CBX4 antibody - N-terminal region (ARP30002_P050)
- Known as:
- CBX4 (anti-) - N-terminal region (ARP30002_P050)
- Catalog number:
- arp30002_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CBX4 antibody - N-terminal region (ARP30002_P050)
Related genes to: CBX4 antibody - N-terminal region (ARP30002_P050)
- Gene:
- CBX4 NIH gene
- Name:
- chromobox 4
- Previous symbol:
- -
- Synonyms:
- hPC2, PC2, NBP16
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-20
- Date modifiied:
- 2015-11-24
Related products to: CBX4 antibody - N-terminal region (ARP30002_P050)
Related articles to: CBX4 antibody - N-terminal region (ARP30002_P050)
- Epigenetic dysregulation is associated with immune evasion and immune checkpoint blockade (ICB) resistance. Here, using in vivo CRISPR-Cas9 screens targeting epigenetic-related factors in mouse tumor models treated with ICB, we identified Chromobox 4 (CBX4) as a key negative regulator of immune tumor microenvironment. Single-cell RNA sequencing and spatial transcriptomics analyses of patients receiving neoadjuvant anti-PD-1 therapy revealed high CBX4 expression in both tumor cells and immunosuppressive tumor-associated macrophage subpopulations, with preferential accumulation in non-responders. Deficiency of CBX4 in macrophages or tumor cells, induced robust anti-tumor immunity, increased infiltration and cytotoxic activity of CD8+ T cells and NK cells, thereby heightening the sensitivity of ICB treatment. Mechanistically, CBX4 targeted H3K9me3 and H3K27me3-marked endogenous retroelements such as RLTR4-Mm-int. Loss of CBX4 derepressed retrotransposons, activating cytosolic RNA-sensing pathways and triggering type I interferon response, ultimately leading to robust inflamed TME. Moreover, we uncovered a negative correlation between CBX4 expression and immune responses, retrotransposon levels as well as the prognosis of patients with hepatocellular carcinoma (HCC) undergoing ICB therapy. Our study establishes CBX4 as an epigenetic immune checkpoint through the epigenetic silencing of retrotransposons, remodeling immune TME and thus providing a promising therapeutic target to enhance tumor immunogenicity and overcoming immunotherapy resistance. - Source: PubMed
Publication date: 2026/03/31
Ma ZhiboJia WenlongZhou XiLiu JingLi QingwenChang RuizhiGu ShiqiYuan NaonaoChen ZhishuiLan Peixiang - : Epigenetic factors are increasingly recognized to contribute to the pathogenesis of intestinal diseases, yet the precise mechanisms through which these factors influence ulcerative colitis (UC) remain poorly understood. : Transcriptome profiles pertaining to UC and genes associated with epigenetic factors (EFRGs) were retrieved from publicly accessible datasets. Candidate genes were ascertained through the intersection of differentially expressed genes (DEGs) and EFRGs. Key genes were screened through machine learning algorithms and validated via the Artificial Neural Network (ANN) model. Enrichment analysis and immune infiltration assays were conducted to elucidate the underlying mechanisms of these genes. The hub gene, CBX4 (Chromobox homolog 4), was validated through immunohistochemical analysis of both healthy controls and patients with UC, and the correlation was evaluated using UC-related clinical parameters. Additionally, CBX4 expression was knocked down in dextran sulphate sodium (DSS)-treated mice to examine its regulatory function. Unlike conventional broad-spectrum biomarker screens, this study specifically integrated epigenetic factor-related genes (EFRGs) with machine learning and experimental validation using both clinical samples and animal models. : , , , and were identified as key genes, with SMARCB1, JAK2, and CBX4 being upregulated in the UC group, while PPARGC1A was significantly downregulated. The ANN model exhibited excellent diagnostic performance. Enrichment analysis revealed that the key genes were associated with pathways such as the "chemokine signaling pathway". Immune cell infiltration analysis results revealed marked differences in the abundances of 13 immune cell types between the UC and control groups, and there were notable associations between immune cell infiltration and key genes. Notably, CBX4 expression was elevated in both DSS-treated mice and patients with UC, showing positive correlations with clinical indicators of UC. Further in vivo experiments revealed that silencing CBX4 alleviated DSS-induced colon damage and inflammation. : This study identifies four EFRG-related key genes (SMARCB1, JAK2, CBX4, PPARGC1A) in UC, suggesting that CBX4 may play a significant role as an epigenetic regulator. CBX4 is upregulated in UC intestinal tissues, and its knockdown mitigates DSS-induced colitis. These findings provide critical theoretical support for developing targeted therapies for UC. - Source: PubMed
Publication date: 2026/03/17
Ma XiaohanLiu GuangpengGong TingtingLiu Xueqi - Enterovirus 71 (EV71) is a primary etiological agent of hand-foot-mouth disease (HFMD) in children under 5 years of age and can cause severe neurological disorders even death. Therefore, elucidating the infection mechanism and pathogenicity of EV71 is essential for developing more effective and targeted therapies to prevent and control EV71-associated diseases. Here, we initially reported that the SUMO E3 ligase CBX4 is important for EV71 replication. Furthermore, we found that CBX4 interacts with the EV71 3D polymerase, and overexpression of CBX4 significantly extends the half-life of 3D, whereas knockdown of CBX4 reduces the stability of 3D protein. Subsequent investigations demonstrated that CBX4 mediates both SUMOylation and ubiquitination modifications of 3D, and treatment with protein SUMOylation inhibitor 2-D08 remarkably depresses EV71 replication and the expression of ectopically transfected 3D. The regulatory role of CBX4 and the effect of 2-D08 were also observed in other enteroviruses, including coxsackievirus B3 (CVB3) and poliovirus 1 (PV1). These findings revealed that CBX4 facilitates EV71 infection through inducing SUMOylation and stabilization of 3D polymerase, hinting its potential as a novel target for antiviral development. - Source: PubMed
Publication date: 2026/03/04
Su RuiNiu YifanSun AipingZhao TiesuoWang Hui - - Source: PubMed
Publication date: 2026/03/04
Sun XinguoZhang JianxinYan QiongDeng Xiaojun - Chromobox 4 (CBX4), a polycomb protein family member linked to tumor pathogenesis via dysregulation, has an incompletely defined role in gastric cancer (GC). The study aimed to investigate the role and mechanism of CBX4 in GC progression and evaluate its potential as a therapeutic target. - Source: PubMed
Publication date: 2025/12/30
Jia WendongZhang TingZhang ZiyingWu LingzhiFu XihaoWang ZhenxinYin Ni