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Gene Review:

USP18 - ubiquitin specific peptidase 18

Homo sapiens

Synonyms: 43 kDa ISG15-specific protease, ISG15-specific-processing protease, ISG43, UBP43, Ubl carboxyl-terminal hydrolase 18, ...

Randall, G. et al., Zou, W. et al., Genini, S. et al., Babcock, M. et al., Malakhova, O.A. et al., et al.

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Disease relevance of USP18

Silencing of USP18 Potentiates the Antiviral Activity of Interferon Against Hepatitis C Virus Infection [1].
Results: The siRNA knockdown of USP18 in human cells consistently potentiated the ability of IFN to inhibit HCV-RNA replication and infectious virus particle production by a factor of 1-2 log(10) [1].
These results provide excellent biochemical support for the high resistance of viral and bacterial infection of Ubp43 knockout mice, suggesting that Ubp43 is a potential therapeutic target for the enhancement of immune responses against infections [2].

High impact information on USP18

Role of ISG15 protease UBP43 (USP18) in innate immunity to viral infection [3].
Decreasing USP18 expression led to increased cellular protein ISGylation in response to exogenous IFN-alfa, prolonged tyrosine phosphorylation of signal transducer and activation of transcription (STAT1), and a general enhancement of IFN-stimulated gene expression [1].
Methods: The role of USP18 in IFN antiviral activity was examined using an in vitro model of HCV replication that reproduces the full viral life cycle [1].
These data implicate Ubp43 as a novel in vivo inhibitor of signal transduction pathways that are specifically triggered by type I IFN [4].
We found Alu (SINE) elements at the breakpoints in the substrates and at the junctions in the truncated products of recombination for USP18, GGT, and GGTLA, consistent with Alu-mediated unequal crossing-over events [5].

Biological context of USP18

The delayed shut-off kinetics of ISG43 mRNA corresponded to an increase in its half-life in RNase-L-deficient cells [6].
Here, we show that Ubp43 regulates IFN-beta stimulated genes at genome level [2].

Anatomical context of USP18

Microarray analysis reveals that Type I interferon strongly increases the expression of immune-response related genes in Ubp43 (Usp18) deficient macrophages [2].

Other interactions of USP18

In addition, we provide evidence that a small chromosomal region of HSA22q11.2 evolutionarily corresponds to SSC5q12-q22 (and contains the human homologues of porcine SW152, Q6ZUQ4, TUBA8 and USP18), while the regions flanking HSA22q11.2 on SSC5 correspond to HSA12p13 and HSA12q12 [7].

References

Silencing of USP18 Potentiates the Antiviral Activity of Interferon Against Hepatitis C Virus Infection. Randall, G., Chen, L., Panis, M., Fischer, A.K., Lindenbach, B.D., Sun, J., Heathcote, J., Rice, C.M., Edwards, A.M., McGilvray, I.D. Gastroenterology (2006) [Pubmed]
Microarray analysis reveals that Type I interferon strongly increases the expression of immune-response related genes in Ubp43 (Usp18) deficient macrophages. Zou, W., Kim, J.H., Handidu, A., Li, X., Kim, K.I., Yan, M., Li, J., Zhang, D.E. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
Role of ISG15 protease UBP43 (USP18) in innate immunity to viral infection. Ritchie, K.J., Hahn, C.S., Kim, K.I., Yan, M., Rosario, D., Li, L., de la Torre, J.C., Zhang, D.E. Nat. Med. (2004) [Pubmed]
UBP43 is a novel regulator of interferon signaling independent of its ISG15 isopeptidase activity. Malakhova, O.A., Kim, K.I., Luo, J.K., Zou, W., Kumar, K.G., Fuchs, S.Y., Shuai, K., Zhang, D.E. EMBO J. (2006) [Pubmed]
Shuffling of genes within low-copy repeats on 22q11 (LCR22) by Alu-mediated recombination events during evolution. Babcock, M., Pavlicek, A., Spiteri, E., Kashork, C.D., Ioshikhes, I., Shaffer, L.G., Jurka, J., Morrow, B.E. Genome Res. (2003) [Pubmed]
RNase-L-dependent destabilization of interferon-induced mRNAs. A role for the 2-5A system in attenuation of the interferon response. Li, X.L., Blackford, J.A., Judge, C.S., Liu, M., Xiao, W., Kalvakolanu, D.V., Hassel, B.A. J. Biol. Chem. (2000) [Pubmed]
Radiation hybrid mapping of 18 positional and physiological candidate genes for arthrogryposis multiplex congenita on porcine chromosome 5. Genini, S., Nguyen, T.T., Malek, M., Talbot, R., Gebert, S., Rohrer, G., Nonneman, D., Stranzinger, G., Vögeli, P. Anim. Genet. (2006) [Pubmed]

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