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Protein Coding Gene : Nbr1 NBR1, autophagy cargo receptor

Primary Identifier  MGI:108498 Organism  mouse, laboratory
Chromosome  11 NCBI Gene Number  17966
Mgi Type  protein coding gene
description  FUNCTION: Automated description from the Alliance of Genome Resources (Release 7.1.0)

Enables mitogen-activated protein kinase binding activity. Involved in negative regulation of osteoblast differentiation; regulation of bone mineralization; and regulation of stress-activated MAPK cascade. Located in late endosome; mitochondrial intermembrane space; and phagophore assembly site. Colocalizes with autophagosome. Is expressed in several structures, including central nervous system; genitourinary system; gut; hemolymphoid system; and liver and biliary system. Orthologous to human NBR1 (NBR1 autophagy cargo receptor).
PHENOTYPE: Homozygous mice of the genetic truncation allele had an age-dependent increase in bone mass and bone mineral density. Mice homozygous for a floxed allele activated in T cells exhibit decreased ovalbumin-induced inflammation and defective Th2 polarization. [provided by MGI curators]
  • synonyms:
  • MGD-MRK-37542,
  • NBR1, autophagy cargo receptor,
  • mKIAA0049,
  • Nbr1

Features --> Cross References

Genome

Sequence Feature Displayer

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0 Canonical

0 CDSs

0 Exons

0 Genomic Clusters

1 Involved In Mutations

0 Strain

0 Transcripts

0 Transgenic Expressors

0 UTRs

Canonical gene --> CDSs in specific strains.

Canonical gene --> Exons in specific strains

Canonical gene --> Strain-specific IDs, biotypes, and locations

Canonical gene --> Transcripts in specific strains.

Features --> Overlapping features

Proteins

Gene --> Proteins

Function

Mouse features --> Functions (GO terms)

Homology

Genes --> Homologs

Interactions

4 Pathways

0 Targeted By

Gene --> Protein-Protein Interactions

Expression

Gene --> Expression annotations

Phenotype

Genes/Features --> Phenotypes (MP terms)

Disease

Mouse features --> Human diseases

Literature

Mouse features --> Publications

 

Other

0 Driver For