Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.
Identifieur interne : 001663 ( Ncbi/Merge ); précédent : 001662; suivant : 001664Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.
Auteurs : Xiao-Nan Zhang [République populaire de Chine] ; Jiang-Xia Liu ; Yun-Wen Hu ; Hui Chen ; Zheng-Hong YuanSource :
- Biochimica et biophysica acta [ 0006-3002 ]
Descripteurs français
- KwdFr :
- Carcinome hépatocellulaire (génétique), Carcinome hépatocellulaire (métabolisme), Dimérisation, Expression des gènes (), Facteur de transcription STAT-1 (), Facteur de transcription STAT-1 (métabolisme), Facteur-1 de régulation d'interféron (antagonistes et inhibiteurs), Facteur-1 de régulation d'interféron (génétique), Facteur-1 de régulation d'interféron (métabolisme), Humains, Interféron de type I (pharmacologie), Interféron gamma (pharmacologie), Lignée cellulaire tumorale, Petit ARN interférent (génétique), Phosphorylation, Protéines proto-oncogènes c-bcl-2 (génétique), Protéines recombinantes, Régions promotrices (génétique), Séquence nucléotidique, Transfection, Tumeurs du foie (génétique), Tumeurs du foie (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Facteur-1 de régulation d'interféron.
- génétique : Carcinome hépatocellulaire, Facteur-1 de régulation d'interféron, Petit ARN interférent, Protéines proto-oncogènes c-bcl-2, Tumeurs du foie.
- métabolisme : Carcinome hépatocellulaire, Facteur de transcription STAT-1, Facteur-1 de régulation d'interféron, Tumeurs du foie.
- pharmacologie : Interféron de type I, Interféron gamma.
- Dimérisation, Expression des gènes, Facteur de transcription STAT-1, Humains, Lignée cellulaire tumorale, Phosphorylation, Protéines recombinantes, Régions promotrices (génétique), Séquence nucléotidique, Transfection.
English descriptors
- KwdEn :
- Base Sequence, Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (metabolism), Cell Line, Tumor, Dimerization, Gene Expression (drug effects), Humans, Interferon Regulatory Factor-1 (antagonists & inhibitors), Interferon Regulatory Factor-1 (genetics), Interferon Regulatory Factor-1 (metabolism), Interferon Type I (pharmacology), Interferon-gamma (pharmacology), Liver Neoplasms (genetics), Liver Neoplasms (metabolism), Phosphorylation, Promoter Regions, Genetic, Proto-Oncogene Proteins c-bcl-2 (genetics), RNA, Small Interfering (genetics), Recombinant Proteins, STAT1 Transcription Factor (chemistry), STAT1 Transcription Factor (metabolism), Transfection.
- MESH :
- chemical , antagonists & inhibitors : Interferon Regulatory Factor-1.
- chemical , chemistry : STAT1 Transcription Factor.
- drug effects : Gene Expression.
- genetics : Carcinoma, Hepatocellular, Interferon Regulatory Factor-1, Liver Neoplasms, Proto-Oncogene Proteins c-bcl-2, RNA, Small Interfering.
- metabolism : Carcinoma, Hepatocellular, Interferon Regulatory Factor-1, Liver Neoplasms, STAT1 Transcription Factor.
- chemical , pharmacology : Interferon Type I, Interferon-gamma.
- Base Sequence, Cell Line, Tumor, Dimerization, Humans, Phosphorylation, Promoter Regions, Genetic, Recombinant Proteins, Transfection.
Abstract
Previous reports suggest that type I and type II Interferon can co-operatively inhibit some virus replication, e.g. HCV, SARS-CoV, HSV-1. To find out the molecular mechanism underlying this phenomenon, we analyzed the transcription profile stimulated by IFN-alpha and IFN-gamma in Huh-7 cells and found that the transcription of a subset of IFN stimulated genes (ISGs) including BclG, XAF1, TRAIL and TAP1 was enhanced when IFN-alpha and gamma were both present. Promoter analysis of BclG revealed that IRF-1 and STAT1 were both required in this process. Enhanced IRF-1/DNA complex formation was observed in interferon co-treatment group by gel shift analysis. Furthermore, IRF-1 activation was found to be generally required in this cluster of ISGs. STAT1 tyrosine phosphorylation was elevated by IFN combination treatment, however, only the hyper-transactivation of GAS but not ISRE was observed. In conclusion, hyper-activation of IRF-1 and elevated STAT1 dimer formation may be two general switches which contribute to a much more robust antiviral symphony against virus replication when type I and type II IFNs are co-administered.
DOI: 10.1016/j.bbaexp.2006.08.003
PubMed: 16987558
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To find out the molecular mechanism underlying this phenomenon, we analyzed the transcription profile stimulated by IFN-alpha and IFN-gamma in Huh-7 cells and found that the transcription of a subset of IFN stimulated genes (ISGs) including BclG, XAF1, TRAIL and TAP1 was enhanced when IFN-alpha and gamma were both present. Promoter analysis of BclG revealed that IRF-1 and STAT1 were both required in this process. Enhanced IRF-1/DNA complex formation was observed in interferon co-treatment group by gel shift analysis. Furthermore, IRF-1 activation was found to be generally required in this cluster of ISGs. STAT1 tyrosine phosphorylation was elevated by IFN combination treatment, however, only the hyper-transactivation of GAS but not ISRE was observed. In conclusion, hyper-activation of IRF-1 and elevated STAT1 dimer formation may be two general switches which contribute to a much more robust antiviral symphony against virus replication when type I and type II IFNs are co-administered.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16987558</PMID><DateCompleted><Year>2006</Year><Month>11</Month><Day>20</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>1759</Volume><Issue>8-9</Issue><PubDate><MedlineDate>2006 Aug-Sep</MedlineDate></PubDate></JournalIssue><Title>Biochimica et biophysica acta</Title><ISOAbbreviation>Biochim. Biophys. Acta</ISOAbbreviation></Journal><ArticleTitle>Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.</ArticleTitle><Pagination><MedlinePgn>417-25</MedlinePgn></Pagination><Abstract><AbstractText>Previous reports suggest that type I and type II Interferon can co-operatively inhibit some virus replication, e.g. HCV, SARS-CoV, HSV-1. To find out the molecular mechanism underlying this phenomenon, we analyzed the transcription profile stimulated by IFN-alpha and IFN-gamma in Huh-7 cells and found that the transcription of a subset of IFN stimulated genes (ISGs) including BclG, XAF1, TRAIL and TAP1 was enhanced when IFN-alpha and gamma were both present. Promoter analysis of BclG revealed that IRF-1 and STAT1 were both required in this process. Enhanced IRF-1/DNA complex formation was observed in interferon co-treatment group by gel shift analysis. Furthermore, IRF-1 activation was found to be generally required in this cluster of ISGs. STAT1 tyrosine phosphorylation was elevated by IFN combination treatment, however, only the hyper-transactivation of GAS but not ISRE was observed. In conclusion, hyper-activation of IRF-1 and elevated STAT1 dimer formation may be two general switches which contribute to a much more robust antiviral symphony against virus replication when type I and type II IFNs are co-administered.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiao-Nan</ForeName><Initials>XN</Initials><AffiliationInfo><Affiliation>Key Laboratory of Medical Molecular Virology, Institute of Microbiology and Biomedical Sciences, Shanghai Medical College, Fudan University, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jiang-Xia</ForeName><Initials>JX</Initials></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yun-Wen</ForeName><Initials>YW</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hui</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Zheng-Hong</ForeName><Initials>ZH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta</MedlineTA><NlmUniqueID>0217513</NlmUniqueID><ISSNLinking>0006-3002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C428448">BCL2L14 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050856">Interferon Regulatory Factor-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene 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MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019281" MajorTopicYN="N">Dimerization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050856" MajorTopicYN="N">Interferon Regulatory Factor-1</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007370" MajorTopicYN="N">Interferon Type I</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008113" MajorTopicYN="N">Liver Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050794" MajorTopicYN="N">STAT1 Transcription Factor</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>05</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2006</Year><Month>07</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>08</Month><Day>10</Day></PubMedPubDate><PubMedPubDate 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IdType="pubmed">9759489</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2004 Mar 26;279(13):12232-41</Citation><ArticleIdList><ArticleId IdType="pubmed">14709551</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Eur J Biochem. 2003 Oct;270(20):4052-8</Citation><ArticleIdList><ArticleId IdType="pubmed">14519116</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Immunol. 2002 Feb 1;168(3):1356-61</Citation><ArticleIdList><ArticleId IdType="pubmed">11801676</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>EMBO J. 2002 Mar 1;21(5):954-65</Citation><ArticleIdList><ArticleId IdType="pubmed">11867523</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Annu Rev Immunol. 2001;19:623-55</Citation><ArticleIdList><ArticleId IdType="pubmed">11244049</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2001 Jan 26;276(4):2780-5</Citation><ArticleIdList><ArticleId IdType="pubmed">11054413</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2002 Aug 9;277(32):28504-11</Citation><ArticleIdList><ArticleId IdType="pubmed">12029096</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4650-5</Citation><ArticleIdList><ArticleId IdType="pubmed">11904369</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Genes Immun. 2004 Jan;5(1):26-35</Citation><ArticleIdList><ArticleId IdType="pubmed">14735146</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Med Virol. 1991 Sep;35(1):32-7</Citation><ArticleIdList><ArticleId IdType="pubmed">1940881</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nat Cell Biol. 2001 Feb;3(2):128-33</Citation><ArticleIdList><ArticleId IdType="pubmed">11175744</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2002 Mar 15;277(11):9103-11</Citation><ArticleIdList><ArticleId IdType="pubmed">11781315</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Med Virol. 2003 Feb;69(2):188-94</Citation><ArticleIdList><ArticleId IdType="pubmed">12683406</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Apoptosis. 2003 Jun;8(3):237-49</Citation><ArticleIdList><ArticleId IdType="pubmed">12766484</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Interferon Cytokine Res. 2002 Jan;22(1):5-14</Citation><ArticleIdList><ArticleId IdType="pubmed">11846971</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Viral Hepat. 2001 May;8(3):180-5</Citation><ArticleIdList><ArticleId IdType="pubmed">11380795</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Virology. 2004 Nov 10;329(1):11-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15476870</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nature. 1986 Jul 3-9;322(6074):32-8</Citation><ArticleIdList><ArticleId IdType="pubmed">2425263</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Virol. 1999 Aug;73(8):6506-16</Citation><ArticleIdList><ArticleId IdType="pubmed">10400746</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Genes Cells. 1998 Jan;3(1):29-37</Citation><ArticleIdList><ArticleId IdType="pubmed">9581980</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Interferon Cytokine Res. 2003 May;23(5):247-57</Citation><ArticleIdList><ArticleId IdType="pubmed">12804067</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Cytokine Growth Factor Rev. 2002 Dec;13(6):441-54</Citation><ArticleIdList><ArticleId IdType="pubmed">12401479</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Virol. 2000 Feb;74(3):1513-23</Citation><ArticleIdList><ArticleId IdType="pubmed">10627563</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Cell Death Differ. 2001 Feb;8(2):113-26</Citation><ArticleIdList><ArticleId IdType="pubmed">11313713</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Antiviral Res. 2005 Jan;65(1):23-34</Citation><ArticleIdList><ArticleId IdType="pubmed">15652968</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Virol. 2002 Nov;76(22):11541-50</Citation><ArticleIdList><ArticleId IdType="pubmed">12388715</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nat Rev Immunol. 2005 May;5(5):375-86</Citation><ArticleIdList><ArticleId IdType="pubmed">15864272</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Virol. 2004 Sep;78(18):9713-20</Citation><ArticleIdList><ArticleId IdType="pubmed">15331704</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Science. 2000 Jun 30;288(5475):2357-60</Citation><ArticleIdList><ArticleId IdType="pubmed">10875919</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Annu Rev Immunol. 2001;19:65-91</Citation><ArticleIdList><ArticleId IdType="pubmed">11244031</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Virol J. 2005 Feb 23;2:14</Citation><ArticleIdList><ArticleId IdType="pubmed">15727684</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>EMBO J. 2004 Aug 4;23(15):3051-60</Citation><ArticleIdList><ArticleId IdType="pubmed">15241475</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nat Immunol. 2004 Nov;5(11):1181-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15467722</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>N Engl J Med. 1997 Dec 11;337(24):1733-45</Citation><ArticleIdList><ArticleId IdType="pubmed">9392700</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Chen, Hui" sort="Chen, Hui" uniqKey="Chen H" first="Hui" last="Chen">Hui Chen</name><name sortKey="Hu, Yun Wen" sort="Hu, Yun Wen" uniqKey="Hu Y" first="Yun-Wen" last="Hu">Yun-Wen Hu</name><name sortKey="Liu, Jiang Xia" sort="Liu, Jiang Xia" uniqKey="Liu J" first="Jiang-Xia" last="Liu">Jiang-Xia Liu</name><name sortKey="Yuan, Zheng Hong" sort="Yuan, Zheng Hong" uniqKey="Yuan Z" first="Zheng-Hong" last="Yuan">Zheng-Hong Yuan</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Xiao Nan" sort="Zhang, Xiao Nan" uniqKey="Zhang X" first="Xiao-Nan" last="Zhang">Xiao-Nan Zhang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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