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
- 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 - The interplay between host innate immunity and pathogen evasion is a dynamic battle shaping infection outcomes. The Topical Collection "Regulation of Antiviral and Antimicrobial Innate Immunity and Immune Evasion" synthesizes findings from thirteen recent studies to elucidate the molecular mechanisms of innate immune signaling and pathogen countermeasures. Host pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and DNA sensor cyclic GMP-AMP synthase (cGAS), drive type I interferon (IFN-I) and interferon-stimulated genes (ISGs) responses, alongside processes like autophagy and inflammasome activation, to combat viral and bacterial infections. Pathogens, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), cytomegalovirus, and porcine reproductive and respiratory syndrome virus, deploy sophisticated strategies to target immune sensors and adaptors, enabling replication and persistence. Novel insights, including the roles of ISG15, autophagy protein ATG7, and host factors such as THAP11 and PSMB4, highlight complex interactions influencing viral replication and host defense. These studies propose targeted therapeutic strategies, such as inflammasome modulation for human immunodeficiency viruses (HIV), and prostaglandin E2 regulation for foot-and-mouth disease virus vaccine production, offering promising avenues to enhance host immunity and counter pathogen evasion. - Source: PubMed
Publication date: 2025/08/29
Wang LingHe DandanSatoh-Takayama NaokoZheng ChunfuXing Junji - The biological basis of the development of cancer of unknown primary (CUP) remains largely unknown, with no evidence of whether a common biological basis exists at present. Our previous multicenter clinical study predicted the primary site of CUP for site‑specific therapy. Concomitantly with the study, a microarray analysis of tumor mRNA samples obtained from 60 participants of the study with CUP was performed, and a gene expression profile specific to CUP was constructed. Several of the genes identified as being upregulated/downregulated in CUP could potentially be clinically useful common biomarkers of CUP. In the present study, to identify genes that may be more closely related to the development of CUP (characterized by its metastatic potential) among the upregulated genes, cell‑based small interfering RNA screening was performed , and two genes, protein kinase DNA‑activated catalytic subunit (PRKDC) and proteasome subunit β type‑4 (PSMB4), were identified to be possibly involved in the metastatic ability of CUP, since knockdown of these genes resulted in reduced migration of A549 cells. These genes were further knocked down in A549 cells using short hairpin RNAs (shRNAs) and the cells were implanted into the footpad of mice. Marked suppression of the metastatic ability of implanted cells from the footpad to the popliteal lymph node (LN) was observed in cells transfected with the shRNAs for PRKDC and PSMB4. In addition, bortezomib, a proteasome inhibitor, markedly reduced the ability of cells implanted into the footpad to metastasize to the LNs, as well as cell growth at the metastatic site, compared with vehicle or NU7447 (inhibitor of PRKDC). These findings indicated that proteasomal function activation augmented the metastatic ability of malignant CUP cells. - Source: PubMed
Publication date: 2025/05/02
Fujita YoshihikoDe Velasco Marco AHayashi HidetoshiNakagawa KazuhikoNishio Kazuto