EPHB2 monoclonal antibody (M02), clone 3B3
- Known as:
- EPHB2 mab (anti-) (M02), clonality 3B3
- Catalog number:
- H00002048-M02
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- EPHB2 monoclonal antibody (M02) clone 3B3
Related genes to: EPHB2 monoclonal antibody (M02), clone 3B3
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- Gene:
- EPHB2 NIH gene
- Name:
- EPH receptor B2
- Previous symbol:
- DRT, ERK, EPHT3
- Synonyms:
- Hek5, Tyro5
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2019-04-23
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- Gene:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
Related products to: EPHB2 monoclonal antibody (M02), clone 3B3
Related articles to: EPHB2 monoclonal antibody (M02), clone 3B3
- Src-family kinases (SFKs) regulate proliferation in colonic epithelial cells (CECs), but the mechanisms that restrain their activity remain poorly defined. We identify Src-like adaptor protein (SLAP), a negative regulator of receptor tyrosine kinase signaling, as a key suppressor of SFK activity in the colon. Constitutive and inducible epithelial-specific Slap deletion using a villin-CreERT2 model increases CEC proliferation and accelerates tumorigenesis in the azoxymethane/dextran sodium sulfate model. Slap deficiency also enhances SFK-dependent expansion of normal and tumor-derived colonic organoids. Mechanistically, we identify the receptor tyrosine kinase EPHB2 as a critical upstream activator of SFKs and a direct target of SLAP-mediated regulation. Loss of Slap increased EphB2 protein abundance and tyrosine phosphorylation, and enhanced its association with active SRC. Pharmacological inhibition of EPHB2 suppressed SRC activation and reversed the hyperproliferative phenotype induced by Slap deficiency. Together, these findings uncover a non-genetic mechanism driving SFK activation during colonic transformation and establish SLAP as a tumor suppressor that constrains oncogenic EPHB2-SFK signaling in the colonic epithelium. - Source: PubMed
Publication date: 2026/09/08
Naim DanaHouhou ZouheirCauchois FlorentEspie KevinSimon ValerieBoublik YvanLanga Vives FrancinaHomayed ZeinabPaul ConceptionMaillard MorganHahne MichaelPannequin JulieNguyen JulieSirvent AudreyRoche Serge - Male accessory sex glands are essential components of the reproductive system, providing secretions that support sperm function, fertility, and androgen-dependent reproductive processes. Despite the widespread use of mice as experimental models, comprehensive biometrical, histomorphometrical, and molecular characterization of their accessory sex glands remains limited. The present study investigated the vesicular, bulbourethral, and preputial glands of adult male mice with particular emphasis on biometric parameters, histological organization, and the expression of EphB2, EphB4, and ephrin-B1 membrane proteins. Ten-week-old male ICR mice ( = 6) were used for morphometric profiling, RT-PCR, and immunofluorescence analyses. The vesicular glands showed highly folded mucosa lined by pseudostratified columnar epithelial cells and enclosed by well-developed smooth muscle layers. Bulbourethral glands were multilobular, composed of arborized acini lined by tall columnar epithelial cells, whereas preputial glands were modified sebaceous glands characterized by lobulated sebaceous acini with prominent basal cells. RT-PCR analysis revealed the presence of EphB4 and ephrin-B1 transcripts in all three glands, while EphB2 expression was detected only in the vesicular and bulbourethral glands. Immunofluorescence staining demonstrated that EphB4 and ephrin-B1 were predominantly localized in basal cells of vesicular and preputial glands and in secretory epithelial cells in the bulbourethral gland, with weaker expression in principal cells in the vesicular gland. Faint expression of EphB2, EphB4, and ephrin-B1 was observed in α-SMA-positive smooth muscle cells of vesicular and bulbourethral glands. The findings provide the first integrated biometric and histomorphometric data and demonstrate distinct expression profiles of EphB2/B4 and ephrin-B1 membrane proteins in mouse accessory sex glands, suggesting their involvement in glandular structure and functional regulation. - Source: PubMed
Publication date: 2026/06/22
Gofur Md RoyhanToma Mst Suriya TanjumNakajima TakayukiTanida Takashi - - Source: PubMed
Publication date: 2026/06/25
Chai XingxingXu YanqiuChai JiaxinDeng WenfangWang JiandongWang SiliZhuang Wanchuan - IntroductionColorectal cancer (CRC) is a common malignancy characterized by high recurrence rates and frequent late-stage diagnoses, highlighting the need for reliable prognostic biomarkers. Despite the existence of several multi-gene prognostic models, these often fail to account for individual molecular heterogeneity and the influence of neuromodulatory pathways. The Axon Guidance pathway, a critical regulator of the nervous system, has been implicated in tumor progression; however, its prognostic significance in CRC remains largely unexplored.MethodTo address this gap, a novel prognostic index, the Optimal Prognostic Index of Survival Variables (OPISV), was developed. Using transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) CRC cohort, survival-associated genes were first identified through Kaplan-Meier analysis, and differentially expressed genes were determined via the Wilcoxon rank-sum test. Key prognostic variables were rigorously selected through univariate Cox regression, least absolute shrinkage and selection operator (LASSO) regression, and stepwise multivariate Cox regression. The final OPISV model incorporated four variables: age, M stage, EPHB2, and ZNF346. Its predictive performance was robustly evaluated using time-dependent receiver operating characteristic (ROC) curves, Kaplan-Meier survival analysis, and calibration curves, with external validation in two independent Gene Expression Omnibus (GEO) datasets (GSE39582 and GSE17537). Protein expression levels of the target genes were further validated by Western blotting in CRC tissues and matched adjacent non-tumor tissues from our hospital.ResultThe OPISV model effectively stratified patients into high- and low-risk groups with significantly different overall survival (p < 0.001). Functional enrichment analysis revealed significant activation of the Axon Guidance pathway in the high-risk group. Unsupervised clustering of related genes confirmed the pathway's central role and highlighted distinct immune and mutational landscapes between subtypes. Western blotting analysis of clinical samples confirmed significant upregulation of EPHB2 and ZNF346 proteins in CRC tissues, highlighting their biological and clinical relevance.ConclusionThe OPISV model is a reliable and practical tool for predicting CRC prognosis and offers valuable mechanistic insights into the role of the Axon Guidance pathway in tumor progression. - Source: PubMed
Publication date: 2026/06/22
Wei YiLi BinBinChu WeiJianRao ChunHui - Dengue fever, a mosquito-borne disease caused by dengue virus (DENV), has become a global health problem, and no FDA-approved drug is currently available. Qingwen Baidu Decoction (QBD) is used to treat the critical phase of dengue fever in China, but its mechanism of action remains unclear. In this work, we integrated bioinformatics analysis, machine learning, and network pharmacology to investigate the possible molecular targets and potential active chemical components of QBD. Common targets between differentially expressed genes from DENV infected samples and predicted targets of QBD were identified by bioinformatics analysis and refined by machine learning algorithms including LASSO, random forest and SVM-RFE. Three core genes, CXCL10, EZH2 and EPHB2 were significantly overexpressed in dengue fever patients, indicating their potential diagnostic and therapeutic value. Single cell transcriptome analysis further revealed that QBD primarily targets dendritic cells, monocytes and macrophages. Immune infiltration analysis using ssGSEA showed that these three core genes were significantly associated with CD4 and CD8 T cell subtypes, suggesting their involvement in host immune regulation. Molecular docking and molecular dynamics simulations identified eight chemical components of QBD as potential active ingredients. Based on these computational predictions, we hypothesize that QBD may exert its therapeutic effects through dual mechanisms, including directly binding to DENV proteins to inhibit viral replication, while also regulating the function of CXCL10 and EZH2 to alleviate DENV-induced inflammatory responses and modulate host immunity. These results provide a theoretical reference for future experimental validation and drug development. - Source: PubMed
Publication date: 2026/06/23
Xiao YanLiu ZhanchenHu ShengjieYao PengLiu YajunCheng Maosheng