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Ubiquitin specific peptidase 18

UBP43, USP18
The protein encoded by this gene belongs to the ubiquitin-specific proteases (UBP) family of enzymes that cleave ubiquitin from ubiquitinated protein substrates. It is highly expressed in liver and thymus, and is localized to the nucleus. This protein efficiently cleaves only ISG15 (a ubiquitin-like protein) fusions, and deletion of this gene in mice results in a massive increase of ISG15 conjugates in tissues, indicating that this protein is a major ISG15-specific protease. Mice lacking this gene are also hypersensitive to interferon, suggesting a function of this protein in downregulating interferon responses, independent of its isopeptidase activity towards ISG15. [provided by RefSeq, Sep 2011] (from NCBI)
Top mentioned proteins: ISG15, Ubiquitin, CAN, STAT1, V1a
Papers on UBP43
Endothelial RSPO3 Controls Vascular Stability and Pruning through Non-canonical WNT/Ca(2+)/NFAT Signaling.
New
Augustin et al., Heidelberg, Germany. In Dev Cell, Feb 2016
An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified Rnf213, Usp18, and Trim30α.
Differential mRNA expression profiling in ovarian endometriotic tissue with versus without leuprolide acetate treatment.
New
Watanabe et al., Japan. In J Obstet Gynaecol Res, Oct 2015
These genes included CARD11 and USP18.
Global transcriptomic profiling of bovine endometrial immune response in vitro. II. Effect of bovine viral diarrhea virus on the endometrial response to lipopolysaccharide.
New
Wathes et al., United Kingdom. In Biol Reprod, Oct 2015
Top down-regulated genes were RSAD2, ISG15, BST2, MX2, OAS1, USP18, IFIT3, IFI27, SAMD9, IFIT1, and DDX58, whereas TRIM56, C3, and OLFML1 were most up-regulated.
Roles of unphosphorylated ISGF3 in HCV infection and interferon responsiveness.
New
Shin et al., Taejŏn, South Korea. In Proc Natl Acad Sci U S A, Sep 2015
As a mechanism of U-ISGF3-induced resistance to IFN-α, we found that ISG15, a U-ISGF3-induced protein, sustains the abundance of ubiquitin-specific protease 18 (USP18), a negative regulator of IFN signaling.
[Research progress on ubiquitin-specific protease in antiviral immunity].
Review
New
Wei-Lin et al., Hangzhou, China. In Zhejiang Da Xue Xue Bao Yi Xue Ban, Jun 2015
USP2b, USP3, USP18, USP25, UL36USP and HAUSP play a role of antivirus; while USP4, USP13, USP15 and USP17 negatively regulate antiviral immune response.
Human intracellular ISG15 prevents interferon-α/β over-amplification and auto-inflammation.
Impact
Pellegrini et al., Wuhan, China. In Nature, 2015
We further show that an absence of intracellular ISG15 in the patients' cells prevents the accumulation of USP18, a potent negative regulator of IFN-α/β signalling, resulting in the enhancement and amplification of IFN-α/β responses.
USP18 Sensitivity of Peptide Transporters PEPT1 and PEPT2.
Lang et al., Tübingen, Germany. In Plos One, 2014
USP18 (Ubiquitin-like specific protease 18) is an enzyme cleaving ubiquitin from target proteins.
Mice null for the deubiquitinase USP18 spontaneously develop leiomyosarcomas.
Dmitrovsky et al., United States. In Bmc Cancer, 2014
BACKGROUND: USP18 (ubiquitin-specific protease 18) removes ubiquitin-like modifier interferon stimulated gene 15 (ISG15) from conjugated proteins.
USP18 negatively regulates NF-κB signaling by targeting TAK1 and NEMO for deubiquitination through distinct mechanisms.
Cui et al., Key West, United States. In Sci Rep, 2014
In this study, we identified a member of the deubiquitinases family, ubiquitin-specific protease 18 (USP18), as a novel negative regulator in Toll-like receptor (TLR)-mediated NF-κB activation in human macrophages.
USP18 downregulation in peripheral blood mononuclear cells predicts nonresponse to interferon-based triple therapy in patients with chronic hepatitis C, genotype 1: a pilot study.
Sperl et al., Praha, Czech Republic. In Ther Clin Risk Manag, 2014
PATIENTS AND METHODS: Expression of IFNG, IFNLR1, and interferon-sensitive genes CXCL9, IFI16, IFI27, ISG15, and USP18 in peripheral blood mononuclear cells was assessed before and during the initial 12 weeks of treatment.
Activation of endogenous type I IFN signaling contributes to persistent HCV infection.
Review
Chen et al., Chengdu, China. In Rev Med Virol, 2014
In this review, we briefly summarize the findings from high-throughput gene expression profiling from patients chronically infected with HCV, then focus on a novel ubiquitin-like signaling pathway (ISG15/USP18) and its potential role in HCV persistence.
Candidate genes for type 1 diabetes modulate pancreatic islet inflammation and β-cell apoptosis.
Review
Eizirik et al., Brussels, Belgium. In Diabetes Obes Metab, 2013
PTPN2 and USP18), and genes related to β-cell phenotype and susceptibility to pro-apoptotic stimuli (i.e.
USP18 establishes the transcriptional and anti-proliferative interferon α/β differential.
GeneRIF
Pellegrini et al., Paris, France. In Biochem J, 2012
USP18 establishes the transcriptional and anti-proliferative interferon alpha/beta differential
Interferon-γ-stimulated genes, but not USP18, are expressed in livers of patients with acute hepatitis C.
GeneRIF
Heim et al., Basel, Switzerland. In Gastroenterology, 2012
USP18 is up-regulated in liver samples of patients with chronic hepatitis C that did not respond to therapy, but not in patients with acute hepatitis C.
The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-α/β-mediated apoptosis in Ubp43-deficient hematopoietic cells.
GeneRIF
Kim et al., Seoul, South Korea. In Biochem Biophys Res Commun, 2012
although UBP43 depletion can cause hypersensitivity to interferon-alpha/beta-mediated apoptosis in a broad range of cell types, the downstream pathway may vary depending on the cell type.
Usp18 promotes conventional CD11b+ dendritic cell development.
GeneRIF
Zhang et al., San Diego, United States. In J Immunol, 2012
Usp18 modulates conventional CD11b+ dendritic cell development via its inhibitory effect on type I IFN signaling.
Two independent mechanisms promote expression of an N-terminal truncated USP18 isoform with higher DeISGylation activity in the nucleus.
GeneRIF
Zhang et al., San Diego, United States. In J Biol Chem, 2012
the existence of an N-terminal truncated isoform of USP18, whose expression is controlled on translational level by two independent mechanisms providing translational flexibility
The ISG15/USP18 ubiquitin-like pathway (ISGylation system) in hepatitis C virus infection and resistance to interferon therapy.
Review
McGilvray et al., Chengdu, China. In Int J Biochem Cell Biol, 2011
The ISG15/USP18 pathway modulates cellular functions and is important for the host innate immune response to chronic viral infections such as Hepatitis C Virus (HCV).
Interferon-stimulated gene 15 and the protein ISGylation system.
Review
Zhang et al., Los Angeles, United States. In J Interferon Cytokine Res, 2011
The process to remove ISG15 from its conjugated proteins, termed de-ISGylation, is performed by a cellular ISG15-specific protease, ubiquitin-specific proteases with molecular mass 43 kDa (UBP43)/ubiquitin-specific proteases 18.
Role of ISG15 protease UBP43 (USP18) in innate immunity to viral infection.
Impact
GeneRIF
Zhang et al., Los Angeles, United States. In Nat Med, 2004
UBP43 (USP18), an ISG15 protease, and possibly protein ISGylation have a role in innate immunity against viral infection.
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