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https://www.readbyqxmd.com/read/27980214/the-isg15-specific-protease-usp18-regulates-stability-of-pten
#1
Lisa Maria Mustachio, Masanori Kawakami, Yun Lu, Jaime Rodriguez-Canales, Barbara Mino, Carmen Behrens, Ignacio Wistuba, Neus Bota-Rabassedas, Jun Yu, J Jack Lee, Jason Roszik, Lin Zheng, Xi Liu, Sarah J Freemantle, Ethan Dmitrovsky
The ubiquitin-like modifier interferon-stimulated gene 15 (ISG15) is implicated in both oncogenic and tumor suppressive programs. Yet, few ISGylation substrates are known and functionally validated in cancer biology. We previously found specific oncoproteins were substrates of ISGylation and were stabilized by the ISG15-specific deubiquitinase (DUB) ubiquitin specific peptidase 18 (USP18). Using reverse-phase protein arrays (RPPAs), this study reports that engineered loss of the DUB USP18 destabilized the tumor suppressor protein phosphatase and tensin homologue (PTEN) in both murine and human lung cancer cell lines...
December 12, 2016: Oncotarget
https://www.readbyqxmd.com/read/27923569/gender-differences-of-b-cell-signature-related-to-estrogen-induced-ifi44l-baff-in-systemic-lupus-erythematosus
#2
Hongye Fan, Guangfeng Zhao, Deshan Ren, Fei Liu, Guanjun Dong, Yayi Hou
Systemic lupus erythematosus (SLE) possesses a gender-dependent incidence characterized by a male/female ratio 1:9. B-cell, a vital part of the immune system, plays an important role in pathogenesis of SLE. Thus, we hypothesize that gender differences of B cells may exist in SLE and relate to the onset and the progression of SLE. Here, we showed that the genes expression pattern is similar between healthy female and male. However, SLE female and SLE male showed more upregulated genes, in which the trendline of SLE male is higher than that of SLE female...
December 5, 2016: Immunology Letters
https://www.readbyqxmd.com/read/27882925/isgylation-controls-exosome-secretion-by-promoting-lysosomal-degradation-of-mvb-proteins
#3
Carolina Villarroya-Beltri, Francesc Baixauli, María Mittelbrunn, Irene Fernández-Delgado, Daniel Torralba, Olga Moreno-Gonzalo, Sara Baldanta, Carlos Enrich, Susana Guerra, Francisco Sánchez-Madrid
Exosomes are vesicles secreted to the extracellular environment through fusion with the plasma membrane of specific endosomes called multivesicular bodies (MVB) and mediate cell-to-cell communication in many biological processes. Posttranslational modifications are involved in the sorting of specific proteins into exosomes. Here we identify ISGylation as a ubiquitin-like modification that controls exosome release. ISGylation induction decreases MVB numbers and impairs exosome secretion. Using ISG15-knockout mice and mice expressing the enzymatically inactive form of the de-ISGylase USP18, we demonstrate in vitro and in vivo that ISG15 conjugation regulates exosome secretion...
November 24, 2016: Nature Communications
https://www.readbyqxmd.com/read/27809302/multiple-functions-of-usp18
#4
REVIEW
Nadine Honke, Namir Shaabani, Dong-Er Zhang, Cornelia Hardt, Karl S Lang
Since the discovery of the ubiquitin system and the description of its important role in the degradation of proteins, many studies have shown the importance of ubiquitin-specific peptidases (USPs). One special member of this family is the USP18 protein (formerly UBP43). In the past two decades, several functions of USP18 have been discovered: this protein is not only an isopeptidase but also a potent inhibitor of interferon signaling. Therefore, USP18 functions as 'a' maestro of many biological pathways in various cell types...
November 3, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27801882/usp18-recruits-usp20-to-promote-innate-antiviral-response-through-deubiquitinating-sting-mita
#5
Man Zhang, Meng-Xin Zhang, Qiang Zhang, Gao-Feng Zhu, Lei Yuan, Dong-Er Zhang, Qiyun Zhu, Jing Yao, Hong-Bing Shu, Bo Zhong
STING (also known as MITA) mediates the innate antiviral signaling and ubiquitination of STING is key to its function. However, the deubiquitination process of STING is unclear. Here we report that USP18 recruits USP20 to deconjugate K48-linked ubiquitination chains from STING and promotes the stability of STING and the expression of type I IFNs and proinflammatory cytokines after DNA virus infection. USP18 deficiency or knockdown of USP20 resulted in enhanced K48-linked ubiquitination and accelerated degradation of STING, and impaired activation of IRF3 and NF-κB as well as induction of downstream genes after infection with DNA virus HSV-1 or transfection of various DNA ligands...
December 2016: Cell Research
https://www.readbyqxmd.com/read/27716962/acetaldehyde-disrupts-interferon-alpha-signaling-in-hepatitis-c-virus-infected-liver-cells-by-up-regulating-usp18
#6
Murali Ganesan, Larisa Y Poluektova, Dean J Tuma, Kusum K Kharbanda, Natalia A Osna
BACKGROUND: Alcohol consumption exacerbates the pathogenesis of hepatitis C virus (HCV) infection and worsens disease outcomes. The exact reasons are not clear yet, but they might be partially attributed to the ability of alcohol to further suppress the innate immunity. Innate immunity is known to be already decreased by HCV in liver cells. METHODS: In this study, we aimed to explore the mechanisms of how alcohol metabolism dysregulates IFNα signaling (STAT1 phosphorylation) in HCV(+) hepatoma cells...
September 26, 2016: Alcoholism, Clinical and Experimental Research
https://www.readbyqxmd.com/read/27659523/interferon-stimulated-gene-15-induces-cancer-cell-death-by-suppressing-the-nf-%C3%AE%C2%BAb-signaling-pathway
#7
Hongwu Mao, Man Wang, Biyin Cao, Haibin Zhou, Zubin Zhang, Xinliang Mao
Interferon-stimulated gene 15 (ISG15) is an important cytokine that has been reported in carcinogenesis. However, we found that ISG15 and de-ISGylase USP18 were induced by several anti-cancer agents, which was confirmed by both RT-PCR and immunoblotting assays. Further studies demonstrated that ectopic ISG15 and USP18 inhibited proliferation of myeloma, leukemia and cervical cancer cells. More importantly, ISG15 and USP18 induced cancer cell apoptosis. This finding was confirmed in a cervical xenograft model in which cervical cancer growth was suppressed by lentiviral ISG15...
September 21, 2016: Oncotarget
https://www.readbyqxmd.com/read/27605457/transcriptomic-profiling-of-long-non-coding-rnas-in-dermatomyositis-by-microarray-analysis
#8
Qing-Lin Peng, Ya-Mei Zhang, Han-Bo Yang, Xiao-Ming Shu, Xin Lu, Guo-Chun Wang
Long non-coding RNAs (lncRNAs) are prevalently transcribed in the genome and have been found to be of functional importance. However, the potential roles of lncRNAs in dermatomyositis (DM) remain unknown. In this study, a lncRNA + mRNA microarray analysis was performed to profile lncRNAs and mRNAs from 15 treatment-naive DM patients and 5 healthy controls. We revealed a total of 1198 lncRNAs (322 up-regulated and 876 down-regulated) and 1213 mRNAs (665 up-regulated and 548 down-regulated) were significantly differentially expressed in DM patients compared with the healthy controls (fold change>2, P < 0...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27572150/novel-protective-role-for-ubiquitin-specific-protease-18-in-pathological-cardiac-remodeling
#9
Xiaoying Ying, Yichao Zhao, Tianbao Yao, Ancai Yuan, Longwei Xu, Lingchen Gao, Song Ding, Hongyi Ding, Jun Pu, Ben He
Ubiquitin-specific protease 18 (USP18), a USP family member, is involved in antiviral activity and cancer inhibition. Although USP18 is expressed in heart, the role of USP18 in the heart and in cardiac diseases remains unknown. Here, we show that USP18 expression is elevated in both human dilated hearts and hypertrophic murine models. Cardiomyocyte-specific overexpression of USP18 in mice significantly blunted cardiac remodeling as evidenced by mitigated myocardial hypertrophy, fibrosis, ventricular dilation, and preserved ejection function, whereas USP18-deficient mice displayed exacerbated cardiac remodeling under the same pathological stimuli...
November 2016: Hypertension
https://www.readbyqxmd.com/read/27450445/gene-expression-profile-after-activation-of-rig-i-in-5-ppp-dsrna-challenged-df1
#10
Yang Chen, Qi Xu, Yang Li, Ran Liu, Zhengyang Huang, Bin Wang, Guohong Chen
Retinoic acid inducible gene I (RIG-I) can recognize influenza viruses and evoke the innate immune response. RIG-I is absent in the chicken genome, but is conserved in the genome of ducks. Lack of RIG-I renders chickens more susceptible to avian influenza infection, and the clinical symptoms are more prominent than in other poultry. It is unknown whether introduction of duck RIG-I into chicken cells can establish the immunity as is seen in ducks and the role of RIG-I in established immunity is unknown. In this study, a chicken cell strain with stable expression of duRIG-I was established by lentiviral infection, giving DF1/LV5-RIG-I, and a control strain DF1/LV5 was established in parallel...
December 2016: Developmental and Comparative Immunology
https://www.readbyqxmd.com/read/27434537/full-spectrum-of-lps-activation-in-alveolar-macrophages-of-healthy-volunteers-by-whole-transcriptomic-profiling
#11
Miguel Pinilla-Vera, Zeyu Xiong, Yutong Zhao, Jing Zhao, Michael P Donahoe, Suchitra Barge, William T Horne, Jay K Kolls, Bryan J McVerry, Anastasiya Birukova, Robert M Tighe, W Michael Foster, John Hollingsworth, Anuradha Ray, Rama Mallampalli, Prabir Ray, Janet S Lee
Despite recent advances in understanding macrophage activation, little is known regarding how human alveolar macrophages in health calibrate its transcriptional response to canonical TLR4 activation. In this study, we examined the full spectrum of LPS activation and determined whether the transcriptomic profile of human alveolar macrophages is distinguished by a TIR-domain-containing adapter-inducing interferon-β (TRIF)-dominant type I interferon signature. Bronchoalveolar lavage macrophages were obtained from healthy volunteers, stimulated in the presence or absence of ultrapure LPS in vitro, and whole transcriptomic profiling was performed by RNA sequencing (RNA-Seq)...
2016: PloS One
https://www.readbyqxmd.com/read/27379545/correction-suppression-of-usp18-potentiates-the-anti-hbv-activity-of-interferon-alpha-in-hepg2-2-15-cells-via-jak-stat-signaling
#12
Lin Li, Qing-Song Lei, Shu-Jun Zhang, Ling-Na Kong, Bo Qin
[This corrects the article DOI: 10.1371/journal.pone.0156496.].
2016: PloS One
https://www.readbyqxmd.com/read/27325888/human-usp18-deficiency-underlies-type-1-interferonopathy-leading-to-severe-pseudo-torch-syndrome
#13
Marije E C Meuwissen, Rachel Schot, Sofija Buta, Grétel Oudesluijs, Sigrid Tinschert, Scott D Speer, Zhi Li, Leontine van Unen, Daphne Heijsman, Tobias Goldmann, Maarten H Lequin, Johan M Kros, Wendy Stam, Mark Hermann, Rob Willemsen, Rutger W W Brouwer, Wilfred F J Van IJcken, Marta Martin-Fernandez, Irenaeus de Coo, Jeroen Dudink, Femke A T de Vries, Aida Bertoli Avella, Marco Prinz, Yanick J Crow, Frans W Verheijen, Sandra Pellegrini, Dusan Bogunovic, Grazia M S Mancini
Pseudo-TORCH syndrome (PTS) is characterized by microcephaly, enlarged ventricles, cerebral calcification, and, occasionally, by systemic features at birth resembling the sequelae of congenital infection but in the absence of an infectious agent. Genetic defects resulting in activation of type 1 interferon (IFN) responses have been documented to cause Aicardi-Goutières syndrome, which is a cause of PTS. Ubiquitin-specific peptidase 18 (USP18) is a key negative regulator of type I IFN signaling. In this study, we identified loss-of-function recessive mutations of USP18 in five PTS patients from two unrelated families...
June 27, 2016: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/27302182/ifn-%C3%AE-4-desensitizes-the-response-to-ifn-%C3%AE-treatment-in-chronic-hepatitis-c-through-long-term-induction-of-usp18
#14
Weiguo Fan, Shiqi Xie, Xinhao Zhao, Nan Li, Chong Chang, Li Li, Ge Yu, Xiumei Chi, Yu Pan, Junqi Niu, Jin Zhong, Bing Sun
The recently discovered interferon lambda 4 (IFN-λ4) is a new member of the human type III interferons which could induce a strong antiviral effect through the JAK-STAT cascade. However, hepatitis C virus (HCV) patients who are capable of expressing IFN-λ4 usually have poor response to IFN-α treatment, and the mechanism behind this paradox remains unknown. Here, we reported that IFN-λ4 desensitized IFN-α-stimulated JAK-STAT signalling. Microarray analysis revealed that IFN-λ4 could induce ubiquitin specific peptidase 18 (USP18), a known inhibitor of the type I IFN signalling pathway, in a more sustained pattern compared with type I interferon induction...
September 2016: Journal of General Virology
https://www.readbyqxmd.com/read/27260842/genome-wide-identification-of-quantitative-trait-transcripts-for-blood-traits-in-the-liver-samples-of-a-white-duroc-%C3%A3-erhualian-f2-pig-resource-population
#15
Pan Xu, Leilei Cui, Tao Huang, Zhen Zhang, Bin Yang, Congying Chen, Lusheng Huang, Yanyu Duan
Blood cell counts are important clinical indicators for health status. The liver plays a crucial role in food digestion and metabolism and is also a blood-forming organ. Here, we conducted a whole-genome quantitative trait transcript (QTT) analysis on 497 liver samples for 16 hematological traits in a White Duroc × Erhualian F2 pig resource population. A total of 20,108 transcripts were explored to detect their association with hematological traits. By using Spearman correlation coefficients, we identified 1,267 QTTs for these 16 hematological traits at the significance threshold of P < 0...
August 1, 2016: Physiological Genomics
https://www.readbyqxmd.com/read/27227879/suppression-of-usp18-potentiates-the-anti-hbv-activity-of-interferon-alpha-in-hepg2-2-15-cells-via-jak-stat-signaling
#16
Lin Li, Qing-Song Lei, Shu-Jun Zhang, Ling-Na Kong, Bo Qin
Ubiquitin-specific protease 18 (USP18, also known as UBP43) has both interferon stimulated gene 15 (ISG15) dependent and ISG15-independent functions. By silencing the expression of USP18 in HepG2.2.15 cells, we studied the effect of USP18 on the anti-HBV activity of IFN-F and demonstrated that knockdown of USP18 significantly Inhibited the HBV expression and increased the expression of ISGs. Levels of hepatitis B virus surface antigen (HBsAg), hepatitis B virus e antigen (HBeAg), HBV DNA and intracellular hepatitis B virus core antigen (HBcAg) were dramatically decreased with or without treatment of indicated dose of IFN-F...
2016: PloS One
https://www.readbyqxmd.com/read/27193971/isg15-deficiency-and-increased-viral-resistance-in-humans-but-not-mice
#17
Scott D Speer, Zhi Li, Sofija Buta, Béatrice Payelle-Brogard, Li Qian, Frederic Vigant, Erminia Rubino, Thomas J Gardner, Tim Wedeking, Mark Hermann, James Duehr, Ozden Sanal, Ilhan Tezcan, Nahal Mansouri, Payam Tabarsi, Davood Mansouri, Véronique Francois-Newton, Coralie F Daussy, Marisela R Rodriguez, Deborah J Lenschow, Alexander N Freiberg, Domenico Tortorella, Jacob Piehler, Benhur Lee, Adolfo García-Sastre, Sandra Pellegrini, Dusan Bogunovic
ISG15 is an interferon (IFN)-α/β-induced ubiquitin-like protein. It exists as a free molecule, intracellularly and extracellularly, and conjugated to target proteins. Studies in mice have demonstrated a role for Isg15 in antiviral immunity. By contrast, human ISG15 was shown to have critical immune functions, but not in antiviral immunity. Namely, free extracellular ISG15 is crucial in IFN-γ-dependent antimycobacterial immunity, while free intracellular ISG15 is crucial for USP18-mediated downregulation of IFN-α/β signalling...
May 19, 2016: Nature Communications
https://www.readbyqxmd.com/read/27193023/elevated-hepatic-lipid-and-interferon-stimulated-gene-expression-in-hcv-gt3-patients-relative-to-non-alcoholic-steatohepatitis
#18
Shikha Shrivastava, Eric G Meissner, Emily Funk, Seerat Poonia, Virender Shokeen, Arun Thakur, Bhawna Poonia, Shiv Kumar Sarin, Nirupma Trehanpati, Shyamasundaran Kottilil
BACKGROUND AND AIMS: HCV GT-3 has a more pronounced effect on hepatic steatosis and host lipids than other HCV genotypes and is proving less responsive to all oral interferon-free treatment with direct acting antiviral agents. As both HCV GT3 infection and NASH can result in steatosis and cirrhosis, we asked whether hepatic transcriptional profiles reflective of the host response to inflammation differed based on the etiology of injury. METHODS: Hepatic gene expression was determined for 48 pre-selected genes known to be associated with hepatic interferon signaling and lipid metabolic pathways in treatment-naïve HCV GT-3 (n = 9) and NASH (n = 14) patients...
November 2016: Hepatology International
https://www.readbyqxmd.com/read/27133094/molecular-cloning-and-functional-analysis-of-duck-ubiquitin-specific-protease-18-usp18-gene
#19
Wei Qian, Xiaoqin Wei, Hongbo Zhou, Meilin Jin
In mammals, ubiquitin-specific protease 18 (USP18) is an interferon (IFN)-inducible gene and is a negative regulator of Toll-like receptor-mediated nuclear factor kappa B (NF-κB) activation. The role of USP18 in ducks (duUSP18) remains poorly understood. In the present study, we cloned and characterized the full-length coding sequence of duUSP18 from duck embryo fibroblasts (DEFs). In healthy ducks, duUSP18 transcripts were broadly expressed in different tissues, with higher expression levels in the spleen, lung and kidney...
September 2016: Developmental and Comparative Immunology
https://www.readbyqxmd.com/read/27016605/elevated-response-to-type-i-ifn-enhances-rankl-mediated-osteoclastogenesis-in-usp18-knockout-mice
#20
Hwa Young Yim, Cheolkyu Park, Yong Deok Lee, Kei-Ichiro Arimoto, Raok Jeon, Sung Hee Baek, Dong-Er Zhang, Hong-Hee Kim, Keun Il Kim
A balance between bone formation and bone resorption is critical for the maintenance of bone mass. In many pathological conditions, including chronic inflammation, uncontrolled activation of osteoclast differentiation often causes excessive bone resorption that results in osteoporosis. In this study, we identified the osteopenia phenotype of mice lacking Usp18 (also called Ubp43), which is a deISGylating enzyme and is known as a negative regulator of type I IFN signaling. The expression of Usp18 was induced in preosteoclasts upon receptor activator of NF-κB ligand (RANKL) treatment...
May 1, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
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