Ask about this productRelated genes to: PSME3 Blocking Peptide
- Gene:
- PSME3 NIH gene
- Name:
- proteasome activator subunit 3
- Previous symbol:
- -
- Synonyms:
- Ki, PA28-gamma, REG-GAMMA, PA28G
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-04
- Date modifiied:
- 2016-01-15
Related products to: PSME3 Blocking Peptide
Related articles to: PSME3 Blocking Peptide
- Gain or amplification of chromosome 1q (+1q) is a common genomic alteration occurring in the plasma cells in nearly 40% of multiple myeloma patients. Although it is associated with inferior outcomes and is more common in the relapsed or refractory stages, the impact of +1q at the proteomic level remains unclear. Here, we studied enriched CD138+ plasma cells in newly diagnosed multiple myeloma to uncover molecular alterations associated with +1q. Differential expression analysis revealed significantly increased expression of over 100 proteins encoded by the 1q region, indicating a potential gene dosage effect. Pathway enrichment analysis identified enrichment of cell cycle proteins such as CDK1, MCM complex, CHEK2, PSME3 and NEK7 in cases with +1q gain. Further, protein-protein interaction network analysis showed enrichment of MYC transcriptional targets in +1q cases, including increased expression of TIPRL that is encoded on 1q24. In agreement with these findings, increased TIPRL transcript expression was correlated with +1q across different cytogenetic subgroups in the CoMMpass dataset. Further, high TIPRL expression was associated with poor prognosis in patients from the hyperdiploidy subgroup. Overall, this study highlights the role of proteomics in understanding molecular events associated with chromosomal alterations in MM and identifying potential targets for further functional analysis. - Source: PubMed
Publication date: 2026/04/14
Mangalaparthi Kiran KHsu Joel-SeanWiedmeier-Nutor J ErinSen ParthoStaub JulieBhat Firdous AStein Caleb KAhmann Greg JKumar Shaji KRajkumar S VincentBergsagel P LeifFonseca RafaelBraggio EstebanKandasamy Richard KPandey Akhilesh - Sarcandra glabra (S. glabra) has been traditionally used to promote diuresis and reduce swelling, which is employed to treat facial and lower limb edema, one of the earliest and most visible external signs of chronic kidney disease (CKD). The alleviating effect of S. glabra on CKD and its mechanism remains unclear. - Source: PubMed
Publication date: 2026/02/10
Tang PengfeiZheng ZeYu MengmengZhang DanyangXiao ZhiqiKong LingyiLuo Jun - Porcine reproductive and respiratory syndrome virus (PRRSV) poses a significant threat to the global swine industry, employing complex mechanisms to interact with the host and evade host immune responses. The ubiquitin-proteasome system (UPS) is central to host antiviral innate immunity, yet its interplay with PRRSV remains poorly understood. In this study, Proteasome 20S Subunit Alpha 2 (PSMA2) was identified as a novel host restriction factor against highly pathogenic PRRSV (HP-PRRSV). Through overexpression and siRNA knockdown experiments, it was demonstrated that PSMA2 effectively inhibits PRRSV replication in a time- and dose-dependent manner, exerting antiviral effects during the mid-to-late post-entry stages of replication. Mechanistically, PSMA2 overexpression enhances overall cellular proteasome activity and specifically upregulates transcription of immunoproteasome activator subunits PSME1, PSME2, and PSME3. As a countermeasure, the PRRSV JXA1 strain induces the degradation of PSMA2 protein via the autophagy pathway, a process contingent on active viral replication. Further screening identified PRRSV nonstructural protein 12 (Nsp12) as a viral factor associated with the autophagy-dependent reduction of PSMA2. In parallel, PRRSV infection suppresses global proteasome activity, indicating that the virus adopts a two-pronged strategy to undermine this host defense pathway. These findings demonstrate that PRRSV hijacks autophagy machinery to eliminate a key proteasome-associated restriction factor. Collectively, our results highlight the intricate interplay between PRRSV and the host proteasome system and provide novel insights into viral pathogenesis. - Source: PubMed
Publication date: 2025/12/10
Li WeiYang DanjiaoWang RuiqingLan LanQiu XinxinWang Xinglong - Lung cancer remains a major cause of cancer-related death, highlighting the need for new molecular targets and novel therapeutics. Matrix metalloproteinases are key regulators of invasion and microenvironment remodeling, and among them, matrix metalloproteinase-12 (MMP12) is a particularly attractive candidate whose network-level effects in cancer are still poorly defined. Herein, we applied an integrative strategy that combines bioinformatics methods with experimental validation in non-small cell lung cancer (NSCLC) cells. Protein-protein interaction (PPI) and pathway analyses of MMP12-regulated genes identified 113 downstream targets enriched in the extracellular matrix, PI3K-AKT, and immune pathways, from which an eight-gene panel (MMP12, CD44, ADAM9, NFKBIA, PSME3, SPARCL1, CCL15, and APOA1) was prioritized as a biomarker signature. Guided by these predictions, we screened a 31-compound MMP12 inhibitor library and selected five leads (, , , , and ) for testing in H1299 cells, with showing the strongest antiproliferative activity. These compounds showed antimigratory activity ( achieving a 90% inhibition of wound closure at its IC concentration), reduced clonogenic growth, cell cycle perturbation, and induction of apoptosis. Gene- and protein-expression analyses confirmed MMP12 suppression and modulation of the eight-gene panel. Upstream regulator predictions implicated reduced AKT signaling alongside an ADAM9-centered adaptive axis. Collectively, these findings highlight , , , , and as promising MMP12 inhibitors, supporting their further development in preclinical lung cancer and nominating the eight-gene panel as a pharmacodynamic signature for MMP12-targeted therapies. - Source: PubMed
Publication date: 2025/12/06
Almutairi ShriefaHajjo RimaSabbah Dima ASweidan KamalRashid Zainab AhmedBardaweel Sanaa K - Regulatory T cells (Tregs) contribute to the immune escape of hepatocellular carcinoma (HCC). However, the drivers of the accelerated Treg accumulation in HCC remain unclear. In this study, Treg infiltration-related genes were analysed, and proteasome activator subunit 3 (PSME3) was identified as a pivotal driver using bioinformatics analysis. Functional experiments were performed to investigate the correlation between PSME3 expression and programmed cell death-1 (PD-1) monoclonal antibody therapy resistance in HCC. Elevated levels of PSME3 lead to metabolic reprogramming towards glycolysis and upregulation of osteopontin (OPN) expression. This glycolysis-induced OPN secretion by HCC cells promotes the differentiation and enrichment of Tregs while inhibiting CD8 T cells in vivo and in vitro. Mechanistically, PSME3 enhanced PTEN-FBXL7 binding and promoted PTEN degradation through FBXL7-mediated ubiquitination, thereby enhancing glycolysis. The combination of PSME3 inhibition and PD-1 blockade is a promising strategy for HCC treatment. In conclusion, our data showed the critical role played by PSME3 in triggering Treg infiltration and inducing anti-PD1 tolerance. - Source: PubMed
Publication date: 2025/10/15
Chen QiuyangLiang YuanLi YuLi XiangyuZhou JinrenXu XiaozhangShao QingQian QufeiHuang TianningSong ZiyanTakashi MaruyamaLin MinjieLu LingGu Jian