Ask about this productRelated genes to: CBX3 antibody
- Gene:
- CBX3 NIH gene
- Name:
- chromobox 3
- Previous symbol:
- -
- Synonyms:
- HP1Hs-gamma
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-12
- Date modifiied:
- 2015-11-24
Related products to: CBX3 antibody
Related articles to: CBX3 antibody
- Hydrogen sulfide (H₂S), generated by cystathionine γ-lyase (CSE), protects against aortic aneurysm and dissection (AAD), yet its role in extracellular matrix (ECM) regulation remains unclear. Here, we demonstrate that CSE expression is markedly attenuated in vascular smooth muscle cells (VSMCs) from human AAD specimens and AngII-induced male murine models. VSMC-specific Cse deletion exacerbated AAD formation. Mechanistically, Cse deficiency downregulated CBX3, thereby relieving transcriptional repression of Adamts4. Cbx3 overexpression rescued the aggravated AAD phenotype in Cse-deficient male mice. We further identified a CBX3-centered epigenetic complex (SUV39H1, KDM2A, HDAC1, RING1) that coordinates H3K9/4 methylation and acetylation to regulate ECM remodeling, apoptosis and inflammation-related genes. Notably, CSE/H₂S induced CBX3 sulfhydration at C69, C160, and C177, enhancing protein stability by reducing ubiquitin-mediated degradation; Therapeutically, AAV-mediated Cse or Cbx3 delivery via an extravascular carrier attenuated AAD incidence and progression in male mice. Collectively, these findings define a VSMCs CSE/H₂S-CBX3 epigenetic axis that constrains AAD through regulation of the ADAMTS4-versican pathway. - Source: PubMed
Publication date: 2026/06/04
Zhao YingCui ChangtingGao HuiminYao YanNiu YapingCheng LingShao XiaodieZhang HaizengWang YuanLin YuanzhenDong ZengxiangWu HeChen ZhenzhenYang LimingGeng Bin - Synovial sarcoma (SS) is a malignant mesenchymal tumor of uncertain histogenesis, representing approximately 5% to 10% of all soft tissue sarcomas. It predominantly affects adolescents and young adults. The role of CBX3 (Chromobox homolog 3) in Synovial sarcoma progression, particularly in relation to epithelial mesenchymal transition (EMT), remains unclear. This study aimed to investigate the functional role of CBX3 in synovial sarcoma and to elucidate the underlying molecular mechanisms by which it regulates EMT. Human synovial sarcoma cell lines (SYO-1, HS-SY-II, YaFuSS, and Fuji) and the immortalized human keratinocyte line (HaCaT) were used for studies. For modeling, mice were inoculated with Fuji cells. CBX3 expression was significantly upregulated in human synovial sarcoma tumor specimens compared to control tissues. Clinically, patients with high CBX3 expression exhibited significantly shorter overall survival than those with low expression. In vitro, CBX3 promoted cell proliferation, induced EMT, and suppressed mitochondrial oxidative metabolism. Conversely, siRNA-mediated knockdown of CBX3 (si-CBX3) enhanced mitochondrial oxidative activity. Moreover, CBX3 overexpression inhibited ferroptosis in SS cells, whereas its knockdown (sh-CBX3) promoted both ferroptosis and mitochondrial oxidation - effects consistently observed in both in vitro assays and the mouse xenograft model. Mechanistically, CBX3 activated the Sonic Hedgehog (SHH) signaling pathway. Pharmacological inhibition of SHH signaling abrogated CBX3-mediated suppression of ferroptosis and restoration of mitochondrial oxidation. Furthermore, co-immunoprecipitation assays demonstrated that CBX3 physically interacts with SHH protein and stabilizes it by reducing its polyubiquitination. CBX3 drives EMT and tumor progression in SS by activating the SHH/Gli1 signaling axis. Mechanistically, CBX3 binds directly to and SHH and prevents its ubiquitin-mediated degradation, thereby stabilizing the protein. CBX3-SHH subsequently suppresses mitochondrial oxidative metabolism, which in turn inhibits ferroptosis and facilitates EMT - ultimately promoting SS aggressiveness. - Source: PubMed
Publication date: 2026/03/25
Sun YachaoDai ZhibingDu JunweiMaihemuti MaierdanjianJi SuzhiJiang Renbing - Brain metastases (BM) remain a devastating disease with dismal prognosis. How circulating tumor cells (CTCs) penetrate the blood brain barrier (BBB) and reprogram the brain microenvironment remain unclear. Using spatially resolved multi-omic profiling of CTCs and brain metastases, integrated with experimental and clinical analyses, we identified Glycoprotein Non-Metastatic Melanoma Protein B (GPNMB) as a CTC-secreted driver of vascular disruption and brain colonization. CBX3 upregulation induced GPNMB expression, which bound endothelial EGFR, triggering CBL-mediated ubiquitination and degradation. Attenuated EGFR signaling suppressed FTO and disrupted endothelial junctions via YTHDF2-dependent TJP1 m6A methylation. Remarkably, GPNMB-induced BBB remodeling promoted immune infiltration via CXCL12-CXCR4 axis, and induced time course-dependent T cell exhaustion within the brain microenvironment. Clinically, elevated CBX3⁺GPNMB⁺ CTCs and plasma CXCL12 were significantly associated with BM progression in lung cancer and melanoma. Therapeutically, dual blockade of GPNMB and PD1 enhanced anti-BM efficacy in mice, unveiling GPNMB as a promising target for precision immunotherapy. - Source: PubMed
Publication date: 2026/04/15
Liu XuefeiTan JunWu ChunHuang GuanyinCheng YixinHu JianyangZhang BinyuZhao MaoZhao BoxiLian JingruZheng ShuqianZeng LinXu MengXu YangZeng ShanYu HaoYang HuiZuo ZhixiangLiu ChuanyuFeng WeinengGuo WeinanLi ChunyingLiu Sai-LanLiu QingWen FeiqiuHong Xin - Kinase gene fusions are critical oncogenic drivers and key targets in precision oncology. Here, we report a CBX3::ALK out-of-frame fusion identified in a case of metastatic melanoma, which produces functional ALK isoforms via alternative translation start sites. The patient demonstrates a remarkable clinical response to the ALK inhibitor alectinib. Functional studies confirm that the CBX3::ALK-derived isoforms retain oncogenic signaling and tumorigenic potential. Our findings reveal limitations in current tertiary analysis strategies for functional gene fusion detection that may overlook clinically relevant out-of-frame fusions. Additional analysis of pan-cancer RNA sequencing data from 5,725 tumors and genomic datasets comprising 6,977 melanomas demonstrates that such events are rare but potentially significant. This study highlights the need to consider alternative translation mechanisms and incorporate additional analytic filters, such as 5'/3' expression imbalance, to better capture actionable out-of-frame fusion events in the era of precision oncology. - Source: PubMed
Publication date: 2026/03/25
Hang Jen-FanCheng Han-YingTsai Yu-ShuenLin Sin-YingSong Jie-HongChung Chih-HungYang Muh-Hwa - IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Its pathogenesis is widely described by a multi-hit hypothesis in which galactose-deficient IgA1 (Gd-IgA1) serves as a central disease driver. Advances in the understanding of IgAN pathophysiology, together with the establishment of proteinuria reduction as a surrogate endpoint in 2019, have led to revisions of recent KDIGO Clinical Practice Guideline. As of 2025, multiple therapeutic agents are under active development and in clinical trials, with several already approved, highlighting the need for individualized treatment strategies. Optimizing the use of these emerging therapies requires a deeper understanding of disease mechanisms. One of the key unresolved questions in pathogenesis of IgAN is why Gd-IgA1-containing immune complexes selectively deposit in the glomerular mesangial region, a disease hallmark of IgAN. Long before the identification of Gd-IgA1, it has been debated whether mesangial immune complex deposition reflects passive trapping of circulating complexes or active deposition mediated by antibodies recognizing glomerular antigens. In this regard, we recently discovered IgA-type anti-mesangial cell antibodies (IgA-MESCA) in serum from patients with IgAN and demonstrated that these antibodies target the mesangial cell-surface antigens β2-spectrin and CBX3. In this review, we summarize evidence from early studies to recent findings, including ours, on autoantibodies in IgAN, with a particular focus on glomerular-specific autoantibodies, and discuss the potential involvement of these autoantibodies in the pathogenesis of IgAN. - Source: PubMed
Publication date: 2026/03/09
Nihei YoshihitoSuzuki Yusuke