Ask about this productRelated genes to: PSMB4 antibody
- Gene:
- PSMB4 NIH gene
- Name:
- proteasome subunit beta 4
- Previous symbol:
- -
- Synonyms:
- HN3, PROS26
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-03
- Date modifiied:
- 2016-10-05
Related products to: PSMB4 antibody
Related articles to: PSMB4 antibody
- Swine Acute Diarrhea Syndrome Coronavirus (SADS-CoV) is an emerging porcine enteric coronavirus that causes severe diarrhea in piglets. Type III interferon (IFN) are crucial for intestinal antiviral defense, and the capacity of SADS-CoV to disrupt IFN-III responses is critical for its replication. This study found that SADS-CoV inhibits IFN-III production through its nonstructural protein 1 (Nsp1), which degrades interferon regulatory factor 1 (IRF1) by promoting its ubiquitination and proteasomal degradation. Mass spectrometry and co-immunoprecipitation analyses revealed that SADS-CoV Nsp1 interacts with proteasomal subunits. Further research indicates that PSMB4, PSMB5, and PSMC5 are key proteasomal subunits involved in SADS-CoV Nsp1-induced IRF1 degradation. Similarly, Porcine Epidemic Diarrhea Virus (PEDV) and Transmissible Gastroenteritis Virus (TGEV) Nsp1 exhibit similar functions, highlighting the conserved role of coronavirus Nsp1 in immune evasion. Collectively, our findings uncover a new mechanism where SADS-CoV Nsp1 exploits the proteasome to degrade IRF1, countering IFN-III responses. - Source: PubMed
Publication date: 2026/09/06
Xiang YingjieZhu QinyuanCheng YueZhao XingShi KaichuangFeng ShupingHuang YuChen ZhenhaiLin ChanghuaMou Chunxiao - Parkinson's disease (PD) is characterized by progressive dopaminergic neuronal loss driven by mitochondrial dysfunction, oxidative stress, and proteostasis collapse, for which current therapies remain symptomatic. This study investigated the neuroprotective effects of Eucalyptus citriodora essential oil (ECEO) on 6-hydroxydopamine (6-OHDA)-induced toxicity in N2a neuroblastoma cells. GC-MS analysis showed that ECEO was dominated by oxygenated monoterpenes, mainly citronellal (60.7%), isopulegol (16%), and citronellol (5.7%). In silico analysis of these constituents showed favorable ADMET profiles, predicted blood-brain barrier permeability, and non-overlapping multitarget engagement across enzymes, GPCRs and nuclear receptors. At the cellular level, ECEO pretreatment significantly restored cell viability (86.7% of control), reduced LDH release, attenuated ROS and NO, and limited mitochondrial depolarization. Quantitative 2D-gel/MALDI-TOF/TOF proteomics identified 94 differentially abundant proteins, of which 20 showed validated PD-related associations (KEGG, Gene4PD, and DisGeNET databases). ECEO pretreatment modulated 12 of these proteins across mechanistically coherent pathways: (i) reversal of 6-OHDA-induced reprogramming of energy metabolism, by normalizing the glycolytic enzymes PKM and PGK1 and restoring the TCA enzyme SUCLG2; (ii) reinforcement of proteostasis through PSMB4 and PSMA3 induction, VCP upregulation and attenuation of ER stress marker HSPA5/BiP; (iii) preservation of mitochondrial and cytoskeletal integrity through PHB1 induction and bilateral TUBB5 restoration. Overall, our results suggest that ECEO exerts significant neuroprotective effects in a cellular PD model by coordinately modulating energy metabolism, proteostasis, antioxidant defense, and structural integrity. Given its predominance in oxygenated monoterpenes the neuroprotective activity of ECEO may result from the combined contribution of the major constituents supporting further investigation in age-related neurodegeneration. - Source: PubMed
Publication date: 2026/08/17
Abidi AmelShaba EnxhiVantaggiato LorenzaKouki OumaymaMasmoudi-Kouki OlfaBini LucaUlivieri CristinaLandi ClaudiaGhrairi Taoufik - Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality, largely due to frequent metastasis to the brain and bones. Therapeutic outcomes are often limited by drug resistance, tumor heterogeneity, and the lack of effective treatment options across different stages and metastatic sites. Identifying druggable targets that are conserved between primary tumors and metastases is critical for advancing precision oncology. - Source: PubMed
Publication date: 2026/06/19
Nagarajan NagasundaramShakyawar Sushil KumarRaheem KayodeGuda Chittibabu - Neuroinflammation is increasingly implicated in depression pathogenesis, yet the underlying mechanisms are still unclear. This study explores whether PSMB4/MHC-I signaling in the cerebrospinal fluid (CSF)-contacting nucleus mediates neuroinflammatory depression. A persistent neuroinflammation-associated depression model was established in mice by repeated intracerebroventricular lipopolysaccharide (LPS) administration. Depressive-like behaviors were evaluated using established assays. Neuroinflammatory responses and target protein expression were assessed by immunofluorescence, Western blotting, RT-qPCR, and laser capture microdissection. Neuronal activity was mapped by c-Fos staining and manipulated using chemogenetics, alongside pharmacological and genetic interventions. Repeated LPS administration induced significant depressive-like behaviors and obvious neuroinflammation in the CSF-contacting nucleus. Under these conditions, neuronal activity in this nucleus was selectively enhanced. Crucially, chemogenetic activation of these neurons alleviated depressive phenotypes, whereas their inhibition induced depression. Molecularly, LPS significantly upregulated PSMB4 and MHC-I expression. Pharmacological suppression of upstream neuroinflammation reversed this PSMB4 upregulation, and targeted PSMB4 knockdown reduced MHC-I expression, ultimately ameliorating depressive-like behaviors. These findings identify the CSF-contacting nucleus as a critical node in neuroinflammation-induced depression and reveal a novel PSMB4/MHC-I signaling axis linking central inflammatory responses to behavioral deficits. - Source: PubMed
Publication date: 2026/05/26
Zhang Yi-JunMa Yu-WeiGui BinWang Xin-LingQian JinPeng YuZhang Li-Cai - Aristolochic acids (AA) are naturally occurring carcinogens found in traditional herbal medicines derived from Aristolochia species. This study explores the potential link between AA and hepatocellular carcinoma (HCC), aiming to uncover key molecular targets driving AA-induced hepatocarcinogenesis. - Source: PubMed
Publication date: 2025/09/06
Liu CanQiao RuHe PengChen WangGao XiangtingHe Fuyuan