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Gene: Edem3 (ER degradation enhancer, mannosidase alpha-like 3) Mus musculus
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Symbol: Edem3
Name: ER degradation enhancer, mannosidase alpha-like 3
Description: Exhibits mannosyl-oligosaccharide 1,2-alpha-mannosidase activity. Involved in mannose trimming involved in glycoprotein ERAD pathway. Localizes to endoplasmic reticulum lumen. Orthologous to human EDEM3 (ER degradation enhancing alpha-mannosidase like protein 3); PARTICIPATES IN Endoplasmic Reticulum-associated degradation pathway; INTERACTS WITH 2,2',4,4'-Tetrabromodiphenyl ether; 2,3,7,8-tetrachlorodibenzodioxine; carbon nanotube.
Type: protein-coding
RefSeq Status: VALIDATED
Also known as: 2310050N11Rik; alpha-1,2-mannosidase EDEM3; ER degradation enhancing alpha-mannosidase-like; ER degradation-enhancing alpha-mannosidase-like 3; ER degradation-enhancing alpha-mannosidase-like protein 3
Orthologs:
Latest Assembly: GRCm38 - Mouse Genome Assembly GRCm38
Position:
Mouse AssemblyChrPosition (strand)SourceGenome Browsers
JBrowseNCBIUCSCEnsembl
GRCm38 Ensembl1151,755,371 - 151,822,051 (+)EnsemblGRCm38mm10GRCm38
GRCm381151,755,344 - 151,822,328 (+)NCBIGRCm38GRCm38mm10GRCm38
MGSCv371153,602,504 - 153,669,458 (+)NCBIGRCm37mm9NCBIm37
MGSCv361153,517,592 - 153,584,546 (+)NCBImm8
Celera1154,180,540 - 154,247,550 (+)NCBICelera
Cytogenetic Map1G1-G2NCBI
JBrowse: View Region in Genome Browser (JBrowse)
Model


Disease Annotations
Gene-Chemical Interaction Annotations
Gene Ontology Annotations
Molecular Pathway Annotations
Phenotype Annotations
References - curated
References - uncurated

Genomics

Comparative Map Data
QTLs in Region (GRCm38)
miRNA Target Status

Expression


Sequence

Nucleotide Sequences
Protein Sequences
Promoters

Additional Information

External Database Links
 
More on Edem3
Alliance Gene
NCBI Gene
Ensembl Gene
JBrowse: mm9 mm10
MGI Report
NCBI Genome Data Viewer

RGD Object Information
RGD ID: 1619192
Created: 2007-05-01
Species: Mus musculus
Last Modified: 2020-06-30
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.