Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ
IκB-ζ, a new negative-regulator of nuclear factor-κB (NF-κB), is strongly induced by lipopolysaccharide or interleukin-1β stimulation, but not by tumor necrosis factor-α. Here, we analyzed the mechanisms for transcriptional induction of IκB-ζ. IκB-ζ mRNA was induced by overexpression of MyD88 or TRA...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2003-02, Vol.301 (2), p.495-501 |
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| creator | Eto, Akiko Muta, Tatsushi Yamazaki, Soh Takeshige, Koichiro |
| description | IκB-ζ, a new negative-regulator of nuclear factor-κB (NF-κB), is strongly induced by lipopolysaccharide or interleukin-1β stimulation, but not by tumor necrosis factor-α. Here, we analyzed the mechanisms for transcriptional induction of IκB-ζ. IκB-ζ mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in IκB-ζ induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for IκB-ζ induction. The induction was inhibited by treatment with various inhibitors of NF-κB activation or by overexpressing IκB-α or β, indicating essential roles for NF-κB in IκB-ζ induction. However, overexpression of the NF-κB subunits induced IκB-α, but not IκB-ζ. These results indicate the existence of another signal essential for IκB-ζ induction, which is specifically mediated by the TIR domain-mediated signaling pathway. |
| doi_str_mv | 10.1016/S0006-291X(02)03082-6 |
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Here, we analyzed the mechanisms for transcriptional induction of IκB-ζ. IκB-ζ mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in IκB-ζ induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for IκB-ζ induction. The induction was inhibited by treatment with various inhibitors of NF-κB activation or by overexpressing IκB-α or β, indicating essential roles for NF-κB in IκB-ζ induction. However, overexpression of the NF-κB subunits induced IκB-α, but not IκB-ζ. These results indicate the existence of another signal essential for IκB-ζ induction, which is specifically mediated by the TIR domain-mediated signaling pathway.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Animals</subject><subject>Antigens, Differentiation - genetics</subject><subject>Antigens, Differentiation - metabolism</subject><subject>Cell Line</subject><subject>CpG Islands</subject><subject>Cysteine Proteinase Inhibitors - pharmacology</subject><subject>Drosophila Proteins</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Glucans - metabolism</subject><subject>Humans</subject><subject>I-kappa B Proteins</subject><subject>Innate immunity</subject><subject>IκB-ζ</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophage</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Myeloid Differentiation Factor 88</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - metabolism</subject><subject>Nuclear factor-κB</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Peptidoglycan - metabolism</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Receptors, Interleukin-1 - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>TNF Receptor-Associated Factor 6</subject><subject>Toll-like receptor</subject><subject>Toll-Like Receptor 2</subject><subject>Toll-Like Receptors</subject><subject>Toll/interleukin-1 receptor domain</subject><subject>Transcriptional induction</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkLFuFDEQhi0EIpfAI4BcoaQwmbH3vLsVClECJ52gIEh0ltceg9He-rD3kHgxijxEngknd4KSaor5_n80H2MvEF4joD7_BABayB6_nII8AwWdFPoRWyD0ICRC85gt_iJH7LiU7wCIje6fsiOUS73sun7B4lUpNM3RjjynkQoPKfMP1-Lu9i23k-eW36RxPF-tBfJMjrZz3fu0sXESZUsuhuh4iV8nO56WMx4nPn-jOvzOzTFNPAW-ql3i7vcz9iTYsdDzwzxhn6-vbi7fi_XHd6vLi7VwSuMsKFDjJWmpOud7RHLYDt4NbQ_oMDTNoAY9KAxDK71q0fadJK9kH6RFOXh1wl7te7c5_dhRmc0mFkfjaCdKu2JaBVAzXQWXe9DlVEqmYLY5bmz-ZRDMvWPz4NjcCzQgzYNjo2vu5eHAbtiQ_5c6SK3Amz1A9c2fkbIpLtLkyMeqcDY-xf-c-AN-Jo1N</recordid><startdate>20030207</startdate><enddate>20030207</enddate><creator>Eto, Akiko</creator><creator>Muta, Tatsushi</creator><creator>Yamazaki, Soh</creator><creator>Takeshige, Koichiro</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20030207</creationdate><title>Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ</title><author>Eto, Akiko ; Muta, Tatsushi ; Yamazaki, Soh ; Takeshige, Koichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-efe4d2e6238cd911ec17bdcb7901c1f44b3b6b31fb72d371a982ed329f2a12bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Animals</topic><topic>Antigens, Differentiation - genetics</topic><topic>Antigens, Differentiation - metabolism</topic><topic>Cell Line</topic><topic>CpG Islands</topic><topic>Cysteine Proteinase Inhibitors - pharmacology</topic><topic>Drosophila Proteins</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Glucans - metabolism</topic><topic>Humans</topic><topic>I-kappa B Proteins</topic><topic>Innate immunity</topic><topic>IκB-ζ</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophage</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mice</topic><topic>Myeloid Differentiation Factor 88</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - metabolism</topic><topic>Nuclear factor-κB</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Peptidoglycan - metabolism</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Receptors, Interleukin-1 - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>TNF Receptor-Associated Factor 6</topic><topic>Toll-like receptor</topic><topic>Toll-Like Receptor 2</topic><topic>Toll-Like Receptors</topic><topic>Toll/interleukin-1 receptor domain</topic><topic>Transcriptional induction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eto, Akiko</creatorcontrib><creatorcontrib>Muta, Tatsushi</creatorcontrib><creatorcontrib>Yamazaki, Soh</creatorcontrib><creatorcontrib>Takeshige, Koichiro</creatorcontrib><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><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eto, Akiko</au><au>Muta, Tatsushi</au><au>Yamazaki, Soh</au><au>Takeshige, Koichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003-02-07</date><risdate>2003</risdate><volume>301</volume><issue>2</issue><spage>495</spage><epage>501</epage><pages>495-501</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>IκB-ζ, a new negative-regulator of nuclear factor-κB (NF-κB), is strongly induced by lipopolysaccharide or interleukin-1β stimulation, but not by tumor necrosis factor-α. Here, we analyzed the mechanisms for transcriptional induction of IκB-ζ. IκB-ζ mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in IκB-ζ induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for IκB-ζ induction. The induction was inhibited by treatment with various inhibitors of NF-κB activation or by overexpressing IκB-α or β, indicating essential roles for NF-κB in IκB-ζ induction. However, overexpression of the NF-κB subunits induced IκB-α, but not IκB-ζ. These results indicate the existence of another signal essential for IκB-ζ induction, which is specifically mediated by the TIR domain-mediated signaling pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12565889</pmid><doi>10.1016/S0006-291X(02)03082-6</doi><tpages>7</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2003-02, Vol.301 (2), p.495-501 |
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| subjects | Adaptor Proteins, Signal Transducing Animals Antigens, Differentiation - genetics Antigens, Differentiation - metabolism Cell Line CpG Islands Cysteine Proteinase Inhibitors - pharmacology Drosophila Proteins Gene Expression Regulation Genes, Reporter Glucans - metabolism Humans I-kappa B Proteins Innate immunity IκB-ζ Lipopolysaccharides - pharmacology Macrophage Macrophages - cytology Macrophages - drug effects Macrophages - metabolism Membrane Glycoproteins - metabolism Mice Myeloid Differentiation Factor 88 NF-kappa B - antagonists & inhibitors NF-kappa B - metabolism Nuclear factor-κB Nuclear Proteins - genetics Nuclear Proteins - metabolism Peptidoglycan - metabolism Protein Isoforms - genetics Protein Isoforms - metabolism Proteins - genetics Proteins - metabolism Receptors, Cell Surface - metabolism Receptors, Immunologic - genetics Receptors, Immunologic - metabolism Receptors, Interleukin-1 - metabolism RNA, Messenger - metabolism Signal Transduction - physiology TNF Receptor-Associated Factor 6 Toll-like receptor Toll-Like Receptor 2 Toll-Like Receptors Toll/interleukin-1 receptor domain Transcriptional induction |
| title | Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ |
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