Ask about this productRelated genes to: MSA2 protein
- Gene:
- PSMA2 NIH gene
- Name:
- proteasome subunit alpha 2
- Previous symbol:
- -
- Synonyms:
- MU, HC3, PMSA2
- Chromosome:
- 7p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-03
- Date modifiied:
- 2016-10-05
Related products to: MSA2 protein
Related articles to: MSA2 protein
- Epilepsy, ischemic stroke, and depression, as common neurological diseases, pose a serious threat to human health. Although vagus nerve stimulation (VNS) has been applied in the treatment of these diseases, its exact mechanism of action remains unclear. This study aims to deeply analyze the relationships between the core target genes of VNS and epilepsy, ischemic stroke, and depression by integrating network pharmacology, bioinformatics, and Mendelian randomization. The results showed that, compared with the control group, 159 differentially expressed genes were identified in the VNS-treated group. These genes were involved in biological processes such as "protein-RNA complex organization" and are enriched in metabolism-related pathways such as the "AMPK signaling pathway." There were 73, 54, and 108 overlapping genes between VNS-related genes and genes related to epilepsy, ischemic stroke, and depression, respectively. Through network analysis and Mendelian randomization analysis, several core genes that may play a protective role in the corresponding diseases were identified, such as CPT1A, SUCLG1, IMMT, IVD, and PSMA2. This study has revealed the potential molecular mechanisms possibly involved in VNS treatment of these neurological diseases. The findings offer crucial clues for further in-depth study of VNS treatment mechanisms, and may boost the development of more precise and effective treatment strategies. - Source: PubMed
Yang XiaobingChen YeHuang TaoYang RongLiu QiangMan DulegeqiWang WeiZhang BijiangLuo BangweiZhang YangmingNiu BenLi Jinghui - 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 - Aberrant activation of the androgen receptor (AR) pathway drives prostate cancer (PCa). Androgen deprivation therapy (ADT) and next-generation AR blockade (e.g., enzalutamide) are initially effective, but virtually all patients develop castration-resistant prostate cancer (CRPC), which frequently transitions to treatment-emergent neuroendocrine PCa (tNEPC) following AR suppression. The molecular logic that links AR blockade to lineage plasticity remains incompletely understood. Here, we identify PSMA2 (Proteasome Subunit Alpha 2) as a treatment-induced effector that mechanistically connects AR blockade to tNEPC evolution. Enzalutamide induces PSMA2 expression in AR-expressing PCa cells. Enforced PSMA2 expression accelerates HSP90 turnover, hypersensitizes AR to residual post-castration androgen, drives AR nuclear activity under androgen-poor conditions, and confers enzalutamide resistance. Conversely, PSMA2 silencing stabilizes HSP90, desensitizes CRPC to androgen, and re-sensitizes resistant cells to enzalutamide-induced cell death. Importantly, PSMA2 also promotes lineage plasticity: treatment-induced PSMA2 enhances transcriptional and phenotypic conversion toward tNEPC. Thus, we uncover a single stress-induced node (PSMA2) that both maintains AR-dependent survival under ADT and fuels the neuroendocrine transition. PSMA2 marks an AR-hypersensitized transitional state and is itself a therapeutically actionable driver of tNEPC evolution, revealing an opportunity for rational interception of the lethal ADT-CRPC-tNEPC trajectory. - Source: PubMed
Publication date: 2025/11/29
Patterson NBadoi AVadla G PHasani MMoyer JDe la Nuez Ramirez CChabu Y C - Nasopharyngeal carcinoma (NPC), highly prevalent in southern China, often leads to treatment failure in advanced stages due to recurrence or metastasis. While METTL14 plays a crucial role in cancer, its regulation of immune- and inflammation-related genes remains poorly understood. This study aims to investigate whether METTL14 is involved in regulating the expression of genes associated with tumor necrosis factor (TNF), interferon (IFN), interleukin (IL), and MHC class I in NPC cells. - Source: PubMed
Zhou ZhihaoWang JingShen LingjunHan LiuxinLi QiwenWu AibingLi JingLiang ZumingZhu LitongHe DanhuaZhou YingHuang ShihaoZhao ZhanlinCong JingePeng ZhitaoZhao PingYe ShunaBai BinyiHong XuanjiaDai GuanqiLei YeZhao WentaoJia JunshuangLin XiaolinXiao DongZhang YuqinLin Taoyan - To identify protein markers that may be associated with ulcerative colitis (UC) by analyzing differential proteins in the salivary exosomes from newly diagnosed patients with active UC and healthy controls (HC), and to investigate the function of salivary exosome-specific high-expression proteins in UC patients and their potential role in the pathogenesis of UC. - Source: PubMed
Yang CongyiZheng XiaowenChen JingyiXu JunChen FengChen YangChen Ning