Grb3-3 Is Up-regulated in HIV-1-infected T-cells and Can Potentiate Cell Activation through NFATc
The MAPK pathway is required for T-cell activation; however, its role in modulating T-cell function following human immunodeficiency virus type 1 (HIV-1) infection is poorly understood. In this report, we investigated whether Grb3-3, an isoform of the Grb2 (growth factorreceptor-bound protein-2) ada...
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| Veröffentlicht in: | The Journal of biological chemistry 2000-10, Vol.275 (40), p.30925-30933 |
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| creator | Li, Xuguang Multon, Marie-Christine Henin, Yvette Schweighoffer, Fabien Venot, Corinne Josef, Juliana Zhou, Changhong LaVecchio, Joyce Stuckert, Patricia Raab, Monika Mhashilkar, Abner Tocqué, Bruno Marasco, Wayne A. |
| description | The MAPK pathway is required for T-cell activation; however, its role in modulating T-cell function following human immunodeficiency virus type 1 (HIV-1) infection is poorly understood. In this report, we investigated whether Grb3-3, an isoform of the Grb2 (growth factorreceptor-bound protein-2) adaptor molecule that is associated with the MAPK pathway, could be involved. We found that Grb3-3, but not its isoform Grb2, is markedly up-regulated in CD4+ peripheral blood mononuclear cells derived from either in vitro HIV-1-infected cultures or HIV-1-infected human subjects. Analysis of HIV-1 gene products indicated that Tat and Nef, both of which have been implicated in modulating T-cell function, can independently induce expression of Grb3-3. By using NFAT/AP-1, AP-1, or NFAT reporter assays, we found that Grb3-3 can potentiate NFAT (but not AP-1) promoter activity in Jurkat T-cells upon engagement of the T-cell receptor and CD28 co-receptor. In addition, potentiation of NFAT by Grb3-3 is substantially suppressed by MEKK1, a kinase that may play an important role in retaining NFAT in the cytoplasm, and by cyclosporin A. Finally, we also found that Grb3-3 potentiates HIV-1 long terminal (LTR) repeat promoter activity following T-cell receptor stimulation, an effect that can be largely suppressed by cyclosporin A. Taken together, this study indicates that Grb3-3 is a cellular factor that can be up-regulated by HIV-1. In addition, Grb3-3 can also function as a positive factor for T-cell activation and, in doing so, may aid in establishing an intracellular environment that can optimally support HIV-1 replication. |
| doi_str_mv | 10.1074/jbc.M005535200 |
| format | Article |
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In this report, we investigated whether Grb3-3, an isoform of the Grb2 (growth factorreceptor-bound protein-2) adaptor molecule that is associated with the MAPK pathway, could be involved. We found that Grb3-3, but not its isoform Grb2, is markedly up-regulated in CD4+ peripheral blood mononuclear cells derived from either in vitro HIV-1-infected cultures or HIV-1-infected human subjects. Analysis of HIV-1 gene products indicated that Tat and Nef, both of which have been implicated in modulating T-cell function, can independently induce expression of Grb3-3. By using NFAT/AP-1, AP-1, or NFAT reporter assays, we found that Grb3-3 can potentiate NFAT (but not AP-1) promoter activity in Jurkat T-cells upon engagement of the T-cell receptor and CD28 co-receptor. In addition, potentiation of NFAT by Grb3-3 is substantially suppressed by MEKK1, a kinase that may play an important role in retaining NFAT in the cytoplasm, and by cyclosporin A. Finally, we also found that Grb3-3 potentiates HIV-1 long terminal (LTR) repeat promoter activity following T-cell receptor stimulation, an effect that can be largely suppressed by cyclosporin A. Taken together, this study indicates that Grb3-3 is a cellular factor that can be up-regulated by HIV-1. In addition, Grb3-3 can also function as a positive factor for T-cell activation and, in doing so, may aid in establishing an intracellular environment that can optimally support HIV-1 replication.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M005535200</identifier><identifier>PMID: 10906142</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; Adult ; Antibodies, Monoclonal - metabolism ; Blotting, Western ; CD28 Antigens - metabolism ; CD4 antigen ; CD4-Positive T-Lymphocytes - metabolism ; CD4-Positive T-Lymphocytes - virology ; Cell Nucleus - metabolism ; Cyclosporine - pharmacology ; Cytoplasm - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Female ; Gene Products, nef - metabolism ; Gene Products, tat - metabolism ; GRB2 Adaptor Protein ; Grb3-3 protein ; HIV Infections - metabolism ; HIV-1 - metabolism ; human immunodeficiency virus 1 ; Humans ; Immunosuppressive Agents - pharmacology ; Jurkat Cells ; Leukocytes, Mononuclear - virology ; Luciferases - metabolism ; Male ; MAP Kinase Kinase Kinase 1 ; MAP Kinase Signaling System ; Middle Aged ; nef Gene Products, Human Immunodeficiency Virus ; NF-AT protein ; NFATC Transcription Factors ; Nuclear Proteins ; Plasmids - metabolism ; Promoter Regions, Genetic ; Protein Isoforms ; Protein-Serine-Threonine Kinases - metabolism ; Proteins - chemistry ; Proteins - genetics ; Proteins - metabolism ; Receptors, Antigen, T-Cell - metabolism ; RNA, Messenger - metabolism ; Signal Transduction ; tat Gene Products, Human Immunodeficiency Virus ; Terminal Repeat Sequences ; Time Factors ; Transcription Factor AP-1 - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transfection ; Up-Regulation</subject><ispartof>The Journal of biological chemistry, 2000-10, Vol.275 (40), p.30925-30933</ispartof><rights>2000 © 2000 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-159361429b92d70a8cf4e60ad3cb56a94baf07c139396b03bbccdc52c42b2d333</citedby><cites>FETCH-LOGICAL-c440t-159361429b92d70a8cf4e60ad3cb56a94baf07c139396b03bbccdc52c42b2d333</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/10906142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xuguang</creatorcontrib><creatorcontrib>Multon, Marie-Christine</creatorcontrib><creatorcontrib>Henin, Yvette</creatorcontrib><creatorcontrib>Schweighoffer, Fabien</creatorcontrib><creatorcontrib>Venot, Corinne</creatorcontrib><creatorcontrib>Josef, Juliana</creatorcontrib><creatorcontrib>Zhou, Changhong</creatorcontrib><creatorcontrib>LaVecchio, Joyce</creatorcontrib><creatorcontrib>Stuckert, Patricia</creatorcontrib><creatorcontrib>Raab, Monika</creatorcontrib><creatorcontrib>Mhashilkar, Abner</creatorcontrib><creatorcontrib>Tocqué, Bruno</creatorcontrib><creatorcontrib>Marasco, Wayne A.</creatorcontrib><title>Grb3-3 Is Up-regulated in HIV-1-infected T-cells and Can Potentiate Cell Activation through NFATc</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>The MAPK pathway is required for T-cell activation; however, its role in modulating T-cell function following human immunodeficiency virus type 1 (HIV-1) infection is poorly understood. In this report, we investigated whether Grb3-3, an isoform of the Grb2 (growth factorreceptor-bound protein-2) adaptor molecule that is associated with the MAPK pathway, could be involved. We found that Grb3-3, but not its isoform Grb2, is markedly up-regulated in CD4+ peripheral blood mononuclear cells derived from either in vitro HIV-1-infected cultures or HIV-1-infected human subjects. Analysis of HIV-1 gene products indicated that Tat and Nef, both of which have been implicated in modulating T-cell function, can independently induce expression of Grb3-3. By using NFAT/AP-1, AP-1, or NFAT reporter assays, we found that Grb3-3 can potentiate NFAT (but not AP-1) promoter activity in Jurkat T-cells upon engagement of the T-cell receptor and CD28 co-receptor. In addition, potentiation of NFAT by Grb3-3 is substantially suppressed by MEKK1, a kinase that may play an important role in retaining NFAT in the cytoplasm, and by cyclosporin A. Finally, we also found that Grb3-3 potentiates HIV-1 long terminal (LTR) repeat promoter activity following T-cell receptor stimulation, an effect that can be largely suppressed by cyclosporin A. Taken together, this study indicates that Grb3-3 is a cellular factor that can be up-regulated by HIV-1. In addition, Grb3-3 can also function as a positive factor for T-cell activation and, in doing so, may aid in establishing an intracellular environment that can optimally support HIV-1 replication.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Adult</subject><subject>Antibodies, Monoclonal - metabolism</subject><subject>Blotting, Western</subject><subject>CD28 Antigens - metabolism</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD4-Positive T-Lymphocytes - virology</subject><subject>Cell Nucleus - metabolism</subject><subject>Cyclosporine - pharmacology</subject><subject>Cytoplasm - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Gene Products, nef - metabolism</subject><subject>Gene Products, tat - metabolism</subject><subject>GRB2 Adaptor Protein</subject><subject>Grb3-3 protein</subject><subject>HIV Infections - metabolism</subject><subject>HIV-1 - metabolism</subject><subject>human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Jurkat Cells</subject><subject>Leukocytes, Mononuclear - virology</subject><subject>Luciferases - metabolism</subject><subject>Male</subject><subject>MAP Kinase Kinase Kinase 1</subject><subject>MAP Kinase Signaling System</subject><subject>Middle Aged</subject><subject>nef Gene Products, Human Immunodeficiency Virus</subject><subject>NF-AT protein</subject><subject>NFATC Transcription Factors</subject><subject>Nuclear Proteins</subject><subject>Plasmids - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Isoforms</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proteins - chemistry</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>tat Gene Products, Human Immunodeficiency Virus</subject><subject>Terminal Repeat Sequences</subject><subject>Time Factors</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transfection</subject><subject>Up-Regulation</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctvEzEQhy1ERUPLlSPyAXFzGL-y8TGK-ohUaA8p4mb5tVlXyW6wvUX89zjaSnBBzMXSzDejnz4j9J7CnEIjPj9ZN_8CICWXDOAVmlFYcsIl_f4azQAYJYrJ5Tl6m_MT1BKKvkHnFBQsqGAzZG6SrTzeZPx4JCnsxr0pwePY49vNN0JJ7NvgTp0tcWG_z9j0Hq9Njx-GEvoSK43XdYBXrsRnU-LQ49KlYdx1-Ov1ausu0Vlr9jm8e3kv0OP11XZ9S-7ubzbr1R1xQkAhVCp-iqSsYr4Bs3StCAswnjsrF0YJa1poHOWKq4UFbq1z3knmBLPMc84v0Kfp7jENP8aQiz7EfIps-jCMWTeMV0_wf5A2DaNARQXnE-jSkHMKrT6meDDpl6agT_Z1ta__2K8LH14uj_YQ_F_4pLsCHyegi7vuZ0xB2zi4Lhw0a6QWoDnU76rYcsJC9fUcQ9LZxdC74OuKK9oP8V8RfgOq1pv8</recordid><startdate>20001006</startdate><enddate>20001006</enddate><creator>Li, Xuguang</creator><creator>Multon, Marie-Christine</creator><creator>Henin, Yvette</creator><creator>Schweighoffer, Fabien</creator><creator>Venot, Corinne</creator><creator>Josef, Juliana</creator><creator>Zhou, Changhong</creator><creator>LaVecchio, Joyce</creator><creator>Stuckert, Patricia</creator><creator>Raab, Monika</creator><creator>Mhashilkar, Abner</creator><creator>Tocqué, Bruno</creator><creator>Marasco, Wayne A.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20001006</creationdate><title>Grb3-3 Is Up-regulated in HIV-1-infected T-cells and Can Potentiate Cell Activation through NFATc</title><author>Li, Xuguang ; Multon, Marie-Christine ; Henin, Yvette ; Schweighoffer, Fabien ; Venot, Corinne ; Josef, Juliana ; Zhou, Changhong ; LaVecchio, Joyce ; Stuckert, Patricia ; Raab, Monika ; Mhashilkar, Abner ; Tocqué, Bruno ; Marasco, Wayne A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-159361429b92d70a8cf4e60ad3cb56a94baf07c139396b03bbccdc52c42b2d333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Adult</topic><topic>Antibodies, Monoclonal - metabolism</topic><topic>Blotting, Western</topic><topic>CD28 Antigens - metabolism</topic><topic>CD4 antigen</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>CD4-Positive T-Lymphocytes - virology</topic><topic>Cell Nucleus - metabolism</topic><topic>Cyclosporine - pharmacology</topic><topic>Cytoplasm - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Gene Products, nef - metabolism</topic><topic>Gene Products, tat - metabolism</topic><topic>GRB2 Adaptor Protein</topic><topic>Grb3-3 protein</topic><topic>HIV Infections - metabolism</topic><topic>HIV-1 - metabolism</topic><topic>human immunodeficiency virus 1</topic><topic>Humans</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Jurkat Cells</topic><topic>Leukocytes, Mononuclear - virology</topic><topic>Luciferases - metabolism</topic><topic>Male</topic><topic>MAP Kinase Kinase Kinase 1</topic><topic>MAP Kinase Signaling System</topic><topic>Middle Aged</topic><topic>nef Gene Products, Human Immunodeficiency Virus</topic><topic>NF-AT protein</topic><topic>NFATC Transcription Factors</topic><topic>Nuclear Proteins</topic><topic>Plasmids - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Isoforms</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proteins - chemistry</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>tat Gene Products, Human Immunodeficiency Virus</topic><topic>Terminal Repeat Sequences</topic><topic>Time Factors</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transfection</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xuguang</creatorcontrib><creatorcontrib>Multon, Marie-Christine</creatorcontrib><creatorcontrib>Henin, Yvette</creatorcontrib><creatorcontrib>Schweighoffer, Fabien</creatorcontrib><creatorcontrib>Venot, Corinne</creatorcontrib><creatorcontrib>Josef, Juliana</creatorcontrib><creatorcontrib>Zhou, Changhong</creatorcontrib><creatorcontrib>LaVecchio, Joyce</creatorcontrib><creatorcontrib>Stuckert, Patricia</creatorcontrib><creatorcontrib>Raab, Monika</creatorcontrib><creatorcontrib>Mhashilkar, Abner</creatorcontrib><creatorcontrib>Tocqué, Bruno</creatorcontrib><creatorcontrib>Marasco, Wayne A.</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>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xuguang</au><au>Multon, Marie-Christine</au><au>Henin, Yvette</au><au>Schweighoffer, Fabien</au><au>Venot, Corinne</au><au>Josef, Juliana</au><au>Zhou, Changhong</au><au>LaVecchio, Joyce</au><au>Stuckert, Patricia</au><au>Raab, Monika</au><au>Mhashilkar, Abner</au><au>Tocqué, Bruno</au><au>Marasco, Wayne A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Grb3-3 Is Up-regulated in HIV-1-infected T-cells and Can Potentiate Cell Activation through NFATc</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2000-10-06</date><risdate>2000</risdate><volume>275</volume><issue>40</issue><spage>30925</spage><epage>30933</epage><pages>30925-30933</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>The MAPK pathway is required for T-cell activation; however, its role in modulating T-cell function following human immunodeficiency virus type 1 (HIV-1) infection is poorly understood. In this report, we investigated whether Grb3-3, an isoform of the Grb2 (growth factorreceptor-bound protein-2) adaptor molecule that is associated with the MAPK pathway, could be involved. We found that Grb3-3, but not its isoform Grb2, is markedly up-regulated in CD4+ peripheral blood mononuclear cells derived from either in vitro HIV-1-infected cultures or HIV-1-infected human subjects. Analysis of HIV-1 gene products indicated that Tat and Nef, both of which have been implicated in modulating T-cell function, can independently induce expression of Grb3-3. By using NFAT/AP-1, AP-1, or NFAT reporter assays, we found that Grb3-3 can potentiate NFAT (but not AP-1) promoter activity in Jurkat T-cells upon engagement of the T-cell receptor and CD28 co-receptor. In addition, potentiation of NFAT by Grb3-3 is substantially suppressed by MEKK1, a kinase that may play an important role in retaining NFAT in the cytoplasm, and by cyclosporin A. Finally, we also found that Grb3-3 potentiates HIV-1 long terminal (LTR) repeat promoter activity following T-cell receptor stimulation, an effect that can be largely suppressed by cyclosporin A. Taken together, this study indicates that Grb3-3 is a cellular factor that can be up-regulated by HIV-1. In addition, Grb3-3 can also function as a positive factor for T-cell activation and, in doing so, may aid in establishing an intracellular environment that can optimally support HIV-1 replication.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>10906142</pmid><doi>10.1074/jbc.M005535200</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 2000-10, Vol.275 (40), p.30925-30933 |
| issn | 0021-9258 1083-351X |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adaptor Proteins, Signal Transducing Adult Antibodies, Monoclonal - metabolism Blotting, Western CD28 Antigens - metabolism CD4 antigen CD4-Positive T-Lymphocytes - metabolism CD4-Positive T-Lymphocytes - virology Cell Nucleus - metabolism Cyclosporine - pharmacology Cytoplasm - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Female Gene Products, nef - metabolism Gene Products, tat - metabolism GRB2 Adaptor Protein Grb3-3 protein HIV Infections - metabolism HIV-1 - metabolism human immunodeficiency virus 1 Humans Immunosuppressive Agents - pharmacology Jurkat Cells Leukocytes, Mononuclear - virology Luciferases - metabolism Male MAP Kinase Kinase Kinase 1 MAP Kinase Signaling System Middle Aged nef Gene Products, Human Immunodeficiency Virus NF-AT protein NFATC Transcription Factors Nuclear Proteins Plasmids - metabolism Promoter Regions, Genetic Protein Isoforms Protein-Serine-Threonine Kinases - metabolism Proteins - chemistry Proteins - genetics Proteins - metabolism Receptors, Antigen, T-Cell - metabolism RNA, Messenger - metabolism Signal Transduction tat Gene Products, Human Immunodeficiency Virus Terminal Repeat Sequences Time Factors Transcription Factor AP-1 - metabolism Transcription Factors - genetics Transcription Factors - metabolism Transfection Up-Regulation |
| title | Grb3-3 Is Up-regulated in HIV-1-infected T-cells and Can Potentiate Cell Activation through NFATc |
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