Ask about this productRelated genes to: MAGEB2 antibody
- Gene:
- MAGEB2 NIH gene
- Name:
- MAGE family member B2
- Previous symbol:
- -
- Synonyms:
- DAM6, MAGE-XP-2, MGC26438, CT3.2
- Chromosome:
- Xp21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-15
- Date modifiied:
- 2016-10-05
Related products to: MAGEB2 antibody
Related articles to: MAGEB2 antibody
- To compare the expression of the MAGEB2 antibody in normal oral mucosa (NOM), oral epithelial dysplasia (OED), and oral squamous cell carcinoma (OSCC) patients, and to evaluate the association of MAGEB2 expression with clinicopathological characteristics and overall survival in OSCC patients. - Source: PubMed
Publication date: 2026/04/01
Hasyim Noratikah AwangManzoor SathickWong Gou ReanZaini Zuraiza MohamadZain Rosnah BintiRamanathan Anand - We conducted a genome-wide interaction analysis between long-term exposure to trihalomethanes in drinking water and colorectal cancer (CRC) risk in a multicenter case-control study in Spain, including 1037 CRC cases and 2100 controls. Exposure categories were estimated based on sex-specific median and quartile values of total trihalomethanes (TTHM), chloroform (CHCl), and brominated trihalomethanes (Br-THMs) among controls. In addition, TTHM exposure was assessed relative to the WHO guideline thresholds. Gene-environment interaction models were computed with the GxEScanR package. To explore biological plausibility, relevant results were inspected in search of expression quantitative trait loci (eQTLs) in two independent resources: BarcUVaSeq and the Genome Tissue Expression (GTEx) v8. Finally, we searched the Comparative Toxicogenomics Database to identify candidate genes previously linked to trihalomethane exposure, retrieved their eQTLs, and evaluated gene-environment interactions with TTHM levels. We found three variants that modulated CRC risk in relation to CHCl and TTHM exposure: rs77985109 near LRRC8B, chr15:28997737 near WHAMMP2, and rs7890183 near MAGEB2. Two additional variants were specifically found for women and one for rectal cancer. Functional assessment suggested a regulatory role of rs77985109 in LRRC8B expression. Moreover, eQTL analysis of candidate genes revealed an additional variant associated with CCL2 which could modulate CRC risk under different TTHM exposure levels. The present study identified novel loci potentially influencing CRC susceptibility under THM exposure, highlighting the importance of integrating environmental and genetic data to better understand environmental driven cancer risks. Further research is needed to confirm these results and clarify underlying mechanisms. - Source: PubMed
Publication date: 2026/01/11
Moratalla-Navarro FerranObón-Santacana MireiaRius-Sansalvador BlancaGuinó ElisabetMoragas NúriaDonat-Vargas Carolinade Larrea-Baz Nerea FernándezMolina-Barceló AnaGuevara MarcelaMorón-Duran Francisco DDierssen-Sotos TrinidadTardón AdoninaCastaño-Vinyals GemmaCabrera-Castro NataliaMolina Antonio JoséAizpurua AmaiaMorales-Suárez-Varela María MMartín VicenteFernández-Navarro PabloVillanueva Cristina MMoreno Victor - Human cancer-germline (CG) genes are a group of testis-specific genes that become aberrantly activated in various tumors. Ongoing studies aim to understand their functions in order to evaluate their potential as anti-cancer therapeutic targets. Evidence suggests the existence of subcategories of CG genes, depending on location on autosomal or sex chromosomes, reliance on DNA methylation for transcriptional regulation, and profile of expression during gametogenesis and early embryogenesis. To clarify this issue, we developed CTexploreR, a R/Bioconductor package that integrates an up-to-date reference list of human CG genes (n = 146) with multiple bulk and single-cell methylomic and transcriptomic datasets. Based on promoter methylation profiles and responsiveness to a DNA methylation inhibitor, 74% of the CG genes were classified as DNA methylation dependent (Methdep). Intriguingly, most X-linked CG genes (69/70) fell into this category, thereby implicating DNA methylation dependency in the well-documented over-representation of testis-specific genes on the X chromosome. We further observed that, whereas X-linked Methdep CG genes become demethylated and activated in pre-spermatogonia in the fetal testis, most of them resist DNA demethylation in female germ cells and remain therefore silent in fetal and adult oocytes. Importantly, a number of X-linked Methdep CG genes (e.g., FMR1NB, GAGE2A, MAGEB2/C2, PAGE2, VCX3A/B) maintained this maternal-specific imprinting after fertilization, and were expressed exclusively in female preimplantation embryos, which inherit a paternal X chromosome. Together, our study using the CTexploreR package has allowed us to show that X-linked CG genes undergo transient maternal imprinting and contribute therefore to transcriptional sexual dimorphism in early embryos. - Source: PubMed
Publication date: 2025/10/15
Loriot AxelleDevis JulieGatto LaurentDe Smet Charles - The Melanoma Antigen Gene (MAGE) family of proteins is the largest family of cancer-testis antigens (CTAs) and shares a MAGE homology domain (MHD). MAGE proteins are divided into Type I and Type II MAGEs depending on their chromosomal location and expression patterns. Type I MAGEs are true CTAs. MAGEB2 is a Type I MAGE, belonging to the MAGEB subfamily, and unlike some MAGE proteins, has not been found to bind to and enhance E3 ligase activity. MAGEB2 has been discovered to be an RNA-binding protein that serves to protect spermatogonial cells in the testis from extraneous stressors. We have discovered that MAGEB2 is necessary and sufficient for the proliferation of cells and is expressed by the differential DNA methylation of its gene promoter. Furthermore, we identified JunD as the transcription factor that regulates MAGEB2 expression. When expressed, MAGEB2 suppresses transforming grown factor-β1 (TGFβ1) signaling by decreasing mRNA levels of Thrombospondin-1 (TSP-1). TSP-1 is an anti-angiogenic protein that activates TGFβ1. Restoring levels of TSP-1 or TGFβ1 results in the inability of MAGEB2 to drive proliferation, suggesting that MAGEB2-expressing tumors might be more susceptible to therapies that induce or activate TSP-1 or TGFβ1 signaling. - Source: PubMed
Publication date: 2025/03/09
Colemon AshleyRomney Carlan VJones Angelle DBagsby ClarkeJackson RichalaRamanathan Saumya - Hepatocellular carcinoma (HCC) ranks sixth in incidence and third in mortality among all cancers. Chronic infection by hepatitis B and C viruses are the predominant risk factors for HCC, but other factors related to metabolic disorders including diabetes and obesity are also involved. - Source: PubMed
Publication date: 2025/02/10
Yang TingWang Si-Yu