c-Fos regulates hepatitis C virus propagation
► In this study we identified c-Fos as a host factor involved in HCV propagation. ► We demonstrated that overexpression of c-Fos significantly increased HCV propagation. ► We showed that c-Fos level was upregulated by HCV infection. ► Collectively, we conclude that c-Fos acts as a positive regulator...
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| Veröffentlicht in: | FEBS letters 2011-10, Vol.585 (20), p.3236-3244 |
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| creator | Kang, Sang-Min Lim, Seri Won, Seung-Jae Shin, Ye-Jin Lim, Yun-Sook Ahn, Byung-Yoon Hwang, Soon B. |
| description | ► In this study we identified c-Fos as a host factor involved in HCV propagation. ► We demonstrated that overexpression of c-Fos significantly increased HCV propagation. ► We showed that c-Fos level was upregulated by HCV infection. ► Collectively, we conclude that c-Fos acts as a positive regulator of HCV propagation.
Hepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non-structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c-Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c-Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)-infected cells; whereas overexpression of c-Fos significantly increased HCV propagation. We further confirmed the positive role of c-Fos in HCV propagation by both HCV-luciferase reporter assay and immunofluorescence analysis. We showed that c-Fos level was upregulated by HCV infection. Furthermore, phorbol 12-myristate 13-acetate (PMA)-induced c-Fos level was synergistically increased by HCV infection. These data suggest that c-Fos acts as a positive regulator of HCV propagation and may contribute to HCV-associated pathogenesis. |
| doi_str_mv | 10.1016/j.febslet.2011.08.041 |
| format | Article |
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Hepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non-structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c-Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c-Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)-infected cells; whereas overexpression of c-Fos significantly increased HCV propagation. We further confirmed the positive role of c-Fos in HCV propagation by both HCV-luciferase reporter assay and immunofluorescence analysis. We showed that c-Fos level was upregulated by HCV infection. Furthermore, phorbol 12-myristate 13-acetate (PMA)-induced c-Fos level was synergistically increased by HCV infection. These data suggest that c-Fos acts as a positive regulator of HCV propagation and may contribute to HCV-associated pathogenesis.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2011.08.041</identifier><identifier>PMID: 21920361</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide ; activator protein 1 ; AP-1 ; c-Fos ; Carcinogens - pharmacology ; Cell Line ; Cellular factor ; GFP ; green fluorescence protein ; HCV ; Hepacivirus - physiology ; Hepatitis C - genetics ; Hepatitis C - metabolism ; Hepatitis C virus ; Humans ; IFN-β ; interferon-beta ; MTT ; non-structural protein ; NS protein ; Pathogenesis ; phorbol 12-myristate 13-acetate ; PMA ; Propagation ; Proto-Oncogene Proteins c-fos - biosynthesis ; Proto-Oncogene Proteins c-fos - genetics ; RNA, Viral - biosynthesis ; RNA, Viral - genetics ; Tetradecanoylphorbol Acetate - pharmacology ; tetramethylrhodamine isothiocyanate ; TRITC ; Up-Regulation ; Virus Replication - drug effects ; Virus Replication - physiology</subject><ispartof>FEBS letters, 2011-10, Vol.585 (20), p.3236-3244</ispartof><rights>2011 Federation of European Biochemical Societies</rights><rights>FEBS Letters 585 (2011) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><rights>Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5080-6e616ccfc6f409a0333c5b6c0b308a62ea15bb219b68a6636d6cd3c6380556133</citedby><cites>FETCH-LOGICAL-c5080-6e616ccfc6f409a0333c5b6c0b308a62ea15bb219b68a6636d6cd3c6380556133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2011.08.041$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014579311006430$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,1427,3537,27901,27902,45550,45551,46384,46808,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21920361$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kang, Sang-Min</creatorcontrib><creatorcontrib>Lim, Seri</creatorcontrib><creatorcontrib>Won, Seung-Jae</creatorcontrib><creatorcontrib>Shin, Ye-Jin</creatorcontrib><creatorcontrib>Lim, Yun-Sook</creatorcontrib><creatorcontrib>Ahn, Byung-Yoon</creatorcontrib><creatorcontrib>Hwang, Soon B.</creatorcontrib><title>c-Fos regulates hepatitis C virus propagation</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>► In this study we identified c-Fos as a host factor involved in HCV propagation. ► We demonstrated that overexpression of c-Fos significantly increased HCV propagation. ► We showed that c-Fos level was upregulated by HCV infection. ► Collectively, we conclude that c-Fos acts as a positive regulator of HCV propagation.
Hepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non-structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c-Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c-Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)-infected cells; whereas overexpression of c-Fos significantly increased HCV propagation. We further confirmed the positive role of c-Fos in HCV propagation by both HCV-luciferase reporter assay and immunofluorescence analysis. We showed that c-Fos level was upregulated by HCV infection. Furthermore, phorbol 12-myristate 13-acetate (PMA)-induced c-Fos level was synergistically increased by HCV infection. These data suggest that c-Fos acts as a positive regulator of HCV propagation and may contribute to HCV-associated pathogenesis.</description><subject>3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide</subject><subject>activator protein 1</subject><subject>AP-1</subject><subject>c-Fos</subject><subject>Carcinogens - pharmacology</subject><subject>Cell Line</subject><subject>Cellular factor</subject><subject>GFP</subject><subject>green fluorescence protein</subject><subject>HCV</subject><subject>Hepacivirus - physiology</subject><subject>Hepatitis C - genetics</subject><subject>Hepatitis C - metabolism</subject><subject>Hepatitis C virus</subject><subject>Humans</subject><subject>IFN-β</subject><subject>interferon-beta</subject><subject>MTT</subject><subject>non-structural protein</subject><subject>NS protein</subject><subject>Pathogenesis</subject><subject>phorbol 12-myristate 13-acetate</subject><subject>PMA</subject><subject>Propagation</subject><subject>Proto-Oncogene Proteins c-fos - biosynthesis</subject><subject>Proto-Oncogene Proteins c-fos - genetics</subject><subject>RNA, Viral - biosynthesis</subject><subject>RNA, Viral - genetics</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>tetramethylrhodamine isothiocyanate</subject><subject>TRITC</subject><subject>Up-Regulation</subject><subject>Virus Replication - drug effects</subject><subject>Virus Replication - physiology</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFO3DAQhq0KVBboI4By6ynpTOzMOidEVyxUQuLQcrYcZ0K9ym62dgLi7fFqt1zhZI31zT-jb4S4QCgQkH6sio6b2PNYlIBYgC5A4RcxQz2XuVSkj8QMAFVezWt5Ik5jXEGqNdZfxUmJdQmScCZyly-HmAV-mno7csz-8taOfvQxW2TPPkwx24Zha5_S57A5F8ed7SN_O7xn4nF582dxl98_3P5aXN_nrgINOTEhOdc56hTUFqSUrmrIQSNBWyrZYtU0aYmGUkmSWnKtdCQ1VBWhlGfi-z43zf43cRzN2kfHfW83PEzR1KCULudIH5K61lqVpMpEVnvShSHGwJ3ZBr-24dUgmJ1SszIHpWan1IA2SWnquzxMmJo1t-9d_x0m4G4PvPieXz-XapY3P8vfu_vszoMIQEpCirraR3GS--w5mOg8bxy3PrAbTTv4D7Z9A_ngnUg</recordid><startdate>20111020</startdate><enddate>20111020</enddate><creator>Kang, Sang-Min</creator><creator>Lim, Seri</creator><creator>Won, Seung-Jae</creator><creator>Shin, Ye-Jin</creator><creator>Lim, Yun-Sook</creator><creator>Ahn, Byung-Yoon</creator><creator>Hwang, Soon B.</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20111020</creationdate><title>c-Fos regulates hepatitis C virus propagation</title><author>Kang, Sang-Min ; Lim, Seri ; Won, Seung-Jae ; Shin, Ye-Jin ; Lim, Yun-Sook ; Ahn, Byung-Yoon ; Hwang, Soon B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5080-6e616ccfc6f409a0333c5b6c0b308a62ea15bb219b68a6636d6cd3c6380556133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide</topic><topic>activator protein 1</topic><topic>AP-1</topic><topic>c-Fos</topic><topic>Carcinogens - pharmacology</topic><topic>Cell Line</topic><topic>Cellular factor</topic><topic>GFP</topic><topic>green fluorescence protein</topic><topic>HCV</topic><topic>Hepacivirus - physiology</topic><topic>Hepatitis C - genetics</topic><topic>Hepatitis C - metabolism</topic><topic>Hepatitis C virus</topic><topic>Humans</topic><topic>IFN-β</topic><topic>interferon-beta</topic><topic>MTT</topic><topic>non-structural protein</topic><topic>NS protein</topic><topic>Pathogenesis</topic><topic>phorbol 12-myristate 13-acetate</topic><topic>PMA</topic><topic>Propagation</topic><topic>Proto-Oncogene Proteins c-fos - biosynthesis</topic><topic>Proto-Oncogene Proteins c-fos - genetics</topic><topic>RNA, Viral - biosynthesis</topic><topic>RNA, Viral - genetics</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>tetramethylrhodamine isothiocyanate</topic><topic>TRITC</topic><topic>Up-Regulation</topic><topic>Virus Replication - drug effects</topic><topic>Virus Replication - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kang, Sang-Min</creatorcontrib><creatorcontrib>Lim, Seri</creatorcontrib><creatorcontrib>Won, Seung-Jae</creatorcontrib><creatorcontrib>Shin, Ye-Jin</creatorcontrib><creatorcontrib>Lim, Yun-Sook</creatorcontrib><creatorcontrib>Ahn, Byung-Yoon</creatorcontrib><creatorcontrib>Hwang, Soon B.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kang, Sang-Min</au><au>Lim, Seri</au><au>Won, Seung-Jae</au><au>Shin, Ye-Jin</au><au>Lim, Yun-Sook</au><au>Ahn, Byung-Yoon</au><au>Hwang, Soon B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-Fos regulates hepatitis C virus propagation</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2011-10-20</date><risdate>2011</risdate><volume>585</volume><issue>20</issue><spage>3236</spage><epage>3244</epage><pages>3236-3244</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>► In this study we identified c-Fos as a host factor involved in HCV propagation. ► We demonstrated that overexpression of c-Fos significantly increased HCV propagation. ► We showed that c-Fos level was upregulated by HCV infection. ► Collectively, we conclude that c-Fos acts as a positive regulator of HCV propagation.
Hepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non-structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c-Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c-Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)-infected cells; whereas overexpression of c-Fos significantly increased HCV propagation. We further confirmed the positive role of c-Fos in HCV propagation by both HCV-luciferase reporter assay and immunofluorescence analysis. We showed that c-Fos level was upregulated by HCV infection. Furthermore, phorbol 12-myristate 13-acetate (PMA)-induced c-Fos level was synergistically increased by HCV infection. These data suggest that c-Fos acts as a positive regulator of HCV propagation and may contribute to HCV-associated pathogenesis.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>21920361</pmid><doi>10.1016/j.febslet.2011.08.041</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elsevier ScienceDirect Journals; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide activator protein 1 AP-1 c-Fos Carcinogens - pharmacology Cell Line Cellular factor GFP green fluorescence protein HCV Hepacivirus - physiology Hepatitis C - genetics Hepatitis C - metabolism Hepatitis C virus Humans IFN-β interferon-beta MTT non-structural protein NS protein Pathogenesis phorbol 12-myristate 13-acetate PMA Propagation Proto-Oncogene Proteins c-fos - biosynthesis Proto-Oncogene Proteins c-fos - genetics RNA, Viral - biosynthesis RNA, Viral - genetics Tetradecanoylphorbol Acetate - pharmacology tetramethylrhodamine isothiocyanate TRITC Up-Regulation Virus Replication - drug effects Virus Replication - physiology |
| title | c-Fos regulates hepatitis C virus propagation |
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