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Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids
Toll-like receptor-4 (TLR4) can be activated by nonbacterial agonists, including saturated fatty acids. However, downstream signaling pathways activated by nonbacterial agonists are not known. Thus, we determined the downstream signaling pathways derived from saturated fatty acid-induced TLR4 activa...
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| Published in: | The Journal of biological chemistry 2003-09, Vol.278 (39), p.37041-37051 |
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| container_title | The Journal of biological chemistry |
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| creator | Lee, Joo Y. Ye, Jianping Gao, Zhanguo Youn, Hyung S. Lee, Won H. Zhao, Ling Sizemore, Nywana Hwang, Daniel H. |
| description | Toll-like receptor-4 (TLR4) can be activated by nonbacterial agonists, including saturated fatty acids. However, downstream signaling pathways activated by nonbacterial agonists are not known. Thus, we determined the downstream signaling pathways derived from saturated fatty acid-induced TLR4 activation. Saturated fatty acid (lauric acid)-induced NFκB activation was inhibited by a dominant-negative mutant of TLR4, MyD88, IRAK-1, TRAF6, or IκBα in macrophages (RAW264.7) and 293T cells transfected with TLR4 and MD2. Lauric acid induced the transient phosphorylation of AKT. LY294002, dominant-negative (DN) phosphatidylinositol 3-kinase (PI3K), or AKT(DN) inhibited NFκB activation, p65 transactivation, and cyclooxygenase-2 (COX-2) expression induced by lauric acid or constitutively active (CA) TLR4. AKT(DN) blocked MyD88-induced NFκB activation, suggesting that AKT is a MyD88-dependent downstream signaling component of TLR4. AKT(CA) was sufficient to induce NFκB activation and COX-2 expression. These results demonstrate that NFκB activation and COX-2 expression induced by lauric acid are at least partly mediated through the TLR4/PI3K/AKT signaling pathway. In contrast, docosahexaenoic acid (DHA) inhibited the phosphorylation of AKT induced by lipopolysaccharide or lauric acid. DHA also suppressed NFκB activation induced by TLR4(CA), but not MyD88(CA) or AKT(CA), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT. Together, these results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility that TLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and unsaturated fatty acids. |
| doi_str_mv | 10.1074/jbc.M305213200 |
| format | article |
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However, downstream signaling pathways activated by nonbacterial agonists are not known. Thus, we determined the downstream signaling pathways derived from saturated fatty acid-induced TLR4 activation. Saturated fatty acid (lauric acid)-induced NFκB activation was inhibited by a dominant-negative mutant of TLR4, MyD88, IRAK-1, TRAF6, or IκBα in macrophages (RAW264.7) and 293T cells transfected with TLR4 and MD2. Lauric acid induced the transient phosphorylation of AKT. LY294002, dominant-negative (DN) phosphatidylinositol 3-kinase (PI3K), or AKT(DN) inhibited NFκB activation, p65 transactivation, and cyclooxygenase-2 (COX-2) expression induced by lauric acid or constitutively active (CA) TLR4. AKT(DN) blocked MyD88-induced NFκB activation, suggesting that AKT is a MyD88-dependent downstream signaling component of TLR4. AKT(CA) was sufficient to induce NFκB activation and COX-2 expression. These results demonstrate that NFκB activation and COX-2 expression induced by lauric acid are at least partly mediated through the TLR4/PI3K/AKT signaling pathway. In contrast, docosahexaenoic acid (DHA) inhibited the phosphorylation of AKT induced by lipopolysaccharide or lauric acid. DHA also suppressed NFκB activation induced by TLR4(CA), but not MyD88(CA) or AKT(CA), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT. Together, these results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility that TLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and unsaturated fatty acids.</description><identifier>ISSN: 0021-9258</identifier><identifier>ISSN: 1083-351X</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M305213200</identifier><identifier>PMID: 12865424</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation - physiology ; Cell Line ; Cyclooxygenase 2 ; docosahexaenoic acid ; Docosahexaenoic Acids - pharmacology ; dodecanoic acid ; Fatty Acids - pharmacology ; gene expression ; gene expression regulation ; Humans ; immune response ; inflammation ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes - biosynthesis ; macrophages ; Membrane Glycoproteins - physiology ; Membrane Proteins ; Mice ; Myeloid Differentiation Factor 88 ; NF-kappa B - metabolism ; nuclear factor kappa B ; phosphatidylinositol 3-kinase ; Phosphatidylinositol 3-Kinases - physiology ; Phosphorylation ; prostaglandin synthase ; Prostaglandin-Endoperoxide Synthases - biosynthesis ; Protein Kinases - physiology ; protein phosphorylation ; Protein-Serine-Threonine Kinases ; Proteins - physiology ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-akt ; receptors ; Receptors, Cell Surface - physiology ; Receptors, Immunologic - physiology ; signal transduction ; Signal Transduction - physiology ; TNF Receptor-Associated Factor 6 ; Toll-Like Receptor 4 ; Toll-Like Receptors ; transcription factors ; transmembrane proteins</subject><ispartof>The Journal of biological chemistry, 2003-09, Vol.278 (39), p.37041-37051</ispartof><rights>2003 © 2003 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-c530t-fd34e2731583267ebe0072ef3088d8b423da0265e042830ad2d5c089cba1d2fb3</citedby><cites>FETCH-LOGICAL-c530t-fd34e2731583267ebe0072ef3088d8b423da0265e042830ad2d5c089cba1d2fb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002192582083258X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>315,783,787,3556,27936,27937,45792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12865424$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Joo Y.</creatorcontrib><creatorcontrib>Ye, Jianping</creatorcontrib><creatorcontrib>Gao, Zhanguo</creatorcontrib><creatorcontrib>Youn, Hyung S.</creatorcontrib><creatorcontrib>Lee, Won H.</creatorcontrib><creatorcontrib>Zhao, Ling</creatorcontrib><creatorcontrib>Sizemore, Nywana</creatorcontrib><creatorcontrib>Hwang, Daniel H.</creatorcontrib><title>Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Toll-like receptor-4 (TLR4) can be activated by nonbacterial agonists, including saturated fatty acids. However, downstream signaling pathways activated by nonbacterial agonists are not known. Thus, we determined the downstream signaling pathways derived from saturated fatty acid-induced TLR4 activation. Saturated fatty acid (lauric acid)-induced NFκB activation was inhibited by a dominant-negative mutant of TLR4, MyD88, IRAK-1, TRAF6, or IκBα in macrophages (RAW264.7) and 293T cells transfected with TLR4 and MD2. Lauric acid induced the transient phosphorylation of AKT. LY294002, dominant-negative (DN) phosphatidylinositol 3-kinase (PI3K), or AKT(DN) inhibited NFκB activation, p65 transactivation, and cyclooxygenase-2 (COX-2) expression induced by lauric acid or constitutively active (CA) TLR4. AKT(DN) blocked MyD88-induced NFκB activation, suggesting that AKT is a MyD88-dependent downstream signaling component of TLR4. AKT(CA) was sufficient to induce NFκB activation and COX-2 expression. These results demonstrate that NFκB activation and COX-2 expression induced by lauric acid are at least partly mediated through the TLR4/PI3K/AKT signaling pathway. In contrast, docosahexaenoic acid (DHA) inhibited the phosphorylation of AKT induced by lipopolysaccharide or lauric acid. DHA also suppressed NFκB activation induced by TLR4(CA), but not MyD88(CA) or AKT(CA), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT. Together, these results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility that TLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and unsaturated fatty acids.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Animals</subject><subject>Antigens, Differentiation - physiology</subject><subject>Cell Line</subject><subject>Cyclooxygenase 2</subject><subject>docosahexaenoic acid</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>dodecanoic acid</subject><subject>Fatty Acids - pharmacology</subject><subject>gene expression</subject><subject>gene expression regulation</subject><subject>Humans</subject><subject>immune response</subject><subject>inflammation</subject><subject>Interleukin-1 Receptor-Associated Kinases</subject><subject>Isoenzymes - biosynthesis</subject><subject>macrophages</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Myeloid Differentiation Factor 88</subject><subject>NF-kappa B - metabolism</subject><subject>nuclear factor kappa B</subject><subject>phosphatidylinositol 3-kinase</subject><subject>Phosphatidylinositol 3-Kinases - physiology</subject><subject>Phosphorylation</subject><subject>prostaglandin synthase</subject><subject>Prostaglandin-Endoperoxide Synthases - biosynthesis</subject><subject>Protein Kinases - physiology</subject><subject>protein phosphorylation</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Proteins - physiology</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>receptors</subject><subject>Receptors, Cell Surface - physiology</subject><subject>Receptors, Immunologic - physiology</subject><subject>signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>TNF Receptor-Associated Factor 6</subject><subject>Toll-Like Receptor 4</subject><subject>Toll-Like Receptors</subject><subject>transcription factors</subject><subject>transmembrane proteins</subject><issn>0021-9258</issn><issn>1083-351X</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkkFvEzEQhVcIREPhyhF8QNw2Hdu7WecYFQpVG1GRVOJmee3ZxMVZh7U31f4e_iiONqInxFxGGn3z9DRvsuwthSmFqrh4qPV0yaFklDOAZ9mEguA5L-mP59kEgNF8zkpxlr0K4QFSFXP6MjujTMzKghWT7Pd31Hbfea0cWXrTOxWtb4lvyNo7lzv7E0lCcB99lxdkZTetcrbdkDsVt49qCOS6PXh3OI6WwychiGoNudv6sN8mKTMk2AcbvSM8v7GtCnixuFmTeiArFftORTTjindD34a_sysV40AW2prwOnvRKBfwzamfZ_dXn9eXX_Pbb1-uLxe3uS45xLwxvEBWcVoKzmYV1ghQMWw4CGFEXTBuFLBZiVAwwUEZZkoNYq5rRQ1ran6efRx10z1-9Rii3Nmg0TnVou-DrMoKCl5U_wWpEMkFZQmcjqDufAgdNnLf2Z3qBklBHvOTKT_5lF9aeHdS7usdmif8FFgCPozA1m62j7ZDWVuvt7iTrBKSzyVPHmnC3o9Yo7xUm84Geb9iQDmk9xDAj9bESGC66MFiJ4O22Go0SVRHabz9l8k_qAy_eQ</recordid><startdate>20030926</startdate><enddate>20030926</enddate><creator>Lee, Joo Y.</creator><creator>Ye, Jianping</creator><creator>Gao, Zhanguo</creator><creator>Youn, Hyung S.</creator><creator>Lee, Won H.</creator><creator>Zhao, Ling</creator><creator>Sizemore, Nywana</creator><creator>Hwang, Daniel H.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>FBQ</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>H94</scope><scope>7X8</scope></search><sort><creationdate>20030926</creationdate><title>Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids</title><author>Lee, Joo Y. ; Ye, Jianping ; Gao, Zhanguo ; Youn, Hyung S. ; Lee, Won H. ; Zhao, Ling ; Sizemore, Nywana ; Hwang, Daniel H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-fd34e2731583267ebe0072ef3088d8b423da0265e042830ad2d5c089cba1d2fb3</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 - physiology</topic><topic>Cell Line</topic><topic>Cyclooxygenase 2</topic><topic>docosahexaenoic acid</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>dodecanoic acid</topic><topic>Fatty Acids - pharmacology</topic><topic>gene expression</topic><topic>gene expression regulation</topic><topic>Humans</topic><topic>immune response</topic><topic>inflammation</topic><topic>Interleukin-1 Receptor-Associated Kinases</topic><topic>Isoenzymes - biosynthesis</topic><topic>macrophages</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>Myeloid Differentiation Factor 88</topic><topic>NF-kappa B - metabolism</topic><topic>nuclear factor kappa B</topic><topic>phosphatidylinositol 3-kinase</topic><topic>Phosphatidylinositol 3-Kinases - physiology</topic><topic>Phosphorylation</topic><topic>prostaglandin synthase</topic><topic>Prostaglandin-Endoperoxide Synthases - biosynthesis</topic><topic>Protein Kinases - physiology</topic><topic>protein phosphorylation</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Proteins - physiology</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>receptors</topic><topic>Receptors, Cell Surface - physiology</topic><topic>Receptors, Immunologic - physiology</topic><topic>signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>TNF Receptor-Associated Factor 6</topic><topic>Toll-Like Receptor 4</topic><topic>Toll-Like Receptors</topic><topic>transcription factors</topic><topic>transmembrane proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Joo Y.</creatorcontrib><creatorcontrib>Ye, Jianping</creatorcontrib><creatorcontrib>Gao, Zhanguo</creatorcontrib><creatorcontrib>Youn, Hyung S.</creatorcontrib><creatorcontrib>Lee, Won H.</creatorcontrib><creatorcontrib>Zhao, Ling</creatorcontrib><creatorcontrib>Sizemore, Nywana</creatorcontrib><creatorcontrib>Hwang, Daniel H.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>AGRIS</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>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>Lee, Joo Y.</au><au>Ye, Jianping</au><au>Gao, Zhanguo</au><au>Youn, Hyung S.</au><au>Lee, Won H.</au><au>Zhao, Ling</au><au>Sizemore, Nywana</au><au>Hwang, Daniel H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2003-09-26</date><risdate>2003</risdate><volume>278</volume><issue>39</issue><spage>37041</spage><epage>37051</epage><pages>37041-37051</pages><issn>0021-9258</issn><issn>1083-351X</issn><eissn>1083-351X</eissn><abstract>Toll-like receptor-4 (TLR4) can be activated by nonbacterial agonists, including saturated fatty acids. However, downstream signaling pathways activated by nonbacterial agonists are not known. Thus, we determined the downstream signaling pathways derived from saturated fatty acid-induced TLR4 activation. Saturated fatty acid (lauric acid)-induced NFκB activation was inhibited by a dominant-negative mutant of TLR4, MyD88, IRAK-1, TRAF6, or IκBα in macrophages (RAW264.7) and 293T cells transfected with TLR4 and MD2. Lauric acid induced the transient phosphorylation of AKT. LY294002, dominant-negative (DN) phosphatidylinositol 3-kinase (PI3K), or AKT(DN) inhibited NFκB activation, p65 transactivation, and cyclooxygenase-2 (COX-2) expression induced by lauric acid or constitutively active (CA) TLR4. AKT(DN) blocked MyD88-induced NFκB activation, suggesting that AKT is a MyD88-dependent downstream signaling component of TLR4. AKT(CA) was sufficient to induce NFκB activation and COX-2 expression. These results demonstrate that NFκB activation and COX-2 expression induced by lauric acid are at least partly mediated through the TLR4/PI3K/AKT signaling pathway. In contrast, docosahexaenoic acid (DHA) inhibited the phosphorylation of AKT induced by lipopolysaccharide or lauric acid. DHA also suppressed NFκB activation induced by TLR4(CA), but not MyD88(CA) or AKT(CA), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT. Together, these results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility that TLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and unsaturated fatty acids.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12865424</pmid><doi>10.1074/jbc.M305213200</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing Animals Antigens, Differentiation - physiology Cell Line Cyclooxygenase 2 docosahexaenoic acid Docosahexaenoic Acids - pharmacology dodecanoic acid Fatty Acids - pharmacology gene expression gene expression regulation Humans immune response inflammation Interleukin-1 Receptor-Associated Kinases Isoenzymes - biosynthesis macrophages Membrane Glycoproteins - physiology Membrane Proteins Mice Myeloid Differentiation Factor 88 NF-kappa B - metabolism nuclear factor kappa B phosphatidylinositol 3-kinase Phosphatidylinositol 3-Kinases - physiology Phosphorylation prostaglandin synthase Prostaglandin-Endoperoxide Synthases - biosynthesis Protein Kinases - physiology protein phosphorylation Protein-Serine-Threonine Kinases Proteins - physiology Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-akt receptors Receptors, Cell Surface - physiology Receptors, Immunologic - physiology signal transduction Signal Transduction - physiology TNF Receptor-Associated Factor 6 Toll-Like Receptor 4 Toll-Like Receptors transcription factors transmembrane proteins |
| title | Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids |
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