CRBN — Cereblon
CRBN belongs to a gene co-expression module in 2 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.
CRBN's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | GIMAP survival Immune regulation | ABLIM1, AKT3, ANKRD13D, ARL4C, C16orf54, CA5B, COPA, DYNLT1 +16 more | View in SCUBA |
| Macrophages | Retromer Endosomal Sorting Vesicular traficking | ABHD15, ARHGAP45, ARHGAP9, CNPY3, CTSO, DAB2, DRAM2, FAM217B +20 more | View in SCUBA |
About the gene
| Synonyms | MRT2, MRT2A |
|---|---|
| Chromosome | 3: 3144628-3179727 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Disease related genes, FDA approved drug targets, Human disease related genes, Predicted intracellular proteins, Transporters |
| Biological process | Ubl conjugation pathway |
Function
Substrate recognition component of a DCX (DDB1-CUL4-X-box) E3 protein ligase complex that mediates the ubiquitination and subsequent proteasomal degradation of target proteins, such as MEIS2, ILF2 or GLUL. Normal degradation of key regulatory proteins is required for normal limb outgrowth and expression of the fibroblast growth factor FGF8. Maintains presynaptic glutamate release and consequently cognitive functions, such as memory and learning, by negatively regulating large-conductance calcium-activated potassium (BK) channels in excitatory neurons. Likely to function by regulating the assembly and neuronal surface expression of BK channels via its interaction with KCNT1. May also be involved in regulating anxiety-like behaviors via a BK channel-independent mechanism (By similarity). Plays a negative role in TLR4 signaling by interacting with TRAF6 and ECSIT, leading to inhibition of ECSIT ubiquitination, an important step of the signaling.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.