SCUBA

NBR1 — NBR1 autophagy cargo receptor

NBR1 belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

NBR1's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsMembrane trafficking
Housekeeping
BCL2, CLSTN1, GLB1, GTF2I, HPSE, HSDL2, LENG8, MBIP +19 moreView in SCUBA
Gamma-delta T cellsActin Cytoskeletal Regulation
Cytoskeletal
ACTR2, AP3B1, AP3M1, AZI2, CAPZA1, CEP250, CPSF3, DIDO1 +25 more
MacrophagesMyeloid Innate Signaling
Innate immunity
ADCY7, ARHGAP18, BMP2K, C3AR1, C6orf62, CD46, CD84, CLTC +34 moreView in SCUBA
Mucosal-associated invariant T cellT cell Activation Signaling
TCR Signaling
AGAP2, ARHGAP45, CDK5RAP3, DNMT1, IL10RA, ITGAL, JADE2, PLCB2 +6 more

About the gene

Synonyms1A1-3B, CA125, KIAA0049, M17S2
Chromosome17: 43170481-43211689
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Biological processHost-virus interaction

Function

Ubiquitin-binding autophagy adapter that participates in different processes including host defense or intracellular homeostasis. Possesses a double function during the selective autophagy by acting as a shuttle bringing ubiquitinated proteins to autophagosomes and also by participating in the formation of protein aggregates. Plays a role in the regulation of the innate immune response by modulating type I interferon production and targeting ubiquitinated IRF3 for autophagic degradation. In response to oxidative stress, promotes an increase in SQSTM1 levels, phosphorylation, and body formation by preventing its autophagic degradation (By similarity). In turn, activates the KEAP1-NRF2/NFE2L2 antioxidant pathway (By similarity). Also plays non-autophagy role by mediating the shuttle of IL-12 to late endosome for subsequent secretion (By similarity).

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.