Ubiquitin Specific Peptidase 18 (USP18) ELISA Kits

Human Ubiquitin Specific Peptidase 18 (USP18) interaction partners

1. The structures of ubiquitin-specific protease 18 (USP18) and a USP18-Interferon-stimulated 15-KDa protein (ISG15) complex indicate the molecular basis of the specificity of the protease and its interaction with the type I interferon receptor [Review].

2. These results demonstrate that virus-induced IFN-lambda4 potently blocks IFN-alpha signalling by inducing high protein levels of ISG15 and USP18. Moreover, the data clearly demonstrate that DAA therapy restores IFN-alpha responsiveness in HCV-infected cells.

3. The role of USP18 in breast cancer provides a novel insight into the clinical application of the USP18/AKT/Skp2 pathway.

4. High expression levels of USP18 in the muscles of dermatomyositis patients.

5. study preliminary elucidated the role of USP18 in hepatitis B virus replication and explored the potential key genes in USP18-mediated signaling pathway

6. this study identified PTEN as a previously unrecognized substrate of the ISGylation post-translational modification pathway. The deconjugase USP18 serves as a novel regulator of PTEN stability. This indicates inhibition of ISGylation is therapeutically relevant in cancers.

7. associates with and deubiquitinates TAK1 to protect against hepatic steatosis, insulin resistance, and the inflammatory response

8. that Ubiquitin-specific peptidase 18 directly bind to BCL2L1 and positively regulated its expression in hepatocellular carcinoma cells

9. These findings add USP18 deficiency to the list of genetic disorders collectively termed type I interferonopathies

10. We show that IRF-7 siRNA knockdown enhanced LPS-induced IL-10 production in human monocyte-derived macrophages, and USP-18 overexpression attenuated LPS-induced production of IL-10 in RAW264.7 cells. Quantitative PCR confirmed upregulation of USP18, USP41, IL10, and IRF7. An independent cohort confirmed LPS induction of USP41 and IL10 genes

11. results indicated that USP18 modulates the anti-HBV activity of IFN-F via activation of the JAK/STAT signaling pathway in Hepg2.2.15 cells.

12. USP18's ISG15 specificity is mediated by a small interaction interface.

13. STAT2 recruits USP18 to the type I IFN receptor subunit IFNAR2 via its constitutive membrane-distal STAT2-binding site.

14. findings show that multiple inflammatory stimuli can modulate interferon stimulated gene expression and thus inhibit hepatocyte interferon signaling via USP18 induction

15. USP18 negatively regulates NF-kappaB signaling by targeting TAK1 and NEMO for deubiquitination through distinct mechanisms.

16. Data suggest that USP18 (Ubiquitin-like specific protease 18) sensitive cellular functions include activity of the peptide transporters PEPT1 and PEPT2.

17. Dimerization of IFNAR1 and IFNAR2 and the limiting role of IFNAR1 binding affinity in complex assembly is modulated by USP18.

18. increased expression in the HIV+/HCV+ female patients group compared with HIV-/HCV+ and HIV+/HCV- groups

19. USP18 expression levels induced by IFNbeta did not differ amongst multiple sclerosis patients carrying different rs2542109 genotypes

20. USP18 inhibition induces inflammation by increasing the STAT signaling and exacerbates IFN-induced beta cell apoptosis.

Mouse (Murine) Ubiquitin Specific Peptidase 18 (USP18) interaction partners

1. Usp18 protects the cells from oxidative stress-induced apoptosis which may be through the regulation of p53 and caspase 3.

2. associates with and deubiquitinates TAK1 to protect against hepatic steatosis, insulin resistance, and the inflammatory response

3. this study identifies the osteopenia phenotype of mice lacking Usp18, which is known as a negative regulator of type I IFN signaling

4. USP18 has a protective role in pathological cardiac remodeling in mouse.

5. USP18's ISG15 specificity is mediated by a small interaction interface.

6. findings show that multiple inflammatory stimuli can modulate interferon stimulated gene expression and thus inhibit hepatocyte interferon signaling via USP18 induction

7. Increased ISGylation was accompanied by enhanced viral resistance without causing detrimental side effects suggesting that USP18 protease inhibition might be a suitable antiviral strategy

8. USP18 null mice develop leiomyosarcoma recapitulating key features of clinical leiomyosarcomas and patients with reduced-USP18 tumor levels have an unfavorable outcome.

9. USP18 lack in microglia causes destructive interferonopathy of the mouse brain.

10. results suggest that increasing ISGylation by specific inhibition of USP18 protease activity could constitute a promising antiviral strategy with only a minimal risk of severe adverse effects

11. USP18 is crucial for IFN-gamma-mediated inhibition of B16 melanoma tumorigenesis and antitumor immunity.

12. Usp18-driven enforced viral replication in dendritic cells can break immunological tolerance and critically influences induction of autoimmunity.

13. Hypersensitivity of Usp18 knockout in mammary epithelial cells to IFN-gamma enhances Cxcl10 expression and protects against mammary tumour progression.

14. USP18 inhibits NF-kappaB and NFAT activation during Th17 differentiation by deubiquitinating the TAK1-TAB1 complex.

15. Usp18 upregulation was associated with Wilms Tumor.

16. 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.

17. Usp18 modulates conventional CD11b+ dendritic cell development via its inhibitory effect on type I IFN signaling.

18. These results show the impact of USP18 in the development of Salmonella-induced typhlitis.

19. UBP43 (USP18) specifically removes ISG15 from conjugated proteins

20. UBP43 plays a critical role in maintaining the homeostatic balance of ISG15-conjugated protein, and that regulation of cellular levels of ISG15 protein modification is essential for brain cell function.

Pig (Porcine) Ubiquitin Specific Peptidase 18 (USP18) interaction partners

1. These data highlight USP18 as a host restriction factor during innate immune response to porcine respiratory and reproductive syndrome virus.

2. USP18 is a potential target gene that promotes reduced replication of PRRSV.

3. Results report identification and cloning of the ISG15 and ISG43 genes in pig.