfunction of mitochondrial and lysosomal systems in AD pathogenesis. This research highlights ATP6V1E1 and NDUFB5 as potential early AD indicators, and provides new insights into both the molecular mechanisms underlying AD pathogenesis and novel therapeutic strategies. - Source: PubMed
Publication date: 2025/11/14
Shao JunjieFan XiuzhaoTian ShuangshuangZhang FangLi JunhuZhao ZhiboLi YuanyuanZhou Xiaoshuang