MAGED1 Antibody

1. Our results indicate that NRAGE subcellular localization is related to radiation resistance of esophageal carcinoma cell and EMT may be involved in NRAGE subcellular location. PMID:29516958
2. NRAGE upregulation was correlated with advanced TNM stage, local invasion, and poor survival. Importantly, NRAGE could serve as an independent prognostic factor in patients with gastric cancer. PMID:29778424
3. The nuclear localized NRAGE interacts with RNF8 and BARD1 to mediate the resistance of esophageal carcinomas cells against DNA-damaging agents. PMID:27035619
4. MAGED1 binds and positively regulates the transcriptional activity of family members SIM1, SIM2, NPAS4 and ARNT2, but does not interact with AhR, HIF1alpha and ARNT. This interaction is mediated by PAS repeat regions which also form the interface for bHLH PAS dimerisation, and accordingly MAGED1 is not found in complex with bHLH PAS dimers. PMID:27472814
5. our surprise, NRAGE induces nuclear localization of beta-catenin and increases its DNA binding ability. Further studies reveal that NRAGE leads to the modification of beta-catenin/Arm with O-linked beta-N-acetylglucosamine (O-GlcNAc), and failure of the association between beta-catenin/Arm and pygopus(pygo) protein, which is required for transcriptional activation of Wnt target genes. Therefore, our findings suggest a ... PMID:28427939
6. Loss of GSPT2 and/or MAGED1 function may contribute to the intellectual disability. PMID:28414775
7. The ectopic subcellular localization of NRAGE mediated nuclear translocation of beta-catenin. PMID:26738870
8. High NRAGE expression is associated with esophageal carcinomas. PMID:24710624
9. MAGE-D1 plays important roles in the central nervous system in both developmental and adult stages. PMID:23314527
10. Univariate and multivariate analyses indicated that MAGED1 expression was an independent prognostic factor in colorectal carcinoma PMID:22935435
11. NRAGE may participate in the formation of radioresistance of TE13R120 cells by changing its subcellular localization, but its relationship with cell apoptosis has not been confirmed. PMID:20868560
12. we establish the roles for Dlxin-1, one as an anti-tumorigenic and anti-invasive protein in high-grade gliomas and the other as an inducer of differentiation of glioma stem cells. PMID:21109781
13. Data report that NRAGE, via the same XIAP-Tak1-Tab1 complex, is required for the phosphorylation of IKK -alpha/beta and subsequent transcriptional activation of the p65 subunit of NF-kappaB. PMID:20100315
14. A RING finger protein Praja1 regulates Dlx5-dependent transcription through its ubiquitin ligase activity for the Dlx/Msx-interacting MAGE/Necdin family protein, Dlxin-1. PMID:11959851
15. hNRAGE arrests cell growth through a p53 dependent pathway. hNRAGE also increases the p53 protein level as well as its phosphorylation (Ser392). PMID:15094062
16. The expression pattern of Maged1 roughly summarizes that of Maged2 and Maged3 PMID:15162511
17. MAGE-D1 protein expression was reduced in 6 of 16 breast carcinoma cell lines as compared with untransformed immortal mammary epithelial cell lines; suppression of MAGE-D1 expression may be involved in the tumorigenesis of some sporadic breast cancers. PMID:15930293
18. demonstrate the importance of human NRAGE in homotypic cell-to-cell adhesion and illuminate the mechanism of human NRAGE in the process of inhibition of cell adhesion PMID:16125672
19. Data show that hNRAGE gene can inhibit the growth of 293 cells. PMID:16388736
20. studies indicate for the first time that NRAGE could suppress metastasis of melanoma and pancreatic cancer probably through downregulation of MMP-2 PMID:17140727
21. MAGE-D1 might be a novel inhibitor of angiogenesis in vitro and in vivo. PMID:17149546
22. These findings provide new insight into the ability of MAGE-D1 to suppress the motility and adhesion response of tumor cells by interfering with actin cytoskeleton reorganization and hypoxia inducible factor 1-dependent gene expression. PMID:17453828
23. Che-1 interacts with NRAGE and NRAGE overexpression downregulates endogenous Che-1 by targeting it for proteasome-dependent degradation. PMID:17488777
24. Enhanced expression of MAGE-D1 by gene transfer could reverse the malignant phenotypes of breast cancer cells. PMID:19639218

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HGNC: 6813

UNIGENE: Hs.5258

KEGG: hsa:9500

STRING: 9606.ENSP00000364847

OMIM: 300224