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USP19 suppresses cellular type I interferon signaling by targeting TRAF3 for deubiquitination
To investigate host factors that mediate the immune escape of enterovirus 71 (EV71) in the context of deubiquitinating enzymes. Utilize PCR array to screen candidate genes that may be involved in EV71-induced cellular antiviral immune responses, and utilize protein mass spectrometry analysis to iden...
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| Published in: | Future microbiology 2017-07, Vol.12 (9), p.767-779 |
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| Main Authors: | , , , , |
| Format: | Article |
| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c371t-f24530404624115cc4355afb19b95bea0b57074bd38629c0e983ebd7516e00123 |
| container_end_page | 779 |
| container_issue | 9 |
| container_start_page | 767 |
| container_title | Future microbiology |
| container_volume | 12 |
| creator | Gu, Zhiwen Shi, Weifeng Zhang, Li Hu, Zhilin Xu, Chao |
| description | To investigate host factors that mediate the immune escape of enterovirus 71 (EV71) in the context of deubiquitinating enzymes.
Utilize PCR array to screen candidate genes that may be involved in EV71-induced cellular antiviral immune responses, and utilize protein mass spectrometry analysis to identify the functional targets of the candidate regulator.
EV71 infection induces the upregulation of ubiquitin-specific protease 19 (
) gene expression, which negatively regulates cellular antiviral type I interferon signaling. Additionally, we identify that USP19 suppresses cellular type I interferon signaling by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3) molecule and decreasing TRAF3 ubiquitination of K63-linkage.
This work suggests that USP19 is a previously unrecognized regulator employed by EV71 to evade host antiviral defenses. |
| doi_str_mv | 10.2217/fmb-2017-0006 |
| format | article |
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Utilize PCR array to screen candidate genes that may be involved in EV71-induced cellular antiviral immune responses, and utilize protein mass spectrometry analysis to identify the functional targets of the candidate regulator.
EV71 infection induces the upregulation of ubiquitin-specific protease 19 (
) gene expression, which negatively regulates cellular antiviral type I interferon signaling. Additionally, we identify that USP19 suppresses cellular type I interferon signaling by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3) molecule and decreasing TRAF3 ubiquitination of K63-linkage.
This work suggests that USP19 is a previously unrecognized regulator employed by EV71 to evade host antiviral defenses.</description><identifier>ISSN: 1746-0913</identifier><identifier>EISSN: 1746-0921</identifier><identifier>DOI: 10.2217/fmb-2017-0006</identifier><identifier>PMID: 28391724</identifier><language>eng</language><publisher>England: Future Medicine Ltd</publisher><subject>deubiquitinating enzyme ; Deubiquitinating Enzymes - metabolism ; Endopeptidases - genetics ; Endopeptidases - metabolism ; enterovirus 71 ; Enterovirus A, Human - immunology ; Gene expression ; Genomes ; Glycerol ; HEK293 Cells ; Humans ; Immune Evasion ; Immune response ; Immunity, Cellular ; Immunity, Innate ; Immunoglobulins ; Infections ; Interferon ; Interferon Type I - antagonists & inhibitors ; Interferon Type I - metabolism ; Kinases ; Mass spectrometry ; Mass spectroscopy ; Oligonucleotide Array Sequence Analysis ; Pattern recognition ; Phosphatase ; Plasmids ; Protein Processing, Post-Translational ; Proteins ; Signal Transduction ; TNF Receptor-Associated Factor 3 - genetics ; TNF Receptor-Associated Factor 3 - metabolism ; TRAF3 ; Tumor necrosis factor-TNF ; type I interferon signaling ; Ubiquitin ; Ubiquitin-specific proteinase ; Ubiquitination ; USP19 ; Viral infections ; Viruses</subject><ispartof>Future microbiology, 2017-07, Vol.12 (9), p.767-779</ispartof><rights>Future Medicine Ltd</rights><rights>Copyright Future Medicine Ltd Jul 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-f24530404624115cc4355afb19b95bea0b57074bd38629c0e983ebd7516e00123</citedby><cites>FETCH-LOGICAL-c371t-f24530404624115cc4355afb19b95bea0b57074bd38629c0e983ebd7516e00123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28391724$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, Zhiwen</creatorcontrib><creatorcontrib>Shi, Weifeng</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Hu, Zhilin</creatorcontrib><creatorcontrib>Xu, Chao</creatorcontrib><title>USP19 suppresses cellular type I interferon signaling by targeting TRAF3 for deubiquitination</title><title>Future microbiology</title><addtitle>Future Microbiol</addtitle><description>To investigate host factors that mediate the immune escape of enterovirus 71 (EV71) in the context of deubiquitinating enzymes.
Utilize PCR array to screen candidate genes that may be involved in EV71-induced cellular antiviral immune responses, and utilize protein mass spectrometry analysis to identify the functional targets of the candidate regulator.
EV71 infection induces the upregulation of ubiquitin-specific protease 19 (
) gene expression, which negatively regulates cellular antiviral type I interferon signaling. Additionally, we identify that USP19 suppresses cellular type I interferon signaling by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3) molecule and decreasing TRAF3 ubiquitination of K63-linkage.
This work suggests that USP19 is a previously unrecognized regulator employed by EV71 to evade host antiviral defenses.</description><subject>deubiquitinating enzyme</subject><subject>Deubiquitinating Enzymes - metabolism</subject><subject>Endopeptidases - genetics</subject><subject>Endopeptidases - metabolism</subject><subject>enterovirus 71</subject><subject>Enterovirus A, Human - immunology</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Glycerol</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Immune Evasion</subject><subject>Immune response</subject><subject>Immunity, Cellular</subject><subject>Immunity, Innate</subject><subject>Immunoglobulins</subject><subject>Infections</subject><subject>Interferon</subject><subject>Interferon Type I - antagonists & inhibitors</subject><subject>Interferon Type I - metabolism</subject><subject>Kinases</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Pattern recognition</subject><subject>Phosphatase</subject><subject>Plasmids</subject><subject>Protein Processing, Post-Translational</subject><subject>Proteins</subject><subject>Signal Transduction</subject><subject>TNF Receptor-Associated Factor 3 - genetics</subject><subject>TNF Receptor-Associated Factor 3 - metabolism</subject><subject>TRAF3</subject><subject>Tumor necrosis factor-TNF</subject><subject>type I interferon signaling</subject><subject>Ubiquitin</subject><subject>Ubiquitin-specific proteinase</subject><subject>Ubiquitination</subject><subject>USP19</subject><subject>Viral infections</subject><subject>Viruses</subject><issn>1746-0913</issn><issn>1746-0921</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp1kMtLHTEUh0NR6qNddlsCbroZm5PHZLIU8aogWKwuS0hyz1wic2fGZLK4_31nuOpCcHUefOcH5yPkB7BzzkH_bre-4gx0xRirv5Bj0LKumOFw8N6DOCInOT8zphow8JUc8UYY0Fwek39Pf_-AobmMY8KcMdOAXVc6l-i0G5He0thPmFpMQ09z3PSui_2G-h2dXNrgtAyPDxcrQdsh0TUWH19KnNduikP_jRy2rsv4_bWekqfV1ePlTXV3f317eXFXBaFhqloulWCSyZpLABWCFEq51oPxRnl0zCvNtPRr0dTcBIamEejXWkGNjAEXp-TXPndMw0vBPNltzMsjrsehZAtNUwtZM1AzevYBfR5Kmt_KlgveaGGkXAKrPRXSkHPC1o4pbl3aWWB28W5n73bxbhfvM__zNbX4La7f6TfRM2D2QFumMpsOEfuAdj_NFzHEHj8J_w-6FI_a</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Gu, Zhiwen</creator><creator>Shi, Weifeng</creator><creator>Zhang, Li</creator><creator>Hu, Zhilin</creator><creator>Xu, Chao</creator><general>Future Medicine Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>EHMNL</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170701</creationdate><title>USP19 suppresses cellular type I interferon signaling by targeting TRAF3 for deubiquitination</title><author>Gu, Zhiwen ; Shi, Weifeng ; Zhang, Li ; Hu, Zhilin ; Xu, Chao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-f24530404624115cc4355afb19b95bea0b57074bd38629c0e983ebd7516e00123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>deubiquitinating enzyme</topic><topic>Deubiquitinating Enzymes - metabolism</topic><topic>Endopeptidases - genetics</topic><topic>Endopeptidases - metabolism</topic><topic>enterovirus 71</topic><topic>Enterovirus A, Human - immunology</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Glycerol</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Immune Evasion</topic><topic>Immune response</topic><topic>Immunity, Cellular</topic><topic>Immunity, Innate</topic><topic>Immunoglobulins</topic><topic>Infections</topic><topic>Interferon</topic><topic>Interferon Type I - antagonists & inhibitors</topic><topic>Interferon Type I - metabolism</topic><topic>Kinases</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Pattern recognition</topic><topic>Phosphatase</topic><topic>Plasmids</topic><topic>Protein Processing, Post-Translational</topic><topic>Proteins</topic><topic>Signal Transduction</topic><topic>TNF Receptor-Associated Factor 3 - genetics</topic><topic>TNF Receptor-Associated Factor 3 - metabolism</topic><topic>TRAF3</topic><topic>Tumor necrosis factor-TNF</topic><topic>type I interferon signaling</topic><topic>Ubiquitin</topic><topic>Ubiquitin-specific proteinase</topic><topic>Ubiquitination</topic><topic>USP19</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, Zhiwen</creatorcontrib><creatorcontrib>Shi, Weifeng</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Hu, Zhilin</creatorcontrib><creatorcontrib>Xu, Chao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>UK & Ireland Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Future microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gu, Zhiwen</au><au>Shi, Weifeng</au><au>Zhang, Li</au><au>Hu, Zhilin</au><au>Xu, Chao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>USP19 suppresses cellular type I interferon signaling by targeting TRAF3 for deubiquitination</atitle><jtitle>Future microbiology</jtitle><addtitle>Future Microbiol</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>12</volume><issue>9</issue><spage>767</spage><epage>779</epage><pages>767-779</pages><issn>1746-0913</issn><eissn>1746-0921</eissn><abstract>To investigate host factors that mediate the immune escape of enterovirus 71 (EV71) in the context of deubiquitinating enzymes.
Utilize PCR array to screen candidate genes that may be involved in EV71-induced cellular antiviral immune responses, and utilize protein mass spectrometry analysis to identify the functional targets of the candidate regulator.
EV71 infection induces the upregulation of ubiquitin-specific protease 19 (
) gene expression, which negatively regulates cellular antiviral type I interferon signaling. Additionally, we identify that USP19 suppresses cellular type I interferon signaling by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3) molecule and decreasing TRAF3 ubiquitination of K63-linkage.
This work suggests that USP19 is a previously unrecognized regulator employed by EV71 to evade host antiviral defenses.</abstract><cop>England</cop><pub>Future Medicine Ltd</pub><pmid>28391724</pmid><doi>10.2217/fmb-2017-0006</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1746-0913 |
| ispartof | Future microbiology, 2017-07, Vol.12 (9), p.767-779 |
| issn | 1746-0913 1746-0921 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1886346015 |
| source | PubMed Central |
| subjects | deubiquitinating enzyme Deubiquitinating Enzymes - metabolism Endopeptidases - genetics Endopeptidases - metabolism enterovirus 71 Enterovirus A, Human - immunology Gene expression Genomes Glycerol HEK293 Cells Humans Immune Evasion Immune response Immunity, Cellular Immunity, Innate Immunoglobulins Infections Interferon Interferon Type I - antagonists & inhibitors Interferon Type I - metabolism Kinases Mass spectrometry Mass spectroscopy Oligonucleotide Array Sequence Analysis Pattern recognition Phosphatase Plasmids Protein Processing, Post-Translational Proteins Signal Transduction TNF Receptor-Associated Factor 3 - genetics TNF Receptor-Associated Factor 3 - metabolism TRAF3 Tumor necrosis factor-TNF type I interferon signaling Ubiquitin Ubiquitin-specific proteinase Ubiquitination USP19 Viral infections Viruses |
| title | USP19 suppresses cellular type I interferon signaling by targeting TRAF3 for deubiquitination |
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