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Loss of GSPT2 (show GSPT2 Proteins) and/or MAGED1 function may contribute to the intellectual disability.
The ectopic subcellular localization of NRAGE mediated nuclear translocation of beta-catenin (show CTNNB1 Proteins).
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 (show TRIM31 Proteins) Praja1 (show PJA1 Proteins) regulates Dlx5 (show DLX5 Proteins)-dependent transcription through its ubiquitin ligase activity for the Dlx/Msx-interacting MAGE (show MAGEB10 Proteins)/Necdin (show NDN Proteins) family protein, Dlxin-1.
hNRAGE arrests cell growth through a p53 (show TP53 Proteins) dependent pathway. hNRAGE also increases the p53 (show TP53 Proteins) protein level as well as its phosphorylation (Ser392).
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 (show NFKB1 Proteins) signalling pathway.
Show Ror2 (show ROR2 Proteins) expression is higher in highly metastatic cell line than in low metastatic variant cell line. Our data show that Ror2 (show ROR2 Proteins) is a potential factor in the tumorigenesis and metastasis in a Src (show SRC Proteins)-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 (show BEST1 Proteins))
the present findings suggest a novel role for MAGE-D1 in depressive behaviors: modulating SERT (show SLC6A4 Proteins) ubiquitylation.
XIAP (show XIAP Proteins)-TAB1 (show TAB1 Proteins)-TAK1 (show NR2C2 Proteins) complex is dependent on NRAGE for IKK-alpha (show CHUK Proteins)/beta phosphorylation and NF-kappaB (show NFKB1 Proteins) activation.
MAGED1 binds to nuclear receptor RORalpha to bring about positive and negative effects on core clock genes of Bmal1 (show ARNTL Proteins), Rev-erbalpha (show NR1D1 Proteins) and E4bp4 (show NFIL3 Proteins) expression through the Rev-Erbalpha (show NR1D1 Proteins)/ROR responsive elements (RORE).
NRAGE induces NF-kappaB activation and MIF expression in P19 cells
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