Ask about this productRelated genes to: PSMD12 Blocking Peptide
- Gene:
- PSMD12 NIH gene
- Name:
- proteasome 26S subunit, non-ATPase 12
- Previous symbol:
- -
- Synonyms:
- p55, Rpn5
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-19
- Date modifiied:
- 2016-10-05
Related products to: PSMD12 Blocking Peptide
Related articles to: PSMD12 Blocking Peptide
- To explore the clinical characteristics and genetic etiology of STISS syndrome (an autosomal dominant disorder characterized by ubiquitin-proteasome system dysfunction) in a child. - Source: PubMed
Peng DelongHan ChunxiaoYan LuLuLi HaiboYan Haiya - To explore genetic investigative results in fetuses with isolated horseshoe kidney (HSK). - Source: PubMed
Publication date: 2026/02/16
Yu Qiu-XiaNi Yu-TongZhang Yong-LingXiao Zhi-QingLi Si-YunJiang FanLi Dong-Zhi - The mechanisms underlying carfilzomib (CFZ)-induced cardiotoxicity remain incompletely elucidated. In this study, we used human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to characterize the transcriptional impact of CFZ and to evaluate whether atorvastatin could prevent these deleterious transcriptional changes. hiPSC-CMs were treated with 1 µM CFZ, CFZ + atorvastatin, atorvastatin, or vehicle control, followed by RNA sequencing, differential expression analyses, and pathway analyses. Transcriptomic profiling revealed a marked upregulation of genes in multiple proteasome subunits, including ATPase components (, , , ) and non-ATPase regulatory subunits (, , ), suggesting a strong compensatory activation of proteostasis and protein quality-control pathways in response to CFZ exposure. In addition, several of the most significantly altered genes were those implicated in cardiomyopathy and heart failure, such as and , and many heat-shock proteins, indicating the activation of cardiac stress-response pathways relevant to CFZ-associated cardiotoxicity. Atorvastatin co-treatment partially reversed a subset of CFZ-induced transcriptional changes, particularly within cholesterol biosynthesis and lipid-regulatory pathways (e.g., and ) but did not restore the CFZ-mediated downregulation of sarcomeric genes. Together, these findings define a multifactorial signature of deleterious CFZ-induced transcriptional changes and suggest that atorvastatin may provide partial metabolic, but not structural, cardio protection. - Source: PubMed
Publication date: 2026/01/29
Tantawy MarwaWang DanxinGbadamosi MohammedYu FahongZhang YanpingAlomar Mohammed EShain Kenneth HBaz Rachid CBruno Katelyn AGong Yan - Lung adenocarcinoma (LUAD) is one of the most common cancers and a leading cause of cancer-related mortality worldwide, highlighting the need for novel therapeutic strategies. Proteasome 26S Subunit, Non-ATPase 12 (PSMD12), a component of the proteasomal 19S regulatory particle, is associated with tumorigenesis; however, its role in LUAD remains poorly understood. Integrative bioinformatic analysis of The Cancer Genome Atlas (TCGA) and other publicly available LUAD datasets identified PSMD12 as a candidate driver gene on chromosome 17q, a region frequently amplified in LUAD. Clinicopathological and prognostic analyses revealed that PSMD12 was significantly upregulated in tumor tissues because of DNA copy number gain. High PSMD12 expression was associated with poor prognosis and advanced pathological stages. Gene set enrichment analysis of TCGA LUAD dataset demonstrated that samples with high PSMD12 expression were enriched for cell cycle-related pathways. Using CRISPR-Cas9-mediated PSMD12 knockout and lentivirus-mediated overexpression models, we demonstrated that PSMD12 promoted tumor cell proliferation by accelerating the G2/M cell cycle transition in vitro, and xenograft experiments confirmed its tumor-promoting effect in vivo. Mechanistically, PSMD12 overexpression reduced the ubiquitination of CDK1, a key regulator of mitotic entry. Cycloheximide chase and MG132 assays confirmed that PSMD12 stabilized CDK1 by inhibiting proteasome-mediated degradation. In conclusion, we identified PSMD12 as a novel driver gene and prognostic biomarker of LUAD. PSMD12 promoted LUAD progression by modulating CDK1 ubiquitination and enhancing cell cycle progression. These findings suggest that PSMD12 is a promising molecular target for future LUAD therapies. - Source: PubMed
Publication date: 2026/01/06
Ono YuyaOtsu HajimeMasuda TakaakiKosai KeisukeShibuta ShoheiHirose KosukeOfuchi TakashiAndo YukiKawata KotoTsuda YasuoYonemura YusukeTobo TaroTakenaka TomoyoshiYoshizumi TomoharuMimori Koshi - Neddylation modifications in immune and tumor cells are linked to poor tumor prognosis. This study identifies prognostic genes associated with neddylation-related genes (NRGs) in colorectal cancer (CRC) using single-cell and spatial transcriptome (ST) sequencing, aiming to advance CRC treatment strategies. - Source: PubMed
Publication date: 2025/12/24
Zhu ZimingZhang XinyueWang SongHuang YunsiHan XuedongLai DongpingYao XinLan WeixuanNong HuiZeng WenbinMo YanhuaXu Ri'anZhang Tao