Ask about this productRelated genes to: Psmd10 Blocking Peptide
- Gene:
- PSMD10 NIH gene
- Name:
- proteasome 26S subunit, non-ATPase 10
- Previous symbol:
- -
- Synonyms:
- p28
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-19
- Date modifiied:
- 2015-09-07
Related products to: Psmd10 Blocking Peptide
Related articles to: Psmd10 Blocking Peptide
- Gankyrin (PSMD10) is a 25 kDa oncogenic protein and regulatory subunit of the 26S proteasome, characterized by a sevenfold ankyrin repeat domain. Gankyrin is overexpressed in various malignancies, particularly gastrointestinal (GI) cancers. Gankyrin contributes to tumorigenesis by modulating key signaling pathways and engaging in oncogenic protein-protein interactions with tumor suppressors, including p53 and Rb, thereby promoting cell proliferation, metastasis, and resistance to treatment. Recent advances have shed light on the structural basis of gankyrin's molecular interactions, its potential as a diagnostic and prognostic biomarker, and emerging therapeutic strategies. Together, targeting gankyrin represents a promising strategy for precision oncology in GI cancers. - Source: PubMed
Publication date: 2025/10/15
Li ShuangLam YukyMuth AaronChen Zhe-ShengWang Shanzhi - As synthetic biology advances toward precise design, the construction of high-quality mutant libraries has become essential for large-scale functional screening. Traditional approaches, such as random and saturation mutagenesis, often suffer from low accuracy, high bias, and limited coverage. An ideal method should offer controlled mutagenesis, comprehensive coverage, high throughput, operational simplicity, and controllable outcomes, enabling effective large-scale screening. Here, we developed a high-throughput, precisely controlled method for constructing a mutagenesis library based on chip-based oligonucleotide synthesis. Using as a model, we constructed a full-length amber codon scanning mutagenesis library with 93.75% mutation coverage. Among the five polymerases evaluated, KAPA HiFi HotStart, Platinum SuperFi II and Hot-Start Pfu DNA Polymerase demonstrated higher amplification efficiency and lower chimera formation rates, making them preferred enzymes for optimized library construction. Analysis of unmapped reads highlighted key technical factors, such as oligonucleotide synthesis errors and chimeric sequence formation caused by incomplete extension of DNA polymerase or synthesis across discontinuous templates during PCR. To improve efficiency and fidelity, we recommend refining PCR conditions and strengthening oligo synthesis quality control. We establish an efficient, scalable, precisely controlled mutagenesis library construction strategy tailored for high-throughput functional research and recommend using a high-fidelity, low-bias polymerase to ensure quality. - Source: PubMed
Publication date: 2025/10/25
Lu YuxinMeng ShutingGuan XinyiHe PengyingZhao Dongxin - Epstein-Barr Virus (EBV), a potent viral carcinogen, plays a crucial role in the development of various malignancies. Among its proteins, EBV nuclear antigen-1 (EBNA1) stands out for its ability to modulate gene expression. In this study, we explored the impact of EBNA1 on the expression patterns of four cellular genes-Derlin1, ZEB1, CNN3, and PSMD10-in HeLa cells. - Source: PubMed
Publication date: 2025/08/06
Alipour Amir HosseinHashemi Seyed Mohammad AliGharahkhani FatemehKatanchi AlirezaFarhadi AliSarvari Jamal - Hepatocellular carcinoma (HCC) is the predominant type of liver cancer with a poor prognosis. Treatment methods include surgery, ablation, liver transplantation, and immunotherapy. Programmed cell death (PCD) plays a significant role in the occurrence and treatment of HCC, and disulfidoptosis, as a novel type of PCD, is associated with tumor prognosis and anti-tumor immunity. The purpose of this study is to explore the role and molecular mechanisms of disulfidoptosis-related genes (DRGs) in the occurrence and development of HCC. - Source: PubMed
Publication date: 2025/07/22
Zhang RongzhengZhou KunWu MengQiao HanYu LeJin XiLi JingboDong GuangluZhang Shuyun - This study explores the therapeutic potential of Retinoid analogs to overcome this resistance by modulating autophagy and lysosomal activity in breast cancer. Comprehensive bioinformatics analyses such as gene correlation, mutation, co-expression, and functional network analysis revealed a strong correlation between RARα, NRF2, Gankyrin, p110α, and p110β, alongside the PI3K/Akt/mTOR axis in regulating autophagy. Given its upstream role, RARα was identified as the primary target, with NRF2, Gankyrin, p110α, and p110β serving as co-target macromolecules to influence downstream autophagy pathways. Molecular docking analyses identified six RAR agonists-CD437, BMS961, CD437-C, Adapalene, Adapalene-d, and CD1530-as promising candidates, all exhibiting high-profile binding affinities with all 5 target proteins RARα (< -10 kcal/mol), NRF2 (< -7.6 kcal/mol), Gankyrin (< -7.4 kcal/mol), p110α (< -8.9 kcal/mol), and p110β (< -8.6 kcal/mol). Among all, Adapalene (a synthetic Retinoid analog) was selected as a potent multi-target drug based on average docking score. Further, molecular dynamics simulation studies demonstrated enhanced protein stability with notable binding free energies of -82.712 kJ/mol (Gankyrin) and -25.526 kJ/mol (p110α). Subsequent in vitro validation using MCF7 and MDA-MB-468 breast cancer cell lines corroborated the computational findings. Adapalene markedly inhibited autophagy by downregulating the proteomic conversion of the core autophagy marker LC3B-I/LC3B-II, with reductions of up to 2.99-fold in MCF7 and 1.11-fold in MDA-MB-468 cell lines. In addition, it suppressed lysosomal activity by 2.73-fold in MCF7 and 2.52-fold in MDA-MB-468, as demonstrated by lysotracker assays. These findings underscore the potential of Adapalene as a multi-targeted modulator of RARα-PI3K signaling, effectively disrupting autophagy and cancer cell survival mechanisms in luminal and triple-negative breast cancer cells. - Source: PubMed
Publication date: 2025/06/26
Khanra Pijush KantiKandasamy ThirukumaranGhosh Siddhartha Sankar