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 or ILF2. Normal degradation of key regulatory proteins is required for normal limb outgrowth and expression of the fibroblast growth factor FGF8 (By similarity). 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 (PubMed:29530986). Likely to function by regulating the assembly and neuronal surface expression of BK channels via its interaction with KCNT1 (By similarity). May also be involved in regulating anxiety-like behaviors via a BK channel-independent mechanism (PubMed:29530986). Protein modification; protein ubiquitination. Component of a DCX (DDB1-CUL4-X-box) protein ligase complex, at least composed of CRBN, CUL4A, DDB1 and RBX1. Interacts directly with DDB1 (By similarity). Interacts with KCNT1 (By similarity). Interacts with ILF2 (By similarity). Highly expressed in brain. In brain, expression is abundant in the cerebellum, with less expression in the neocortical, hippocampus and striatum in adult. Neocortical expression increases from embryonic stages to adulthood. The CULT domain binds thalidomide and related drugs. Thalidomide binding leads to a change in substrate specificity of the human DCX (DDB1-CUL4-X-box) E3 protein ligase complex, while no such change is observed in rodents. Ubiquitinated, ubiquitination is mediated by its own DCX protein ligase complex. No obvious phenotype, however mice display increased BK channel activity and a subsequent decrease in synaptic transmission and presynaptic release probability in excitatory synapses (PubMed:29530986). Mice also display cognitive behavioral defects such as abnormal passive avoidance, hyperanxious behavior and decreased preference for new objects (PubMed:29530986). Treatment with the BK blocker paxilline rescues all synaptic and behavioral abnormalities except for hyperanxiety (PubMed:29530986). Brain and synaptic morphology is normal and long-term synaptic plasticity is not affected (PubMed:29530986). Conditional knockout in the forebrain results in no obvious phenotype, however mice display a deficit in contextual fear learning whereas anxiety-like behavior is unaffected (PubMed:21995942). Belongs to the CRBN family.