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NRAGE is significantly upregulated in patients with Hepatocellular Carcinoma. It could possibly be a novel diagnostic biomarker for HCC early detection.
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.
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.
The nuclear localized NRAGE interacts with RNF8 and BARD1 to mediate the resistance of esophageal carcinomas cells against DNA-damaging agents.
these results demonstrate the effective anti-autophagic of NRAGE in non-small-cell lung cancer cells through AMPK/Ulk1/Atg13 autophagy signaling pathways. Therefore, NRAGE could be used as a potential therapeutic target for lung cancer.
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.
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 ...
Loss of GSPT2 and/or MAGED1 function may contribute to the intellectual disability.
The ectopic subcellular localization of NRAGE mediated nuclear translocation of beta-catenin.
High NRAGE expression is associated with esophageal carcinomas.
MAGE-D1 plays important roles in the central nervous system in both developmental and adult stages.
Univariate and multivariate analyses indicated that MAGED1 expression was an independent prognostic factor in colorectal carcinoma
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.
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.
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.
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.
hNRAGE arrests cell growth through a p53 dependent pathway. hNRAGE also increases the p53 protein level as well as its phosphorylation (Ser392).
The expression pattern of Maged1 roughly summarizes that of Maged2 and Maged3
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.
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
Both transient and stable expression of Necdin induced osteoblast-specific markers in an osteogenic cell line through formation of a complex with melanoma-associated antigen D1 (MAGE-D1) and promoter activation.
MAGED1 as a novel regulator of osteoblastogenesis, osteoclastogenesis, and bone remodeling in a mouse model
Maged1 deficiency prevented the interaction of Maged1 with cAMP response element-binding protein (CREB).
NRAGE is a potent regulator of proliferation and odontoblastic differentiation of mouse dental pulp cells, which might be via the NF-kappaB signalling pathway.
Show Ror2 expression is higher in highly metastatic cell line than in low metastatic variant cell line. Our data show that Ror2 is a potential factor in the tumorigenesis and metastasis in a Src-dependent manner that is negatively regulated by NRAGE.
We conclude that Maged1 is required for OT processing or stability. A decrease in mature OT levels in Maged1 mutants affects social interactions and possibly other behavioral processes
Maged1 is involved in osteoblast proliferation and differentiation. Mice deficient in Maged1 protein had decreased bone mineral density (BMD)
the present findings suggest a novel role for MAGE-D1 in depressive behaviors: modulating SERT ubiquitylation.
XIAP-TAB1-TAK1 complex is dependent on NRAGE for IKK-alpha/beta phosphorylation and NF-kappaB activation.
MAGED1 binds to nuclear receptor RORalpha to bring about positive and negative effects on core clock genes of Bmal1, Rev-erbalpha and E4bp4 expression through the Rev-Erbalpha/ROR responsive elements (RORE).
NRAGE induces NF-kappaB activation and MIF expression in P19 cells
MHD2 of NRAGE was not necessary for BMP-induced p38MAPK activation or caspase-mediated apoptosis.
roles for NRAGE as a mediator of precursor apoptosis and a repressor of cell cycle progression in neural development
receptor tyrosine kinase-like orphan receptor 2(Ror2) sequesters Dlxin-1 in membranous compartments, thereby affecting the transcriptional function of Mhomeobox, msh-like 2(msx2)
necdin and MAGE-D1 cooperate to modulate the function of Dlx/Msx homeodomain proteins in cellular differentiation
Our results suggest that interaction of cytosolic PrP and NRAGE could affect neuronal viability.
NRAGE as an integral component in bone morphogenetic proteins signaling and clarify its role during neural progenitor development
NRAGE plays an important role in apoptotic-signaling in vivo.
NRAGE might have multiple roles during renal branching morphogenesis through association with both the BMP and GDNF signaling pathways.
This gene is a member of the melanoma antigen gene (MAGE) family. Most of the genes of this family encode tumor specific antigens that are not expressed in normal adult tissues except testis. Although the protein encoded by this gene shares strong homology with members of the MAGE family, it is expressed in almost all normal adult tissues. This gene has been demonstrated to be involved in the p75 neurotrophin receptor mediated programmed cell death pathway. Three transcript variants encoding two different isoforms have been found for this gene.
melanoma antigen family D, 1
, melanoma-associated antigen D1
, melanoma-associated antigen D1-like
, MAGE tumor antigen CCF
, MAGE-D1 antigen
, neurotrophin receptor-interacting MAGE homolog
, sertoli cell necdin-related gene protein 1