The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4
Our previous studies have revealed that the signaling protein BCL10 plays a major role in adaptive immunity by mediating NF-kappaB activation in the LPS/TLR4 pathway. In this study, we show that IRAK-1 acts as the essential upstream adaptor that recruits BCL10 to the TLR4 signaling complex and media...
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| Veröffentlicht in: | The Journal of biological chemistry 2006-09, Vol.281 (36), p.26029-26040 |
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| container_title | The Journal of biological chemistry |
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| creator | Dong, Wei Liu, Yingle Peng, Jinhong Chen, Lu Zou, Tingting Xiao, Huazhong Liu, Zhengxue Li, Wen Bu, Yiwen Qi, Yipeng |
| description | Our previous studies have revealed that the signaling protein BCL10 plays a major role in adaptive immunity by mediating NF-kappaB activation in the LPS/TLR4 pathway. In this study, we show that IRAK-1 acts as the essential upstream adaptor that recruits BCL10 to the TLR4 signaling complex and mediates signaling to NF-kappaB through the BCL10-MALT1-TRAF6-TAK1 cascade. Following dissociation from IRAK-1, BCL10 is translocated into the cytosol along with TRAF6 and TAK1, in a process bridged by a direct BCL10-Pellino2 interaction. RNA interference against MALT1 markedly reduced the level of NF-kappaB activation stimulated by lipopolysaccharide (LPS) in macrophages, which suggests that MALT1 plays a major role in the LPS/TLR4 pathway. MALT1 interacted with BCL10 and TRAF6 to facilitate TRAF6 self-ubiquitination in the cytosol, which was strictly dependent on the dissociation of BCL10 from IRAK-1. We show that BCL10 oligomerization is a prerequisite for BCL10 function in LPS signaling to NF-kappaB and that IRAK-1 dimerization is an important event in this process. |
| format | Article |
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In this study, we show that IRAK-1 acts as the essential upstream adaptor that recruits BCL10 to the TLR4 signaling complex and mediates signaling to NF-kappaB through the BCL10-MALT1-TRAF6-TAK1 cascade. Following dissociation from IRAK-1, BCL10 is translocated into the cytosol along with TRAF6 and TAK1, in a process bridged by a direct BCL10-Pellino2 interaction. RNA interference against MALT1 markedly reduced the level of NF-kappaB activation stimulated by lipopolysaccharide (LPS) in macrophages, which suggests that MALT1 plays a major role in the LPS/TLR4 pathway. MALT1 interacted with BCL10 and TRAF6 to facilitate TRAF6 self-ubiquitination in the cytosol, which was strictly dependent on the dissociation of BCL10 from IRAK-1. We show that BCL10 oligomerization is a prerequisite for BCL10 function in LPS signaling to NF-kappaB and that IRAK-1 dimerization is an important event in this process.</description><identifier>ISSN: 0021-9258</identifier><identifier>PMID: 16831874</identifier><language>eng</language><publisher>United States</publisher><subject>Adaptor Proteins, Signal Transducing - chemistry ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Amino Acid Sequence ; Animals ; B-Cell CLL-Lymphoma 10 Protein ; Caspases - genetics ; Caspases - metabolism ; Cell Line ; Dimerization ; Humans ; Interleukin-1 Receptor-Associated Kinases - chemistry ; Interleukin-1 Receptor-Associated Kinases - genetics ; Interleukin-1 Receptor-Associated Kinases - metabolism ; Lipopolysaccharides - immunology ; Macrophages - cytology ; Macrophages - metabolism ; MAP Kinase Kinase Kinases - genetics ; MAP Kinase Kinase Kinases - metabolism ; Mice ; Molecular Sequence Data ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; NF-kappa B - metabolism ; Nuclear Proteins - metabolism ; Protein Structure, Quaternary ; RNA Interference ; Signal Transduction - physiology ; TNF Receptor-Associated Factor 6 - genetics ; TNF Receptor-Associated Factor 6 - metabolism ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism</subject><ispartof>The Journal of biological chemistry, 2006-09, Vol.281 (36), p.26029-26040</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16831874$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, Wei</creatorcontrib><creatorcontrib>Liu, Yingle</creatorcontrib><creatorcontrib>Peng, Jinhong</creatorcontrib><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Zou, Tingting</creatorcontrib><creatorcontrib>Xiao, Huazhong</creatorcontrib><creatorcontrib>Liu, Zhengxue</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Bu, Yiwen</creatorcontrib><creatorcontrib>Qi, Yipeng</creatorcontrib><title>The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Our previous studies have revealed that the signaling protein BCL10 plays a major role in adaptive immunity by mediating NF-kappaB activation in the LPS/TLR4 pathway. 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We show that BCL10 oligomerization is a prerequisite for BCL10 function in LPS signaling to NF-kappaB and that IRAK-1 dimerization is an important event in this process.</description><subject>Adaptor Proteins, Signal Transducing - chemistry</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>B-Cell CLL-Lymphoma 10 Protein</subject><subject>Caspases - genetics</subject><subject>Caspases - metabolism</subject><subject>Cell Line</subject><subject>Dimerization</subject><subject>Humans</subject><subject>Interleukin-1 Receptor-Associated Kinases - chemistry</subject><subject>Interleukin-1 Receptor-Associated Kinases - genetics</subject><subject>Interleukin-1 Receptor-Associated Kinases - metabolism</subject><subject>Lipopolysaccharides - immunology</subject><subject>Macrophages - cytology</subject><subject>Macrophages - metabolism</subject><subject>MAP Kinase Kinase Kinases - genetics</subject><subject>MAP Kinase Kinase Kinases - metabolism</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Nuclear Proteins - metabolism</subject><subject>Protein Structure, Quaternary</subject><subject>RNA Interference</subject><subject>Signal Transduction - physiology</subject><subject>TNF Receptor-Associated Factor 6 - genetics</subject><subject>TNF Receptor-Associated Factor 6 - metabolism</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0021-9258</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UMtOwzAQ9AFES-EXkE_cLMXxI84xjShUDSBVvkeOsymmzoM4OfD3RGqZw6w0Go1m5watoyimJI2FWqH7EL6jBTyld2hFpWJUJXyNrP4CvD9mB0LJNi9oRN6zQlOij9lOEp0dKLYmWFMDbqF2ZoKAgzt1xrvuhKcef-zI2QyD2eJm7Fuse--Jd2fAI1gYpn7E_AHdNsYHeLzeDdK7F52_keLzdZ9nBRkE58TKpLIqqgBYbaSQi8agpjKJWSxSmia8iptaQLXQ0t6A4VzZummSJFUUBNug50vsMPY_M4SpbF2w4L3poJ9DKZWKmeDRYny6GudqeaocRtea8bf8X4X9AbHzWYo</recordid><startdate>20060908</startdate><enddate>20060908</enddate><creator>Dong, Wei</creator><creator>Liu, Yingle</creator><creator>Peng, Jinhong</creator><creator>Chen, Lu</creator><creator>Zou, Tingting</creator><creator>Xiao, Huazhong</creator><creator>Liu, Zhengxue</creator><creator>Li, Wen</creator><creator>Bu, Yiwen</creator><creator>Qi, Yipeng</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20060908</creationdate><title>The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4</title><author>Dong, Wei ; Liu, Yingle ; Peng, Jinhong ; Chen, Lu ; Zou, Tingting ; Xiao, Huazhong ; Liu, Zhengxue ; Li, Wen ; Bu, Yiwen ; Qi, Yipeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p544-c67bc80bee3da6565443ed167232591974b2fd5ebfd5831aea448cdff77981e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adaptor Proteins, Signal Transducing - chemistry</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>B-Cell CLL-Lymphoma 10 Protein</topic><topic>Caspases - genetics</topic><topic>Caspases - metabolism</topic><topic>Cell Line</topic><topic>Dimerization</topic><topic>Humans</topic><topic>Interleukin-1 Receptor-Associated Kinases - chemistry</topic><topic>Interleukin-1 Receptor-Associated Kinases - genetics</topic><topic>Interleukin-1 Receptor-Associated Kinases - metabolism</topic><topic>Lipopolysaccharides - immunology</topic><topic>Macrophages - cytology</topic><topic>Macrophages - metabolism</topic><topic>MAP Kinase Kinase Kinases - genetics</topic><topic>MAP Kinase Kinase Kinases - metabolism</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Nuclear Proteins - metabolism</topic><topic>Protein Structure, Quaternary</topic><topic>RNA Interference</topic><topic>Signal Transduction - physiology</topic><topic>TNF Receptor-Associated Factor 6 - genetics</topic><topic>TNF Receptor-Associated Factor 6 - metabolism</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Wei</creatorcontrib><creatorcontrib>Liu, Yingle</creatorcontrib><creatorcontrib>Peng, Jinhong</creatorcontrib><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Zou, Tingting</creatorcontrib><creatorcontrib>Xiao, Huazhong</creatorcontrib><creatorcontrib>Liu, Zhengxue</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Bu, Yiwen</creatorcontrib><creatorcontrib>Qi, Yipeng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</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>Dong, Wei</au><au>Liu, Yingle</au><au>Peng, Jinhong</au><au>Chen, Lu</au><au>Zou, Tingting</au><au>Xiao, Huazhong</au><au>Liu, Zhengxue</au><au>Li, Wen</au><au>Bu, Yiwen</au><au>Qi, Yipeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2006-09-08</date><risdate>2006</risdate><volume>281</volume><issue>36</issue><spage>26029</spage><epage>26040</epage><pages>26029-26040</pages><issn>0021-9258</issn><abstract>Our previous studies have revealed that the signaling protein BCL10 plays a major role in adaptive immunity by mediating NF-kappaB activation in the LPS/TLR4 pathway. In this study, we show that IRAK-1 acts as the essential upstream adaptor that recruits BCL10 to the TLR4 signaling complex and mediates signaling to NF-kappaB through the BCL10-MALT1-TRAF6-TAK1 cascade. Following dissociation from IRAK-1, BCL10 is translocated into the cytosol along with TRAF6 and TAK1, in a process bridged by a direct BCL10-Pellino2 interaction. RNA interference against MALT1 markedly reduced the level of NF-kappaB activation stimulated by lipopolysaccharide (LPS) in macrophages, which suggests that MALT1 plays a major role in the LPS/TLR4 pathway. MALT1 interacted with BCL10 and TRAF6 to facilitate TRAF6 self-ubiquitination in the cytosol, which was strictly dependent on the dissociation of BCL10 from IRAK-1. We show that BCL10 oligomerization is a prerequisite for BCL10 function in LPS signaling to NF-kappaB and that IRAK-1 dimerization is an important event in this process.</abstract><cop>United States</cop><pmid>16831874</pmid><tpages>12</tpages></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - chemistry Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Amino Acid Sequence Animals B-Cell CLL-Lymphoma 10 Protein Caspases - genetics Caspases - metabolism Cell Line Dimerization Humans Interleukin-1 Receptor-Associated Kinases - chemistry Interleukin-1 Receptor-Associated Kinases - genetics Interleukin-1 Receptor-Associated Kinases - metabolism Lipopolysaccharides - immunology Macrophages - cytology Macrophages - metabolism MAP Kinase Kinase Kinases - genetics MAP Kinase Kinase Kinases - metabolism Mice Molecular Sequence Data Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein Neoplasm Proteins - genetics Neoplasm Proteins - metabolism NF-kappa B - metabolism Nuclear Proteins - metabolism Protein Structure, Quaternary RNA Interference Signal Transduction - physiology TNF Receptor-Associated Factor 6 - genetics TNF Receptor-Associated Factor 6 - metabolism Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism |
| title | The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4 |
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