Maged1 MAGE family member D1 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Maged1provided by MGI
Official Full Name: MAGE family member D1provided by MGI
Primary source: MGI:MGI:1930187
See related: Ensembl:ENSMUSG00000025151 AllianceGenome:MGI:1930187
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: NRAGE; Dlixin; Dlxin1; Dlxin-1; MAGE-D1; DXBwg1492e; 2810433C11Rik; 5430405L04Rik
Summary: Enables transcription coactivator activity. Involved in several processes, including positive regulation of MAP kinase activity; positive regulation of branching involved in ureteric bud morphogenesis; and regulation of gene expression. Acts upstream of or within negative regulation of protein localization to nucleus; positive regulation of apoptotic signaling pathway; and regulation of transcription by RNA polymerase II. Located in chromatin and nucleus. Is expressed in several structures, including alimentary system; egg cylinder; genitourinary system; hair follicle; and nervous system. Orthologous to human MAGED1 (MAGE family member D1). [provided by Alliance of Genome Resources, Nov 2024]
Expression: Ubiquitous expression in limb E14.5 (RPKM 316.2), CNS E14 (RPKM 313.7) and 27 other tissues See more
Orthologs: human all
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Genomic context

Location:: X C3; X 41.56 cM

Exon count:: 13

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	X	NC_000086.8 (93579080..93585631, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	X	NC_000086.7 (94535474..94542025, complement)

Chromosome X - NC_000086.8 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

The deficiency of Maged1 attenuates Parkinson's disease progression in mice.
Title: The deficiency of Maged1 attenuates Parkinson's disease progression in mice.
Knockdown of Maged1 inhibits cell cycle progression and causes cell death in mouse embryonic stem cells.
Title: Knockdown of Maged1 inhibits cell cycle progression and causes cell death in mouse embryonic stem cells.
NRAGE is an important regulator of odontogenic differentiation of odontoblasts by inhibiting the NF-kappaB signaling pathway through binding to IKKbeta.
Title: Knockdown of NRAGE induces odontogenic differentiation by activating NF-κB signaling in mouse odontoblast-like cells.
negative regulator of PPARgamma activity, adipogenesis, and insulin sensitivity
Title: Inhibition of PPARγ, adipogenesis and insulin sensitivity by MAGED1.
This work identifies Maged1 as a critical molecule involved in cellular processes and behaviours related to addiction.
Title: Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine.
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.
Title: Necdin modulates osteogenic cell differentiation by regulating Dlx5 and MAGE-D1.
MAGED1 as a novel regulator of osteoblastogenesis, osteoclastogenesis, and bone remodeling in a mouse model
Title: MAGED1 is a negative regulator of bone remodeling in mice.
Maged1 deficiency prevented the interaction of Maged1 with cAMP response element-binding protein (CREB).
Title: Maged1 co-interacting with CREB through a hexapeptide repeat domain regulates learning and memory in mice.
NRAGE is a potent regulator of proliferation and odontoblastic differentiation of mouse dental pulp cells, which might be via the NF-kappaB signalling pathway.
Title: Effects of neurotrophin receptor-mediated MAGE homology on proliferation and odontoblastic differentiation of mouse dental pulp cells.
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.
Title: Ror2-Src signaling in metastasis of mouse melanoma cells is inhibited by NRAGE.

Submit: New GeneRIF Correction See all GeneRIFs (26)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Endonuclease-mediated (5)
Targeted (4) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

NoName (e-PCR)
- UniSTS:546850

Maged1 (e-PCR), detects polymorphism
- UniSTS:546850

Maged1 (e-PCR), detects polymorphism
- UniSTS:142887

AA998497 (e-PCR)
- UniSTS:248620

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables identical protein binding	IEA Inferred from Electronic Annotation more info
enables identical protein binding	ISO Inferred from Sequence Orthology more info
enables protein binding	IPI Inferred from Physical Interaction more info	PubMed
enables transcription coactivator activity	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
involved_in circadian regulation of gene expression	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of DNA-templated transcription	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of epithelial cell proliferation	IEA Inferred from Electronic Annotation more info
involved_in negative regulation of epithelial cell proliferation	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within negative regulation of protein localization to nucleus	IDA Inferred from Direct Assay more info	PubMed
involved_in negative regulation of transcription by RNA polymerase II	IBA Inferred from Biological aspect of Ancestor more info
involved_in positive regulation of DNA-templated transcription	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in positive regulation of MAP kinase activity	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within positive regulation of apoptotic signaling pathway	IGI Inferred from Genetic Interaction more info	PubMed
acts_upstream_of_or_within positive regulation of apoptotic signaling pathway	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in positive regulation of branching involved in ureteric bud morphogenesis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of protein localization to nucleus	IDA Inferred from Direct Assay more info	PubMed
involved_in regulation of circadian rhythm	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within regulation of transcription by RNA polymerase II	IDA Inferred from Direct Assay more info	PubMed

Component	Evidence Code	Pubs
located_in chromatin	IDA Inferred from Direct Assay more info	PubMed
located_in cytosol	TAS Traceable Author Statement more info
is_active_in nucleus	IBA Inferred from Biological aspect of Ancestor more info
located_in nucleus	IDA Inferred from Direct Assay more info	PubMed
located_in plasma membrane	IEA Inferred from Electronic Annotation more info
part_of protein-containing complex	IEA Inferred from Electronic Annotation more info
part_of protein-containing complex	ISO Inferred from Sequence Orthology more info

General protein information

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Preferred Names: melanoma-associated antigen D1

Names: MAGE-D1 antigen; melanoma antigen, family D, 1; neurotrophin receptor-interacting MAGE homolog

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.