Protein cereblon

Definition:

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. 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).

References:

[1]. Anita K Gandhi, et al. Immunomodulatory agents lenalidomide and pomalidomide co-stimulate T cells by inducing degradation of T cell repressors Ikaros and Aiolos via modulation of the E3 ubiquitin ligase complex CRL4(CRBN.). Br J Haematol. 2014 Mar;164(6):811-21. [Content Brief]

[2]. Takumi Ito, et al. Identification of a primary target of thalidomide teratogenicity. Science. 2010 Mar 12;327(5971):1345-50. [Content Brief]

[3]. Eric S Fischer, et al. Structure of the DDB1-CRBN E3 ubiquitin ligase in complex with thalidomide. Nature. 2014 Aug 7;512(7512):49-53. [Content Brief]

[4]. Tae-Yong Choi, et al. Cereblon Maintains Synaptic and Cognitive Function by Regulating BK Channel. J Neurosci. 2018 Apr 4;38(14):3571-3583. [Content Brief]

[5]. Qihui Lian, et al. Cereblon Promotes the Ubiquitination and Proteasomal Degradation of Interleukin Enhancer-Binding Factor 2. Protein J. 2020 Oct;39(5):411-421. [Content Brief]

[6]. Philip P Chamberlain, et al. Structure of the human Cereblon-DDB1-lenalidomide complex reveals basis for responsiveness to thalidomide analogs. Nat Struct Mol Biol. 2014 Sep;21(9):803-9. [Content Brief]

[7]. Joseph J Higgins, et al. Dysregulation of large-conductance Ca2+-activated K+ channel expression in nonsyndromal mental retardation due to a cereblon p.R419X mutation. Neurogenetics. 2008 Jul;9(3):219-23. [Content Brief]

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