EPHB6 Mouse Monoclonal Antibody
- Known as:
- EPHB6 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002051-M03
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- EPHB6 Mouse Monoclonal Antibody
Related genes to: EPHB6 Mouse Monoclonal Antibody
- Gene:
- EPHB6 NIH gene
- Name:
- EPH receptor B6
- Previous symbol:
- -
- Synonyms:
- HEP
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-10
- Date modifiied:
- 2016-10-05
Related products to: EPHB6 Mouse Monoclonal Antibody
Related articles to: EPHB6 Mouse Monoclonal Antibody
- Seven in absentia homologue 2 (SIAH2) has been shown to contribute to the progression of various human tumors, including hepatocellular carcinoma (HCC). However, the precise mechanisms by which SIAH2 promotes HCC cell migration remain to be fully elucidated. In this study, we demonstrate that SIAH2 accelerates the invasion and migration of HCC cells by promoting K48-linked polyubiquitination and degradation of EPH receptor B6 (EPHB6). Notably, the invasion and migration of HCC cells regulated by the SIAH2-EPHB6 axis in association with enhanced filopodia formation, a critical early step in cell motility. Furthermore, our findings indicate that the SIAH2-EPHB6 axis promotes filopodia formation in HCC cells by modulating Ras homolog family member F (RHOF). Finally, we investigated the expression correlations among SIAH2, EPHB6, and RHOF using clinical tissue specimens. In summary, SIAH2 accelerates K48-linked polyubiquitination and degradation of EPHB6 to regulate filopodia formation in HCC cells. - Source: PubMed
Publication date: 2026/04/26
Hu QingheWu KaiLiu ZhiyiXu JiaweiYang WeichaoXia NanHou TianqiZhu YunCao KuanShi HengliangHe YiZhang Bin - Characterizing the relationship between DNA methylation and circulating proteins is critical to understanding the epigenetic regulation of the human plasma proteome. Here, we performed an epigenome-wide association study of 5,032 circulating proteins in 1,449 White and 315 Black participants from the Atherosclerosis Risk in Communities cohort. We identified 12,500 significant protein quantitative trait methylation (pQTM)-protein associations involving 1,647 proteins. Among 7,796 unique pQTMs, 14.7% were classified as cis-pQTMs, which were enriched for fundamental cellular processes, whereas trans-pQTMs were predominantly linked to immune-related functions. Trans-pQTMs also exhibited stronger associations with demographic, lifestyle, and clinical traits as compared with cis-pQTMs. We identified proteins such as GM2A and EPHB6, whose expression appears to be strongly associated with DNA methylation, suggesting potential as targets for epigenetic-based therapeutic interventions. These findings demonstrate the extensive impact of DNA methylation on the circulating proteome through cis- and trans-regulatory mechanisms and underscore the influence of population-level traits on epigenetic regulation. These findings highlight a broad impact of DNA methylation on circulating proteins through both cis- and trans-regulatory mechanisms and the roles of population-level phenotypes. - Source: PubMed
Publication date: 2026/03/03
Li YangSurapaneni AdityaRodriguez-Hernandez ZulemaSchlosser PascalRhee Eugene PBoerwinkle EricYu BingGrove Megan LRuggles Kelly VCoresh JosefGrams Morgan - Triple-negative breast cancers (TNBCs) are among the most aggressive breast tumors, due not only to the absence of clinically functional biomarkers used in other molecular subtypes, but also their marked heterogeneity and pronounced migratory and invasive behavior. The search for new molecules of interest for risk prediction, diagnosis and therapy stems from the class of long non-coding RNAs (lncRNAs), which often display context-dependent ("dual") functions and tissue specificity. Among them, lncRNA LINC01133 stands out for its dysregulation across cancer, although its molecular role in TNBC remains unclear. In the present study, we used the human TNBC cell line Hs578T to generate a cell panel comprising the parental line (Hs578T_wt), the control line (Hs578T_ctr), and the LINC01133 knockout line (Hs578T_ko). Subsequently, we performed bulk RNA-Seq to identify KO-associated Differentially Expressed Genes (DEGs) using as the primary contrast. Functional interpretation was achieved by Over-Representation Analysis (ORA) using Gene Ontology. We then conducted a comparative patient-cohort analysis using TCGA-BRCA Basal-like/TNBC cases (TCGA/BRCA n = 1098; Basal-like/TNBC n = 199), classified with the AIMS algorithm, and evaluated concordance between KO-associated signatures and patient tumor expression patterns via trend-based analyses across the LINC01133 expression levels and associated genes. A total of 265 KO-dominant DEGs were identified in Hs578T_ko, reflecting transcriptional changes consistent with tumor progression, with enrichment of pathways associated with LINC01133 knockout including cell adhesion, cell-cell interactions, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. The main DEGs included , , , , , , , , , and with additional candidates, such as and the lncRNA gene , which have been implicated in migration/invasion, ECM remodeling, or signaling across multiple tumor contexts. Translational analyses in TCGA-BRCA basal-like tumors suggested a descriptive association in which lower LINC01133 levels were accompanied by shifts in the expression trends of genes linked to ECM/EMT programs and modulation of genes related to cell adhesion and protease inhibition. : These results suggest a transcriptional model in which LINC01133 is associated with TNBC-related gene expression programs in a concentration-dependent manner, with loss of LINC01133 being associated with a transcriptomic shift toward pro-migratory/ECM remodeling signatures. While functional validation is required to establish causality, these data support LINC01133 as a molecule of interest in breast cancer research. - Source: PubMed
Publication date: 2026/01/24
Teodoro Júnior LeandroJesus-Ferreira Henrique César deSogayar Mari CleideNishiyama-Jr Milton Yutaka - Age-related macular degeneration (AMD), particularly its non-neovascular (dry) form, is a progressive retinal disorder that causes central vision loss and substantial impairment in daily life. Inflammation and immune dysregulation are recognized as core drivers of AMD, yet the contribution of PANoptosis, a form of programmed cell death that integrates pyroptosis, apoptosis, and necroptosis, remains unclear. In this study, we integrated human single-cell transcriptomic and bulk microarray datasets from the retina and retinal pigment epithelium-choroid to characterize PANoptosis-related transcriptional changes in dry AMD. Dimensionality reduction, cell-type annotation, and PANoptosis gene-set scoring revealed a distinct PANoptosis signature enriched in AMD, with particularly strong activation in myeloid populations. By combining differential expression analysis with machine learning-based feature selection, we identified four PANoptosis-related genes (PON2, BNIP3, EPHB6, and TPD52) that robustly distinguished AMD from control samples and were associated with an altered immune microenvironment. Genetic instrument analysis further suggested a positive association between TPD52 expression and AMD risk. At the cellular level, our data highlighted macrophages, especially pro-inflammatory M1-like macrophages, as key coordinators of PANoptosis-related pathways in dry AMD. To validate these findings in vivo, we used a sodium iodate-induced mouse model of dry AMD and observed significant dysregulation of PON2, BNIP3, EPHB6, and TPD52 in the retina by RT-qPCR, consistent with the human transcriptomic results and supporting their involvement in retinal degeneration and inflammation. Together, these findings implicate PANoptosis as an important and previously underappreciated component of dry AMD pathophysiology, define a four-gene PANoptosis-related signature with diagnostic potential, and suggest new molecular targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/02/13
Li JiamingMa YirongHu MiaoZhang QianWang AnqiTang QiuyuGuo QinshangHuang Binglin - Acute coronary syndrome, driven by vulnerable plaque (VP) instability, is a major cause of cardiovascular mortality. Current diagnostic methods for VPs are limited by invasiveness or low specificity, highlighting the need for non-invasive biomarkers. Using single-cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) from coronary artery disease (CAD) patients with VPs and controls, we identified circulating T cell-platelet aggregates (TPAs) significantly enriched in VP patients and linked to plaque instability via pro-inflammatory pathways. Through high dimensional weighted gene co-expression network analysis, we discovered TPAs' hub genes and demonstrated their role in plaque destabilization. Furthermore, employing machine learning, including Boruta, least absolute shrinkage and selection operator (LASSO) regression and support vector machine-recursive feature elimination (SVM-RFE), we screened for five blood biomarkers that can serve as diagnostic indicators for VPs. Our study demonstrates that TPAs are critically involved in VPs formation. Furthermore, we identified EPHB6, STAT1, RPL23, IKZF3 and AHCY as potential circulating biomarkers for non-invasive detection of VPs. - Source: PubMed
Publication date: 2026/02/04
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