Ubl carboxyl-terminal hydrolase 18

Definition:

Involved in the negative regulation of the inflammatory response triggered by type I interferon. Upon recruitment by STAT2 to the type I IFN receptor subunit IFNAR2 interferes with the assembly of the ternary interferon-IFNAR1-IFNAR2 complex and acts as a negative regulator of the type I IFN signaling pathway. Also regulates protein ISGylation. Can efficiently cleave only ISG15 fusions including native ISG15 conjugates linked via isopeptide bonds. Necessary to maintain a critical cellular balance of ISG15-conjugated proteins in both healthy and stressed organisms.; [Isoform 2]: Has enzymatic activity similar to isoform 1 and interferes with type I interferon signaling. Major deISGylation enzyme for nuclear proteins.

References:

[1]. Michael P Malakhov, et al. UBP43 (USP18) specifically removes ISG15 from conjugated proteins. J Biol Chem. 2002 Mar 22;277(12):9976-81. [Content Brief]

[2]. Kei-Ichiro Arimoto, et al. STAT2 is an essential adaptor in USP18-mediated suppression of type I interferon signaling. Nat Struct Mol Biol. 2017 Mar;24(3):279-289. [Content Brief]

[3]. Marije E C Meuwissen, et al. Human USP18 deficiency underlies type 1 interferonopathy leading to severe pseudo-TORCH syndrome. J Exp Med. 2016 Jun 27;213(7):1163-74. [Content Brief]

[4]. Christoph Burkart, et al. Two independent mechanisms promote expression of an N-terminal truncated USP18 isoform with higher DeISGylation activity in the nucleus. J Biol Chem. 2012 Feb 10;287(7):4883-93. [Content Brief]

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