PSMA4, 1-261aa
- Known as:
- PSMA4, 1-261aa
- Catalog number:
- ATGP1350
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- PSMA4 1-261aa
Related genes to: PSMA4, 1-261aa
- Gene:
- PSMA4 NIH gene
- Name:
- proteasome subunit alpha 4
- Previous symbol:
- -
- Synonyms:
- HC9, HsT17706
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-03
- Date modifiied:
- 2016-10-05
Related products to: PSMA4, 1-261aa
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- Intracranial aneurysms (IAs) represent a significant and potentially life-threatening category of disease, and there is currently a lack of effective treatment options aimed at preventing the progression of the disease. Accordingly, this study is dedicated to exploring and identifying effective drug targets that can help in the prevention of both the formation and rupture of IAs, along with a detailed examination of the underlying potential mechanisms involved in these processes. The data related to IAs for this research was obtained from the ISGC Biobank and UK Biobank. Then, we investigated the possible biological functions and unintended consequences of targeting the specific genes that were highlighted in IAs by using mediation analysis, virtual knockout experiments, and PW-MR studies. A total of 5 unique potential drug targets for IAs (FKTN, MAP3K1, PSMA4, SLC22A4, ADAM17), 4 unique potential drug targets for SAH (PSMA4, ADAM17, GPR160, SLC22A4), and 2 unique potential drug targets for UIA (SLC22A4, PRCP) were identified across brain or blood samples. Among the various candidates identified, SLC22A4 has emerged as a promising potential drug target, showing significant expression levels in both blood and brain tissues. Additionally, phenome-wide MR of SLC22A4 across 32 selected phenotypes did not identify statistically significant adverse associations after FDR correction. Virtual knockout (KO) experiments on SLC22A4 revealed that SLC22A4 KO disrupted 81 genes, all of which are involved in IAs-related pathways. Besides, we recognized BRD-K85337334 as potential candidates for targeting SLC22A4. This research indicates that an increase in SLC22A4 gene expression within the blood or brain is directly linked to a heightened risk of IAs rupture, which will aid in prioritizing the development of drugs for IAs. - Source: PubMed
Wan XichenWan ZhiYingPeng HaoyangZhang ZeyuHuang YiWang MaoqiWang PengHu WenhaoXiong WeiDing HanXiong YeWu Xiao - Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide, and although targeted therapy and immunotherapy have improved clinical outcomes, their long-term efficacy is frequently limited by therapeutic resistance, underscoring the need to identify additional biologically relevant and potentially actionable targets. In this study, we applied summary-data-based Mendelian randomization (SMR) by integrating lung cancer genome-wide association study (GWAS) summary statistics with cis-expression quantitative trait locus (cis-eQTL) and cis-methylation quantitative trait locus (cis-mQTL) datasets to prioritize candidate genes associated with LUAD risk. The robustness of SMR-significant signals was further evaluated using the heterogeneity in dependent instruments (HEIDI) test and Bayesian colocalization analysis. Independent transcriptomic datasets from the Gene Expression Omnibus (GEO), together with multiple public databases, were used for expression and prognostic validation, while protein-protein interaction (PPI) and functional enrichment analyses were performed to provide mechanistic context. Among 13 genes prioritized by integrative genetic analyses, PSMA4 (Proteasome 20S Subunit Alpha 4) emerged as the leading LUAD-relevant candidate on the basis of convergent multi-omics evidence, colocalization support, reproducible overexpression (OE) across independent cohorts, and adverse prognostic association. Functional experiments demonstrated that PSMA4 knockdown (KD) suppressed LUAD cell proliferation, migration, invasion, and xenograft tumor growth, whereas PSMA4 overexpression produced the opposite effects. Mechanistically, PSMA4 interacted with p53 and facilitated the proteasome-dependent turnover of ubiquitinated p53, as supported by co-immunoprecipitation, immunofluorescence, ubiquitination, proteasome inhibition, and cycloheximide chase assays, thereby attenuating p53 signaling. Collectively, these findings support PSMA4 as a biologically relevant and potentially actionable target in LUAD and provide a mechanistic rationale for further translational investigation. - Source: PubMed
Publication date: 2026/04/25
Lu HuiWang SaiMa YuhangShen ZhimingYao LongKang NingningSi PanpanZhang Renquan - Atherosclerosis (AS) is a leading cause of cardiovascular disease, and current treatments often fail to induce plaque regression. This study aims to identify novel, genetically supported therapeutic targets for AS to enable more effective drug development. - Source: PubMed
Publication date: 2026/04/24
Yu YongchaoZhu YuanTian QianShao LijuanZeng JiaoXu DandanMo Xiangang - To identify specific, sensitive, and non-invasive circulating protein biomarkers that could facilitate the diagnosis of brain metastasis (BrM) and improve risk prediction for BrM among patients with non-small cell lung cancer (NSCLC). We performed data-independent acquisition mass spectrometry (DIA-MS)-based proteomic profiling of 14 tissue specimens obtained from 7 patients, together with 89 serum samples from NSCLC and NSCLC-BrM cohorts, to identify candidate biomarkers associated with BrM. A total of 12,808 proteins were identified in the tissue proteome and 6041 proteins in the serum proteome, representing an extensive proteomic analysis of lung cancer with BrM reported to date. Using integrated analyses, we identified a four-protein classifier that served as biomarkers for predicting the risk of NSCLC metastasis to the brain. Notably, PSMA4, LAP3, and LZIC were consistently downregulated in both the sera and tissues of patients with NSCLC-BrM compared with those with NSCLC without BrM. These biomarkers were subsequently validated by ELISA in an additional cohort, demonstrating high concordance with the PRM results. Immunohistochemical analyses further supported the utility of these proteins in distinguishing BrM from primary brain tumors. The integrated analysis of tissue and serum proteomics across the cohorts supports the potential value of proteomics-guided, biomarker-assisted diagnosis and risk prediction in BrM and may help enable more accurate stratification and more targeted treatment strategies. - Source: PubMed
Publication date: 2026/04/13
Zheng YongtaoXiong YuetingMa YuxiaoQiu YijieBu QingfangWang ZhenxiSun QingfangSun YuhaoLiu XiaohuiYuan QuanLi YupingBian LiuguanWang Baofeng - https://bit.ly/435kxK0. - Source: PubMed
Publication date: 2026/04/07
Jin YangXu JiuyangHu QidanLi JingyaWang YemingCao Bin