Genomes and Genes
Gene Symbol: MYD88
Description: myeloid differentiation primary response 88
Alias: MYD88D, myeloid differentiation primary response protein MyD88, mutant myeloid differentiation primary response 88, myeloid differentiation primary response gene (88)
Publications253 found, 100 shown here
- Treatment with glutamine is associated with down-regulation of Toll-like receptor-4 and myeloid differentiation factor 88 expression and decrease in intestinal mucosal injury caused by lipopolysaccharide endotoxaemia in a ratA Kessel
Allergy and Clinical Immunology, Bnai Zion Medical Center, The Bruce Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel
Clin Exp Immunol 151:341-7. 2008..to determine the effects of glutamine (Gln) on Toll-like receptor 4 (TLR-4), myeloid differentiation factor 88 (Myd88) and tumour necrosis factor (TNF)-alpha receptor-associated factor 6 (TRAF6) expression in intestinal mucosa ..
- Induction of beta defensin 2 by NTHi requires TLR2 mediated MyD88 and IRAK-TRAF6-p38MAPK signaling pathway in human middle ear epithelial cellsHaa Yung Lee
The Gonda Department of Cell and Molecular Biology, House Ear Institute, Los Angeles, CA, USA
BMC Infect Dis 8:87. 2008..We believe that this report is the first attempt to elucidate NTHi induced beta-defensin expression in airway mucosa, which includes the middle ear...
- IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokinesJochen Schmitz
Schering Plough Biopharma Formerly DNAX Research, Inc, 901 California Avenue, Palo Alto, California 94304, USA
Immunity 23:479-90. 2005..In vivo, IL-33 induces the expression of IL-4, IL-5, and IL-13 and leads to severe pathological changes in mucosal organs...
- The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signalsKristi L Williams
Lineberger Comprehensive Cancer Center, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina 27599, USA
J Biol Chem 280:39914-24. 2005..Monarch-1 reduces NFkappaB activation by TLR-signaling molecules MyD88, IRAK-1 (type I interleukin-1 receptor-associated protein kinase), and TRAF6 (TNF receptor (TNFR)-associated ..
- Transactivation by the p65 subunit of NF-kappaB in response to interleukin-1 (IL-1) involves MyD88, IL-1 receptor-associated kinase 1, TRAF-6, and Rac1C Jefferies
Department of Biochemistry and Biotechnology Institute, Trinity College, Dublin 2, Ireland
Mol Cell Biol 21:4544-52. 2001..Transient transfection of cells with plasmids encoding wild-type MyD88, IL-1 receptor-associated kinase 1 (IRAK-1), and TRAF-6 drove p65-mediated transactivation...
- The Fas-associated death domain protein suppresses activation of NF-kappa B by LPS and IL-1 betaDouglas D Bannerman
Department of Surgery, University of Washington School of Medicine, Seattle, Washington, USA
J Clin Invest 109:419-25. 2002..of NF-kappa B is dependent upon the interaction of two death domain-containing (DD-containing) proteins, MyD88 and IL-1 receptor-associated kinase IRAK...
- Inhibition of interleukin-1beta -induced NF-kappa B activation by calcium/calmodulin-dependent protein kinase kinase occurs through Akt activation associated with interleukin-1 receptor-associated kinase phosphorylation and uncoupling of MyD88Bing Chang Chen
Department of Pharmacology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
J Biol Chem 277:24169-79. 2002..CaMKKc and Akt overexpression decreases IRAK1-mediated NF-kappaB activity and its association with MyD88 in response to IL-1beta stimulation...
- ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin toleranceElizabeth K Brint
Department of Biochemistry, Trinity College, Dublin 2, Ireland
Nat Immunol 5:373-9. 2004..1 receptor (IL-1RI) and Toll-like receptor 4 (TLR4) but not TLR3 signaling by sequestrating the adaptors MyD88 and Mal. In contrast to wild-type mice, ST2-deficient mice failed to develop endotoxin tolerance...
- Caspase-1 targets the TLR adaptor Mal at a crucial TIR-domain interaction sitePeter Ulrichts
Department of Medical Protein Research, VIB, B 9000 Ghent, Belgium
J Cell Sci 123:256-65. 2010..D198 of Mal is conserved in MyD88 and TLR4 TIR domains and the negatively charged amino acid at this position is crucial for the interactions and ..
- CD300a and CD300f differentially regulate the MyD88 and TRIF-mediated TLR signalling pathways through activation of SHP-1 and/or SHP-2 in human monocytic cell linesEun Ju Kim
School of Life Sciences and Biotechnology, Kyungpook National University, Daegu, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, Korea
Immunology 135:226-35. 2012..of CD300f blocked reporter expression induced by over-expression of both myeloid differentiation factor 88 (MyD88) and toll-interleukin 1 receptor-domain-containing adapter-inducing interferon-β (TRIF), whereas CD300a blocked ..
- Mechanism of bacterial interference with TLR4 signaling by Brucella Toll/interleukin-1 receptor domain-containing protein TcpBMohammed Alaidarous
From the School of Chemistry and Molecular Biosciences
J Biol Chem 289:654-68. 2014..In this study, we show using co-immunoprecipitation analyses that TcpB interacts with MAL, MyD88, and TLR4 but interferes only with the MAL-TLR4 interaction...
- Bacterial lipoprotein-induced self-tolerance and cross-tolerance to LPS are associated with reduced IRAK-1 expression and MyD88-IRAK complex formationChong Hui Li
Department of Academic Surgery, National University of Ireland NUI University College Cork, Cork University Hospital, Cork, Ireland
J Leukoc Biol 79:867-75. 2006..In this study, the effect of BLP-induced tolerance on the myeloid differentiation factor 88 (MyD88)-dependent upstream signaling pathway for NF-kappaB activation in vitro was examined further...
- Identification of essential regions in the cytoplasmic tail of interleukin-1 receptor accessory protein critical for interleukin-1 signalingJurgen Radons
Klinik und Poliklinik für Innere Medizin I, Universitat Regensburg, D 93042 Regensburg, Germany
J Biol Chem 277:16456-63. 2002..Immunoprecipitation data revealed a strong correlation between MyD88 binding with NF-kappaB activation and IL-2 production but not with IL-2 promoter activation...
- Interactive sites in the MyD88 Toll/interleukin (IL) 1 receptor domain responsible for coupling to the IL1beta signaling pathwayChunsheng Li
Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232 2363, USA
J Biol Chem 280:26152-9. 2005Myeloid differentiation factor MyD88 is the essential adaptor protein that integrates and transduces intracellular signals generated by multiple Toll-like receptors including receptor complex for interleukin (IL) 1beta, a key ..
- Smad6 negatively regulates interleukin 1-receptor-Toll-like receptor signaling through direct interaction with the adaptor Pellino-1Kyung Chul Choi
Department of Pathology, Inha University College of Medicine and Inha Research Institute for Medical Sciences, Inha University College of Medicine by BK 21 Project, Incheon 400 712, Republic of Korea
Nat Immunol 7:1057-65. 2006..Thus Smad6 is a critical mediator of the TGF-beta-BMP pathway that mediates anti-inflammatory activity and negatively regulates IL-1R-Toll-like receptor signals...
- MyD88-dependent immune activation mediated by human immunodeficiency virus type 1-encoded Toll-like receptor ligandsAngela Meier
Partners AIDS Research Center, Massachusetts General Hospital, 149 13th Street, Boston, MA 02129, USA
J Virol 81:8180-91. 2007..RNA of HIV-1 encodes multiple uridine-rich Toll-like receptor 7/8 (TLR7/8) ligands that induce strong MyD88-dependent plasmacytoid dendritic cell and monocyte activation, as well as accessory cell-dependent T-cell ..
- Lipoteichoic acid induces HO-1 expression via the TLR2/MyD88/c-Src/NADPH oxidase pathway and Nrf2 in human tracheal smooth muscle cellsI Ta Lee
Department of Physiology and Pharmacology
J Immunol 181:5098-110. 2008..mRNA expression, and promoter activity were attenuated by transfection with dominant negative mutants of TLR2 and MyD88, by pretreatment with the inhibitors of c-Src (PP1), NADPH oxidase (diphenylene iodonium chloride (DPI) and ..
- Activation of ROS/NF-kappaB and Ca2+/CaM kinase II are necessary for VCAM-1 induction in IL-1beta-treated human tracheal smooth muscle cellsShue Fen Luo
Department of Internal Medicine, Chang Gung University, Kwei San, Tao Yuan, Taiwan
Toxicol Appl Pharmacol 237:8-21. 2009..Bay11-7082), HDAC (trichostatin A), and ROS scavenger [N-acetyl-L-cysteine (NAC)] or transfection with siRNAs of MyD88, PKCalpha, Src, p47(phox), p300, and HDAC4...
- HIV-1 Vpr induces TLR4/MyD88-mediated IL-6 production and reactivates viral production from latencyShigeki Hoshino
Research Institute, International Medical Center of Japan, 1 21 1 Toyama, Shinjuku ku, Tokyo 162 8655, Japan
J Leukoc Biol 87:1133-43. 2010..The induction of IL-6 by rVpr was dependent on signaling through TLR4 and its adaptor molecule, MyD88. We next provide evidence that rVpr induced the formation of OxPC and that a mAb against OxPC blocked rVpr-induced ..
- Regulation of MyD88 aggregation and the MyD88-dependent signaling pathway by sequestosome 1 and histone deacetylase 6Takeshi Into
Department of Oral Microbiology, Asahi University School of Dentistry, 1851 1 Hozumi, Mizuho, Gifu 501 0296, Japan
J Biol Chem 285:35759-69. 2010b>MyD88 is an essential adaptor molecule for Toll-like receptors (TLRs) and interleukin (IL)-1 receptor...
- The E3 ubiquitin ligase MARCH8 negatively regulates IL-1β-induced NF-κB activation by targeting the IL1RAP coreceptor for ubiquitination and degradationRui Chen
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China
Proc Natl Acad Sci U S A 109:14128-33. 2012..Our findings suggest that MARCH8-mediated polyubiquitination and degradation of IL1RAP is an important mechanism for negative regulation of IL-1β-induced signaling pathways...
- Poly(I-C)-induced Toll-like receptor 3 (TLR3)-mediated activation of NFkappa B and MAP kinase is through an interleukin-1 receptor-associated kinase (IRAK)-independent pathway employing the signaling components TLR3-TRAF6-TAK1-TAB2-PKR Zhengfan Jiang
Department of Immunology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
J Biol Chem 278:16713-9. 2003..signaling components that associate with the IL-1 receptor, including IL-1 receptor-associated kinase (IRAK), MyD88, and TRAF6...
- Sequential autophosphorylation steps in the interleukin-1 receptor-associated kinase-1 regulate its availability as an adapter in interleukin-1 signalingChristian Kollewe
Department of Pharmacology, Hannover Medical School, D 30623 Hannover, Germany
J Biol Chem 279:5227-36. 2004..Hyperphosphorylation of this region leads to dissociation of IRAK-1 from the upstream adapters MyD88 and Tollip but leaves its interaction with the downstream adapter TRAF6 unaffected...
- The cloning and characterization of human MyD88: a member of an IL-1 receptor related familyT P Bonnert
Immunex Corporation, Seattle, WA 98101, USA
FEBS Lett 402:81-4. 1997Murine MyD88, an RNA with homology both to the interleukin-1 receptor signaling domain and to 'death-domains', is rapidly upregulated during differentiation of the myeloleukemic cell line M1...
- IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signalingM Muzio
University of Michigan Medical School, Department of Pathology, Ann Arbor, MI 48109, USA
Science 278:1612-5. 1997..were identified that are required for IL-1R-induced NF-kappaB activation: IRAK-2, a Pelle family member, and MyD88, a death domain-containing adapter molecule. Both associate with the IL-1R signaling complex...
- MyD88, an adapter protein involved in interleukin-1 signalingK Burns
Institute of Biochemistry, Lausanne Branch, University of Lausanne, Switzerland
J Biol Chem 273:12203-9. 1998b>MyD88 has a modular organization, an N-terminal death domain (DD) related to the cytoplasmic signaling domains found in many members of the tumor necrosis factor receptor (TNF-R) superfamily, and a C-terminal Toll domain similar to that ..
- IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) familyH Wesche
Tularik Inc, South San Francisco, California 94080, USA
J Biol Chem 274:19403-10. 1999..The discovery of IRAK-M adds another level of complexity to our understanding of signaling by members of the Toll/IL-1 receptor family...
- Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptorK Burns
Institute of Biochemistry, University of Lausanne, BIL Biomedical Research Centre, Chemin des Boveresses 155, CH 1066 Epalinges, Switzerland
Nat Cell Biol 2:346-51. 2000..complex that consists of two different receptor chains (IL-1Rs), IL-1RI and IL-1RAcP, the adaptor protein MyD88, the serine/threonine kinase IRAK and a new protein, which we have named Tollip...
- Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4Kimberly Burns
Institute of Biochemistry, University of Lausanne, BIL Biomedical Research Center, CH 1066 Epalinges, Switzerland
J Exp Med 197:263-8. 2003..TLRs) and members of the proinflammatory interleukin 1 receptor (IL-1R) family are dependent on the presence of MyD88 for efficient signal transduction...
- Bruton's tyrosine kinase is a Toll/interleukin-1 receptor domain-binding protein that participates in nuclear factor kappaB activation by Toll-like receptor 4Caroline A Jefferies
Cytokine Research Group, Department of Biochemistry and Biotechnology Institute, Trinity College, Dublin 2, Ireland
J Biol Chem 278:26258-64. 2003..experiments revealed that Btk can also interact with key proteins involved in TLR4 signal transduction, namely, MyD88, Mal (MyD88 adapter-like protein), and interleukin-1 receptor-associated kinase-1, but not TRAF-6...
- MyD88S, a splice variant of MyD88, differentially modulates NF-kappaB- and AP-1-dependent gene expressionSophie Janssens
Department of Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, Ghent University VIB, Technologiepark 927, B 9052, Ghent, Belgium
FEBS Lett 548:103-7. 2003b>MyD88 is an adapter protein that is involved in Toll-like receptor (TLR)- and interleukin-1 receptor (IL-1R)-induced activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK)...
- Interferon-alpha induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6Taro Kawai
ERATO, Akira Innate Immunity Program, Japan Science and Technology Agency, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita, Osaka 565 0871, Japan
Nat Immunol 5:1061-8. 2004..Production of IFN-alpha is dependent on the Toll-interleukin-1 receptor domain-containing adaptor MyD88. Here we show that MyD88 formed a complex with the transcription factor IRF7 but not with IRF3...
- Transforming growth factor-beta differentially inhibits MyD88-dependent, but not TRAM- and TRIF-dependent, lipopolysaccharide-induced TLR4 signalingYoshikazu Naiki
Department of Pediatric Infectious Diseases, Cedars Sinai Medical Center, University of California Los Angeles, 8700 Beverly Blvd, Los Angeles, CA 90048, USA
J Biol Chem 280:5491-5. 2005..TGF-beta1 can specifically interfere with TLR2, -4, or -5 ligand-induced responses involving the adaptor molecule MyD88 (myeloid differentiation factor 88) but not the TRAM/TRIF signaling pathway by decreasing MyD88 protein levels in ..
- A novel splice variant of interleukin-1 receptor (IL-1R)-associated kinase 1 plays a negative regulatory role in Toll/IL-1R-induced inflammatory signalingNavin Rao
Johnson and Johnson Pharmaceutical Research and Development, 3210 Merryfield Row, San Diego, CA 92121, USA
Mol Cell Biol 25:6521-32. 2005..However, IRAK1c retains the ability to strongly interact with IRAK2, MyD88, Tollip, and TRAF6...
- Localization of TLR2 and MyD88 to Chlamydia trachomatis inclusions. Evidence for signaling by intracellular TLR2 during infection with an obligate intracellular pathogenCATHERINE M O'CONNELL
Department of Microbiology Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Biol Chem 281:1652-9. 2006..trachomatis. We found that dominant negative MyD88 inhibited interleukin-8 (IL-8) secretion during a productive infection with chlamydia...
- Suppressor of cytokine signaling 1 negatively regulates Toll-like receptor signaling by mediating Mal degradationAshley Mansell
Centre for Functional Genomics and Human Disease, Monash Institute of Medical Research, Monash University, Melbourne, Victoria, Australia
Nat Immunol 7:148-55. 2006..The transient activation of Mal and subsequent SOCS-1-mediated degradation is a rapid and selective means of limiting primary innate immune response...
- MyD88 and TNF receptor-associated factor 6 are critical signal transducers in Helicobacter pylori-infected human epithelial cellsYoshihiro Hirata
Department of Gastroenterology, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 8655, Japan
J Immunol 176:3796-803. 2006..Protein interactions of exogenously expressed TNFR-associated factor 6 (TRAF6) and MyD88 or receptor-interacting protein 2 and nucleotide-binding oligomerization domain 1 or those of endogenous IkappaB ..
- Mass spectrometric analysis of the endogenous type I interleukin-1 (IL-1) receptor signaling complex formed after IL-1 binding identifies IL-1RAcP, MyD88, and IRAK-4 as the stable componentsConstantinos Brikos
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, London, UK
Mol Cell Proteomics 6:1551-9. 2007..IL-1, IL-1RI, IL-1 receptor accessory protein (IL-1RAcP), and myeloid differentiation primary response protein 88 (MyD88) in the complex. The p60 protein (IRAK-4) was the earliest component of the complex to be phosphorylated...
- Hepatitis C virus nonstructural protein 5A modulates the toll-like receptor-MyD88-dependent signaling pathway in macrophage cell linesTakayuki Abe
Department of Molecular Virology, Graduate School of Medicine, Osaka University, Osaka, Japan
J Virol 81:8953-66. 2007..Various genotypes of NS5A bound to MyD88, a major adaptor molecule in TLR, inhibited the recruitment of interleukin-1 receptor-associated kinase 1 to MyD88,..
- Distinct roles of TIR and non-TIR regions in the subcellular localization and signaling properties of MyD88Tadashi Nishiya
Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
FEBS Lett 581:3223-9. 2007b>MyD88 is a cytoplasmic adaptor protein that is critical for Toll-like receptor (TLR) signaling. The subcellular localization of MyD88 is characterized as large condensed forms in the cytoplasm...
- MyD88 predicts chemoresistance to paclitaxel in epithelial ovarian cancerDan Arin Silasi
Department of Obstetrics, Gynecology, and Reproductive Services, Yale University School of Medicine, New Haven, Connecticut 06520, USA
Yale J Biol Med 79:153-63. 2006..Recently, we described the expression of MyD88 in ovarian cancer cells that were resistant to the cytotoxic agent paclitaxel...
- Inhibition of TLR3 and TLR4 function and expression in human dendritic cells by helminth parasitesRoshanak Tolouei Semnani
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Blood 112:1290-8. 2008..mRNA expression of MyD88, the adaptor molecule involved in TLR4 signaling, was significantly diminished in mhDCs after exposure to mf...
- Pyogenic bacterial infections in humans with MyD88 deficiencyHorst von Bernuth
Human Genetics of Infectious Diseases, INSERM U550, Paris, France
Science 321:691-6. 2008b>MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection...
- Aspergillus fumigatus-induced interleukin-8 synthesis by respiratory epithelial cells is controlled by the phosphatidylinositol 3-kinase, p38 MAPK, and ERK1/2 pathways and not by the toll-like receptor-MyD88 pathwayViviane Balloy
Unité de Défense Innée et Inflammation, Institut Pasteur, Paris 75015, France
J Biol Chem 283:30513-21. 2008..Macrophages detect A. fumigatus via Toll-like receptors 2 and 4 (TLR2 and -4) and respond by the MyD88-NF-kappaB-dependent synthesis of inflammatory mediators...
- Toll-like receptor 9 affects severity of IgA nephropathyHitoshi Suzuki
Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan
J Am Soc Nephrol 19:2384-95. 2008..scan of ddY mice, which spontaneously develop IgAN, was performed, and myeloid differentiation factor 88 (MyD88) was identified as a candidate gene for progression of renal injury (chi(2) = 21.103, P = 0.00017)...
- Structural basis for the multiple interactions of the MyD88 TIR domain in TLR4 signalingHidenori Ohnishi
Department of Pediatrics, Graduate School of Medicine, Center for Emerging Infectious Diseases, and Center for Advanced Drug Research, Gifu University, Gifu, Japan
Proc Natl Acad Sci U S A 106:10260-5. 2009Myeloid differentiating factor 88 (MyD88) and MyD88 adaptor-like (Mal) are adaptor molecules critically involved in the Toll-like receptor (TLR) 4 signaling pathway...
- An oligomeric signaling platform formed by the Toll-like receptor signal transducers MyD88 and IRAK-4Precious G Motshwene
Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom
J Biol Chem 284:25404-11. 2009..to downstream signal transduction by the recruitment of a post-receptor complex containing the adaptor protein MyD88 and the IRAK protein kinases...
- PKC-alpha controls MYD88-dependent TLR/IL-1R signaling and cytokine production in mouse and human dendritic cellsChristelle Langlet
Institute for Medical Immunology, Universite Libre de Bruxelles, Charleroi, Belgium
Eur J Immunol 40:505-15. 2010..cPKC)-alpha regulates TRIF-dependent IFN response factor 3 (IRF3)-mediated gene transcription, but its role in MyD88-dependent TLR signaling remains unknown...
- High expression of Toll-like receptor 4/myeloid differentiation factor 88 signals correlates with poor prognosis in colorectal cancerE L Wang
Department of Human Pathology, Institute of Health Biosciences, University of Tokushima Graduate School, 3 18 15 Kuramoto cho, Tokushima, Japan
Br J Cancer 102:908-15. 2010..To demonstrate the role of TLR4 signalling in colon tumourigenesis, we examined the expression of TLR4 and myeloid differentiation factor 88 (MyD88) in colorectal cancer (CRC).
- Identification of MyD88 as a novel target of miR-155, involved in negative regulation of Helicobacter pylori-induced inflammationBin Tang
Department of Clinical Microbiology and Immunology, College of Medical Laboratory Science, Third Military Medical University, Chongqing, China
FEBS Lett 584:1481-6. 2010..Here, we identified myeloid differentiation protein 88 (MyD88) as a target gene of miR-155, and found that miR-155 decreased MyD88 expression at the protein but not the mRNA ..
- SARM inhibits both TRIF- and MyD88-mediated AP-1 activationJun Peng
Department of Biological Sciences, National University of Singapore, Singapore
Eur J Immunol 40:1738-47. 2010..Both the TRIF- and MyD88-mediated, as well as basal MAPK activity, were repressed, indicating that SARM-mediated inhibition may not be ..
- Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signallingSu Chang Lin
Department of Biochemistry, Weill Cornell Medical College, New York, New York 10021, USA
Nature 465:885-90. 2010b>MyD88, IRAK4 and IRAK2 are critical signalling mediators of the TLR/IL1-R superfamily...
- The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88Bing He
Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
Nat Immunol 11:836-45. 2010..Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-kappaB signaling pathways via a Toll-interleukin 1 (IL-1) ..
- Viral inhibitory peptide of TLR4, a peptide derived from vaccinia protein A46, specifically inhibits TLR4 by directly targeting MyD88 adaptor-like and TRIF-related adaptor moleculeTatyana Lysakova-Devine
Immunology Research Centre, School of Biochemistry and Immunology, Trinity College Dublin, Ireland
J Immunol 185:4261-71. 2010..Indeed, VIPER directly interacted with the TLR4 adaptor proteins MyD88 adaptor-like (Mal) and TRIF-related adaptor molecule (TRAM)...
- Dual function of MyD88 in RAS signaling and inflammation, leading to mouse and human cell transformationIsabelle Coste
CNRS UMR5201, University of Lyon, Centre Leon Berard, Lyon, France
J Clin Invest 120:3663-7. 2010Accumulating evidence points to inflammation as a promoter of carcinogenesis. MyD88 is an adaptor molecule in TLR and IL-1R signaling that was recently implicated in tumorigenesis through proinflammatory mechanisms...
- Oncogenically active MYD88 mutations in human lymphomaVu N Ngo
Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Nature 470:115-9. 2011..Here we describe the dependence of ABC DLBCLs on MYD88, an adaptor protein that mediates toll and interleukin (IL)-1 receptor signalling, and the discovery of highly ..
- Prognostic significance of MyD88 expression by human epithelial ovarian carcinoma cellsYi Zhu
Department of Gynecologic Oncology, Sichuan Cancer Hospital, Sichuan, People s Republic of China
J Transl Med 10:77. 2012b>MyD88 is an adaptor protein for TLR-4 signaling known to mediate paclitaxel resistance in epithelial ovarian carcinoma (EOC). This study examined the clinical significance of MyD88 expression in EOC.
- MYD88 L265P somatic mutation in Waldenström's macroglobulinemiaSteven P Treon
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute, M547, 450 Brookline Ave, Boston, MA 02115, USA
N Engl J Med 367:826-33. 2012..Waldenström's macroglobulinemia is an incurable, IgM-secreting lymphoplasmacytic lymphoma (LPL). The underlying mutation in this disorder has not been delineated...
- IGHV gene features and MYD88 L265P mutation separate the three marginal zone lymphoma entities and Waldenström macroglobulinemia/lymphoplasmacytic lymphomasN Gachard
Laboratoires d Hématologie et d Immunologie, CHU de Limoges, Limoges and Centre National de la Recherche Scientifique, UMR CNRS 7276, Faculté de Médecine de Limoges, Universite de Limoges, Limoges, France
Leukemia 27:183-9. 2013..lymphomas (WM/LPLs), immunoglobulin heavy chain variable gene (IGHV) features were analyzed and the occurrence of MYD88 L265P mutations was identified in a series of 123 patients: 53 MZLs from the spleen (SMZLs), 11 from lymph nodes (..
- MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase chain reactionLian Xu
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute, Boston, MA 02215, USA
Blood 121:2051-8. 2013By whole-genome and/or Sanger sequencing, we recently identified a somatic mutation (MYD88 L265P) that stimulates nuclear factor κB activity and is present in >90% of Waldenström macroglobulinemia (WM) patients...
- Prevalence and clinical significance of the MYD88 (L265P) somatic mutation in Waldenstrom's macroglobulinemia and related lymphoid neoplasmsMarzia Varettoni
Department of Hematology Oncology, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
Blood 121:2522-8. 2013A study has shown that MYD88 (L265P) is a recurring somatic mutation in Waldenström's macroglobulinemia (WM)...
- MYD88 L265P is a marker highly characteristic of, but not restricted to, Waldenström's macroglobulinemiaC Jimenez
Department of Hematology, University Hospital of Salamanca, Salamanca, Spain
Leukemia 27:1722-8. 2013We evaluated the MYD88 L265P mutation in Waldenström's macroglobulinemia (WM) and B-cell lymphoproliferative disorders by specific polymerase chain reaction (PCR) (sensitivity ∼10(-3))...
- MYD88 L265P mutation in Waldenstrom macroglobulinemiaStephanie Poulain
Department of Hematology Immunology Cytogenetic, Centre Hospitalier, Valenciennes, France
Blood 121:4504-11. 2013Mutation of the MYD88 gene has recently been identified in activated B-cell-like diffuse cell lymphoma and enhanced Janus kinase/signal transducer and activator of transcription (JAK-STAT) and nuclear factor κB (NF-κB) signaling ..
- Myeloid differentiation factor 88 promotes growth and metastasis of human hepatocellular carcinomaBeibei Liang
School of Pharmacy, Shanghai Jiao Tong University, Shanghai, PR China
Clin Cancer Res 19:2905-16. 2013To investigate the expression of myeloid differentiation factor 88 (MyD88) in hepatocellular carcinoma (HCC) and its prognostic value in patients with HCC.
- A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemiaGuang Yang
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute, Boston, MA 02215, USA
Blood 122:1222-32. 2013Myeloid differentiation factor 88 (MYD88) L265P somatic mutation is highly prevalent in Waldenström macroglobulinemia (WM) and supports malignant growth through nuclear factor κB (NF-κB)...
- Modification of MyD88 mRNA splicing and inhibition of IL-1beta signaling in cell culture and in mice with a 2'-O-methoxyethyl-modified oligonucleotideTimothy A Vickers
Department of Functional Genomics, Isis Pharmaceuticals, 1896 Rutherfored Road, Carlsbad, CA 92008, USA
J Immunol 176:3652-61. 2006A number of proinflammatory cytokines, including IL-1beta, signal through the adaptor protein MyD88. This signaling leads to phosphorylation of IL-1R-associated kinase-1 (IRAK-1) and, ultimately, activation of the NF-kappaB transcription ..
- Smad6-specific recruitment of Smurf E3 ligases mediates TGF-β1-induced degradation of MyD88 in TLR4 signallingYoun Sook Lee
Department of Biological Sciences, Sungkyunkwan University, Suwon 440 746, Korea
Nat Commun 2:460. 2011..Here we show a novel mechanism where TGF-β1-induced K48-linked polyubiquitination and degradation of the adaptor MyD88 protein is dependent on the Smad6 protein, but not Smad7, and mediated by recruitment of the Smad ubiquitin ..
- Binding specificity of Toll-like receptor cytoplasmic domainsVictoria Brown
Department of Genome Sciences, University of Washington, Seattle 98195, USA
Eur J Immunol 36:742-53. 2006b>MyD88 participates in signal transduction by binding to the cytoplasmic Toll/IL-1 receptor (TIR) domains of activated Toll-like receptors (TLR)...
- TRAF6 distinctively mediates MyD88- and IRAK-1-induced activation of NF-kappaBMasashi Muroi
National Institute of Health Sciences, 1 18 1 Kamiyoga, Setagaya, Tokyo 158 8501, Japan
J Leukoc Biol 83:702-7. 2008b>MyD88 and IL-1R-associated kinase 1 (IRAK-1) play crucial roles as adaptor molecules in signal transduction of the TLR/IL-1R superfamily, and it is known that expression of these proteins leads to the activation of NF-kappaB in a TNFR-..
- Regulation of interleukin-1- and lipopolysaccharide-induced NF-kappaB activation by alternative splicing of MyD88Sophie Janssens
Department of Molecular Biology, Unit of Molecular Signal Transduction in Inflammation, Gent University VIB, K L Ledeganckstraat 35, B 9000 Gent, Belgium
Curr Biol 12:467-71. 2002b>MyD88 is an adaptor protein that is involved in interleukin-1 receptor (IL-1R)- and Toll-like receptor (TLR)-induced activation of NF-kappaB...
- Dysregulation of LPS-induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor-associated kinase 1 activation in endotoxin-tolerant cellsAndrei E Medvedev
Department of Microbiology and Immunology, University of Maryland, Baltimore 21201, USA
J Immunol 169:5209-16. 2002..Comparable levels of mRNA and protein for myeloid differentiation factor 88 (MyD88), IL-1R-associated kinase 1 (IRAK-1), and TNFR-associated factor-6 were found in normal and LPS-tolerant monocytes,..
- MyD88, IRAK1 and TRAF6 knockdown in human chondrocytes inhibits interleukin-1-induced matrix metalloproteinase-13 gene expression and promoter activity by impairing MAP kinase activationRasheed Ahmad
Department of Medicine, University of Montreal and Research Centre of CHUM Notre Dame Hospital, Montreal, Quebec, Canada H2L 4M1
Cell Signal 19:2549-57. 2007..Nothing is known about the involvement of adaptor proteins, MyD88, IRAK1 and TRAF6 in MMP-13 regulation...
- IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinaseShyun Li
Tularik, Inc, 2 Corporate Drive, South San Francisco, CA 94080, USA
Proc Natl Acad Sci U S A 99:5567-72. 2002....
- Toll IL-1 receptors differ in their ability to promote the stabilization of adenosine and uridine-rich elements containing mRNAShyamasree Datta
Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
J Immunol 173:2755-61. 2004..of TIR family members to stabilize ARE-containing mRNAs results from their differential use of signaling adaptors MyD88, MyD88 adaptor-like protein, Toll receptor IFN-inducing factor (Trif), and Trif-related adaptor molecule...
- Contribution of globular death domains and unstructured linkers to MyD88.IRAK-4 heterodimer formation: an explanation for the antagonistic activity of MyD88sElena Mendoza-Barberá
Cardiovascular Research Center and Institut de Recerca, Hospital de la Santa Creu i Sant Pau, Sant Antoni Maria Claret 167, 08025 Barcelona, Spain
Biochem Biophys Res Commun 380:183-7. 2009Homotypic interactions of death domains (DD) mediate complex formation between MyD88 and IL-1 receptor-associated kinases (IRAKs)...
- Polymorphisms in interleukin-1 receptor-associated kinase 4 are associated with total serum IgEM A Tewfik
Department of Otolaryngology Head and Neck Surgery, Montreal General Hospital, McGill University, Montreal, Canada
Allergy 64:746-53. 2009..We sought to investigate the association between single nucleotide polymorphisms (SNPs) in the Toll-like receptor (TLR) signaling pathway and total serum IgE level...
- TLR4 signaling induced by lipopolysaccharide or paclitaxel regulates tumor survival and chemoresistance in ovarian cancerM Szajnik
University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
Oncogene 28:4353-63. 2009..TLRs are also expressed on ovarian cancer (OvCa) cells, but the consequences of signaling by the TLR4/MyD88 pathway in these cells are unclear...
- CD300F blocks both MyD88 and TRIF-mediated TLR signaling through activation of Src homology region 2 domain-containing phosphatase 1Sang Min Lee
School of Life Sciences and Biotechnology, Kyungpook National University, Daegu 702 701, Korea
J Immunol 186:6296-303. 2011..Western blot analysis of THP-1 cells revealed that these inhibitory actions were effective in pathways involving MyD88 and/or TRIF of TLR signaling and associated with marked suppression of IκB kinase activation, phosphorylation/..
- Characterization of a cascade of protein interactions initiated at the IL-1 receptorJason A Boch
Department of Medicine, Harvard Medical School, and the Beth Israel Deaconess Medical Center, Boston, MA, USA
Biochem Biophys Res Commun 303:525-31. 2003..IRAK2 is also capable of associating directly with MyD88 by distinct regions...
- [Role of transduce molecules and modulatory factors of signal pathways of Toll-like receptor in inflammatory response of children with sepsis]Wei Guo Yang
Pediatric Intensive Care Unit, Shenzhen Children Hospital, Shenzhen 518026, Guangdong, China
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 20:561-4. 2008..To investigate the role of transduce molecules and modulatory factors of signal pathways of Toll-like receptors (TLRs) in aberrant inflammatory response in children with sepsis...
- Human lactoferrin activates NF-kappaB through the Toll-like receptor 4 pathway while it interferes with the lipopolysaccharide-stimulated TLR4 signalingKen Ando
Tokyo University of Pharmacy and Life Sciences, Japan
FEBS J 277:2051-66. 2010..TRAF6 is known to be indispensable in leading to NF-kappaB activation in myeloid differentiating factor 88 (MyD88)-dependent signaling pathways, while the role of TRAF6 in the MyD88-independent signaling pathway has not been ..
- Clinical features and outcome of patients with IRAK-4 and MyD88 deficiencyCapucine Picard
Study Center of Primary Immunodeficiencies, Assistance Publique Hopitaux de Paris, Paris, France
Medicine (Baltimore) 89:403-25. 2010..We documented the clinical features and outcome of 48 patients with IRAK-4 deficiency and 12 patients with MyD88 deficiency, from 37 kindreds in 15 countries...
- Identification of critical residues of the MyD88 death domain involved in the recruitment of downstream kinasesMaria Loiarro
Department of Public Health and Cell Biology, University of Rome Tor Vergata, 00133 Rome, Italy
J Biol Chem 284:28093-103. 2009b>MyD88 couples the activation of the Toll-like receptors and interleukin-1 receptor superfamily with intracellular signaling pathways. Upon ligand binding, activated receptors recruit MyD88 via its Toll-interleukin-1 receptor domain...
- Modulation of Toll-interleukin 1 receptor mediated signalingXiaoxia Li
Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
J Mol Med (Berl) 83:258-66. 2005..A group of TIR domain containing adaptors (MyD88, TIRAP, TRIF and TRAM), are differentially recruited to the Toll-IL-1 receptors, contributing to the specificity ..
- Molecular cloning, characterization and expression analysis of TLR9, MyD88 and TRAF6 genes in common carp (Cyprinus carpio)Pawapol Kongchum
Department of Fisheries and Wildlife Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA
Fish Shellfish Immunol 30:361-71. 2011..TLR9 functions as a PRR that recognizes CpG motifs in bacterial and viral DNA and requires adaptor molecules MyD88 and TRAF6 for signal transduction...
- Suppression of allergic reaction by lambda-carrageenan: toll-like receptor 4/MyD88-dependent and -independent modulation of immunityR F Tsuji
Noda Institute for Scientific Research, Noda City, Japan
Clin Exp Allergy 33:249-58. 2003..Because PRRs recognize heterogeneous ligands, daily food intake can potentially regulate immune allergic reaction...
- Wound healing is impaired in MyD88-deficient mice: a role for MyD88 in the regulation of wound healing by adenosine A2A receptorsLisa Macedo
Department of Cell Biology and Molecular Medicine, The Cardiovascular Research Institute, New Jersey Medical School, UMDNJ, 185 South Orange Ave, Newark, NJ 07103, USA
Am J Pathol 171:1774-88. 2007..We show in this study that this switch critically requires signaling through MyD88, IRAK4, and TRAF6...
- Protection against autoimmune nephritis in MyD88-deficient MRL/lpr miceAtsushi Sadanaga
Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
Arthritis Rheum 56:1618-28. 2007..To determine whether innate receptor signals play an important role in the development of autoimmune nephritis in MRL/lpr mice, an experimental model of lupus nephritis...
- Myeloid differentiation factor-88 (MyD88) is essential for control of primary in vivo Francisella tularensis LVS infection, but not for control of intra-macrophage bacterial replicationCarmen M Collazo
Laboratory of Mycobacterial Diseases and Cellular Immunology, Division of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD 20852, USA
Microbes Infect 8:779-90. 2006..Here we wished to explore the contribution of the MyD88/Toll-like receptor signaling pathway in initiating murine responses to F. tularensis Live Vaccine Strain (LVS)...
- Dual role of MyD88 in rapid clearance of relapsing fever Borrelia sppDevin D Bolz
Department of Pathology, University of Utah, 15 North Medical Drive East 2100, Salt Lake City, UT 84112, USA
Infect Immun 74:6750-60. 2006..b>MyD88-deficient mice display defective clearance of many pathogens; however, the IgM response to persistent infection is ..
- Necrotic neurons enhance microglial neurotoxicity through induction of glutaminase by a MyD88-dependent pathwayTeresa F Pais
Instituto Gulbenkian de Ciencia, Rua da Quinta Grande, 6, 2780 156 Oeiras, Portugal
J Neuroinflammation 5:43. 2008..We investigated the molecular mechanisms underlying triggering of microglial activation by necrotic neuronal damage...
- MyD88 adapter-like (Mal)/TIRAP interaction with TRAF6 is critical for TLR2- and TLR4-mediated NF-kappaB proinflammatory responsesBrett Verstak
Centre for Innate Immunity and Infectious Disease, Monash Institute of Medical Research, Monash University, Clayton, Victoria 3168, Australia
J Biol Chem 284:24192-203. 2009..b>MyD88 adapter-like (Mal), also termed TIRAP, is involved in bridging MyD88 to the receptor complex for TLR-2 and TLR4 ..
- Synergism of Toll-like receptor-induced interleukin-12p70 secretion by monocyte-derived dendritic cells is mediated through p38 MAPK and lowers the threshold of T-helper cell type 1 responsesHermann R Bohnenkamp
Cancer Research UK, Breast Cancer Biology Group, Thomas Guy House, 3rd Floor, Guy s Hospital, London SE1 9RT, UK
Cell Immunol 247:72-84. 2007..signalling pathways can be distinguished: The inflammatory signalling pathway acting via the adapter molecule MyD88, leading to the activation of nuclear factor-kappaB (NF-kappaB) and mitogen activated protein kinases (MAPK) such ..
- Functional regulation of MyD88-activated interferon regulatory factor 5 by K63-linked polyubiquitinationMumtaz Yaseen Balkhi
Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21231, USA
Mol Cell Biol 28:7296-308. 2008..IRF-5 is activated by Toll-like receptor 7 (TLR7) and TLR9 via the MyD88 pathway, where it interacts with both MyD88 and the E3 ubiquitin ligase, TRAF6...
- Microglial activation by Citrobacter koseri is mediated by TLR4- and MyD88-dependent pathwaysShuliang Liu
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
J Immunol 183:5537-47. 2009..In this study, we investigated the importance of the LPS receptor TLR4 and MyD88, an adaptor molecule involved in the activation of the majority of TLRs in addition to the IL-1 and IL-18 ..
- MyD88 functions as a negative regulator of TLR3/TRIF-induced corneal inflammation by inhibiting activation of c-Jun N-terminal kinaseAngela C Johnson
Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio 44106, USA
J Biol Chem 283:3988-96. 2008The adaptor molecule MyD88 is necessary for responses to all Toll-like receptors except TLR3 and a subset of TLR4 signaling events, which are mediated by the adaptor molecule TRIF...
- Toll-like receptor 4 agonists adsorbed to aluminium hydroxide adjuvant attenuate ovalbumin-specific allergic airway disease: role of MyD88 adaptor molecule and interleukin-12/interferon-gamma axisJ Bortolatto
Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
Clin Exp Allergy 38:1668-79. 2008..responses through toll-like receptor 4 (TLR4) that in turn activates two major signalling pathways via either MyD88 or TRIF adaptor proteins...
- Mechanisms of Toll-like receptor 4 (TLR4)-mediated inflammation after cold ischemia/reperfusion in the heartDavid J Kaczorowski
Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA
Transplantation 87:1455-63. 2009..hypothesized that the TLR4 coreceptor CD14, the intracellular adaptor proteins myeloid differentiation factor 88 (MyD88) and TIR domain-containing-adaptor inducing IFNbeta (TRIF) would be required for cold I/R induced inflammation...
- [Effect of intrauterine lipopolysaccharide infusion on Toll-like receptor 4 signaling transduction pathway in lungs of perinatal rats]Xiao Yu
Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Zhonghua Er Ke Za Zhi 47:667-71. 2009....
- MyD88 deficiency leads to decreased NK cell gamma interferon production and T cell recruitment during Chlamydia muridarum genital tract infection, but a predominant Th1 response and enhanced monocytic inflammation are associated with infection resolutionUma M Nagarajan
Department of Pediatrics, Arkansas Children s Hospital and University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
Infect Immun 79:486-98. 2011We have previously shown that MyD88 knockout (KO) mice exhibit delayed clearance of Chlamydia muridarum genital infection compared to wild-type (WT) mice...
- MyD88 is pivotal for immune recognition of Citrobacter koseri and astrocyte activation during CNS infectionShuliang Liu
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, 72205, USA
J Neuroinflammation 8:35. 2011..The roles of Toll-like receptor 4 (TLR4) and its signaling adaptor MyD88 during CNS C...
- Astar Winoto; Fiscal Year: 2016..This hypothesis will be tested in aim 1. Using DC-specific FADD-/-/MyD88-/- and dcFADD-/-/RIP3-/- mice, we will address whether constitutive stimulation of DCs through TLRs leads to ..
- Shawn J Skerrett; Fiscal Year: 2016..Specific aim #3. Determine the roles of IL-1[unreadable] and IL-18 in resistance to Lp pneumonia. MyD88, an adaptor that mediates signaling from TLRs and IL-1/IL-18 receptors, is required for survival from pneumonic ..
- Kevin J Tracey; Fiscal Year: 2014..Specific Aim 2. To elucidate whether HMGB1-TLR4 activates TIRAP-MyD88 and TRAM-TRIF dependent signaling. Specific Aim 3...
- Phagosomal Signals Shape Inflammatory Responses to Borrelia BurgdorferiJuan C Salazar; Fiscal Year: 2010..Recent evidence from the investigator's laboratory suggests that the TLR2-independent responses are MyD88-dependent and occur via TLR8...
- MARCEL WUETHRICH; Fiscal Year: 2015..We hypothesize that receptor recognition of Blastomyces mannans by the FcR3-Syk-Card9 and the TLR-Myd88 signaling pathways are essential to induce T17 cells and vaccine immunity...
- Intracellular Targeting of Proinflammatory Pathways to Ameliorate Type 1 DiabetesDaniel J Moore; Fiscal Year: 2010..Signaling through these receptors depends on two key adaptor proteins, MyD88 and TRIP...
- Gary A Jarvis; Fiscal Year: 2016..We recently confirmed that Neisserial LOS activates both MyD88-dependent and TRIF-dependent pathways through NF-:B and IFN regulatory factor 3 (IRF-3) transcription factors, and ..
- HIV-1 regulation by MTb: pathogen and host factorAnne Goldfeld; Fiscal Year: 2010..monocytes requires signaling through the adaptor protein myeloid differentiation primary response gene 88 (MyD88)...
- Orthopaedic Wear Debris, Vitamin D, and Innate ImmunityJohn S Adams; Fiscal Year: 2010..Here TLR-expressing mouse bone marrow-derived macrophages from wild-type and from TLR- and MyD88 (universal adapter protein for TLRs)-deficient mice will be employed to monitor by quantitative PCR and/or ELISA ..
- Yong Jun Liu; Fiscal Year: 2014..Among the TLRs that associate with MyD88, TLR7 and TLR9 strictly depend on MyD88 for signal transduction, and reside in the endoplasmic reticulum (ER) in ..
- Pranoti Mandrekar; Fiscal Year: 2016..alcohol-induced sensitization to LPS-induced inflammatory cytokine production by: A) Studying the interactions of MyD88- depepndent down-stream signaling molecules, IRAK-1 and IKK with co-chaperone cdc37 and hsp90 in alcoholic Kupffer ..
- LAURIE HOLLIS GLIMCHER; Fiscal Year: 2015..TRUC colitis and CRC are, in contrast to most other mouse colitis models, independent of Myd88 signaling giving us the opportunity to identify non- Myd88 driven pathways and mediators that may intersect with ..
- Role of Polymorphonuclear Phagocytes in Malaria SepsisRicardo Gazzinelli; Fiscal Year: 2010..Our studies suggest that the Myeloid Differentiation Factor 88 (MyD88), an adaptor-signaling molecule for the IL-1 receptor (and the related IL-18r and IL-33r) as well as Toll- like ..
- Linking tumor chemoresistance to TLR variants that mediate damage chain reactionNathalie Scholler; Fiscal Year: 2013..b>MyD88 plays a critical role in cancer...
- Role of cytokine induction in APOBEC3-mediated virus restrictionCHIOMA OKEOMA; Fiscal Year: 2011..To determine at which step in the infection pathway mA3 is induced, we will use mice lacking mA3, MyD88, TRIP and TLR4 genes and mice unable to respond to the viral Sag protein...
- Adenosine, Toll-Like Receptors and AngiogenesisSamuel Joseph Leibovich; Fiscal Year: 2011..Mice lacking A2ARs have impaired wound healing, as do mice lacking MyD88, a key mediator of TLR signaling. MyD88-/- mice also fail to respond to the stimulatory effects of A2AR agonists...
- Channe D Gowda; Fiscal Year: 2016..pro-inflammatory cytokines such as TNF-[unreadable] and IL-12 and that pro-inflammatory cytokines produced by TLR9/MyD88-mediated signaling play critical roles in the generation of cell-mediated and antibody-mediated protective ..
- GAMMA DELTA T CELLS IN LYME ARTHRITISRalph C Budd; Fiscal Year: 2011..This will be also studied by in vivo infection with B. burgdorferi in mice lacking TLR, MyD88, or CD1d. A soluble Vd1 TCR will also be made to identify other Vd1 ligands (Aim 1)...
- Inhalation Tolerance, IgE and gamma/delta T cellsWilli K Born; Fiscal Year: 2013..Finally, we will examine if the IgE-regulatory function of the 34 T cells, which requires induction by MyD88+ DCs, relies on Th1-inducing cytokines produced by these DCs, such as IL-12...
- Yingzi Cong; Fiscal Year: 2016..dendritic cells (DC), and negatively regulated by microbiota through the interaction of TLR-TLR ligands via the MyD88 pathway...
- Protein Secretion Pathways of Mycobacterium tuberculosisMIRIAM S BRAUNSTEIN; Fiscal Year: 2013..hypothesize that the role of SecA2 in virulence is to limit host immune responses, possibly through modulation of MyD88-dependent pathways. The specific aims of this proposal are the following...
- Stefanie N Vogel; Fiscal Year: 2014..This proposal details innovative experimental approaches that will: (1) define the earliest interactions between MyD88, IRAK1 and IRAK4, and TRAF6 that mediate TLR-dependent signaling and identify compensatory signaling pathways that ..
- DEBROSKI R HERBERT; Fiscal Year: 2015..TFF2- treated-macrophages selectively expand TH2 cells from naove precursors through an IL-33-dependent, but MyD88-independent mechanism. It is unknown whether macrophages are necessary for TFF2-driven TH2 immunity...
- Der p 2-driven TLR4 signaling in allergic asthmaJaclyn W McAlees; Fiscal Year: 2013..MD-2-dependent TLR4 signaling involves activation of both Mal/MyD88 and TRIF/TRAM pathways of signal transduction...
- Juan C Salazar; Fiscal Year: 2015..provides substantial evidence the TLR2-independent signaling events elicited by Bb in human monocytes are MyD88-dependent and occur via TLR8...
- Cell Type-Specific Roles of TLR Signaling In Immune ResponsesAnthony L DeFranco; Fiscal Year: 2012..of a conditional allele we have engineered into the mouse germ line for the key TLR signaling adaptor molecule MyD88. In this allele, we have placed loxP sites in the introns on either side of the essential exon 3 of the myd88 gene,..
- Role of Innate Immunity in Pathogenesis of Chlamydia Pneumonia InfectionMoshe Arditi; Fiscal Year: 2010..pneumoniae infection. Our studies show that MyD88-/- mice were unable to mount an early inflammatory response, failed to clear the bacteria from their lungs, and ..
- Douglas T Golenbock; Fiscal Year: 2016..MD-2, 2) To characterize the fine details of TLR4/MD-2 receptor activation, 3) To characterize the TLR4 adapters: MyD88, Mai, TRIP and TRAM, 4) To define the biology of MD-2 in vivo...
- Alan A Aderem; Fiscal Year: 2016..2. Delineate the manner by which Sharpin transduces TLR2/MyD88 signals through the IKK complex to regulate transcriptional responses. 3...
- TLR and Notch Ligand in RSV-induced DiseaseNicholas W Lukacs; Fiscal Year: 2012..The upregulation of specific notch ligands on DCs is MyD88-dependent and provides a critical step in mature T cell differentiation...
- Innate Immunity and Mouse Model of Kawasaki DiseaseDanica Jenine Schulte; Fiscal Year: 2010..Our published data indicate that LCCWE potently induces NF-kB via TLR2 and MyD88 but not TLR4 in vitro (in murine and human macrophages and ECs) and in vivo (TLR2-/- and MyD88-/- mice do not ..
- TLR-mediated Signaling Complex Formation and Regulation of Effector FunctionsHans Haecker; Fiscal Year: 2012..pathways have been defined: TLR activation leads to recruitment and oligomerization of the adaptor protein MyD88, which binds to members of the IRAK family, which in turn recruit TRAF6...
- Group B. Streptococci and Toll-like ReceptorsDouglas T Golenbock; Fiscal Year: 2012..factor that induces cytokine formation in dependence on particle uptake and expression of the TLR-adapter protein MyD88, but cannot be assigned to established modes of TLR recognition...
- Toll-Like Receptor-Mediated Photoreceptor Mitochondrial DNA DamageNarsing A Rao; Fiscal Year: 2010..2. Determine the in-vivo effects of TLR upregulation and interaction with MyD88 on mitochondrial oxidative stress, using various TLRs, MyD88, and other adaptor proteins knockout animals. 3...
- Gender Factors Influencing Susceptability to InfluenzaSabra L Klein; Fiscal Year: 2010..sex steroid hormones, production of pro- and anti- inflammatory cytokines/chemokines, and signaling through the Myd88 pathway...
- Gabriel Nunez; Fiscal Year: 2015..aureus and S. pyogenes activate the NLRP3 inflammasome via pore-forming toxins but independently of MyD88/TRIF and the purinergic P2X7 receptor...
- Douglas T Golenbock; Fiscal Year: 2015..studies suggest that Toll-like receptors (TLRs), acting primarily through the Myeloid Differentiation Factor 88 (MyD88) adaptor molecule, are critical for initiation of this early inflammatory response and pathogenesis of malaria...
- Role of TLR-4 in Lung Reperfusion InjuryMICHAEL SCOTT MULLIGAN; Fiscal Year: 2013..TLR-4 has both a rapid MyD88-dependent signaling pathway, involving TIRAP and TRAF-6 leading to SAPK activation and a slower MyD88-independent ..
- Role of Toll-like Receptors in Transplant-Induced Reactivation of CytomegalovirusMichael Abecassis; Fiscal Year: 2010..technology to block expression in vivo, we propose to test the requirement for TLR2 as well as signaling adapters MyD88 and Trif in reactivation of MCMV IE gene expression in this model...
- RICHARD ARTHUR CHOLE; Fiscal Year: 2014..By comparing cytokine profiles from PA LPS stimulated keratinocytes derived from TLR2-/-, TLR4-/- and MyD88-/- knockout mice we hope to delineate the mechanism by which this process occurs...
- Irritable bowel syndrome-diarrhea: the role of gluten intolerance and HLA-DQ2MICHAEL L CAMILLERI; Fiscal Year: 2010..which is well established in celiac disease and involves binding to the chemokine receptor, CXCR3, leading to MyD88-dependent zonulin release (Lammers et al 2008)...
- Eric G Pamer; Fiscal Year: 2016..monocytogenes infection in reporter mice lacking MyD88, TNF, type I interferon receptor and IFN-gamma...
- Calvin B Williams; Fiscal Year: 2014..that the disease can be dissociated into two main components: one that is dependent on the innate immune regulator MyD88 and which involves inflammation at the mucosal surfaces in the skin, gut and lungs, and another that is MyD88-..
- Genhong Cheng; Fiscal Year: 2014..signaling specificity of individual TLRs, initiated through differential recruitment of adaptor molecules such as MyD88 and TRIF, can be further amplified by differential induction of cytokines, which are not only important for innate ..
- DEAN YAW LI; Fiscal Year: 2016..by IL-1[unreadable] but diverges from the canonical NF-?B-pathway at the level of the IL-1R adapter protein MYD88. MYD88 binds to ARNO, an ARF-GEF that activates the small GTPase ARF6...
- Ashok Kumar; Fiscal Year: 2014..TLR2-/- and MyD88-/- mice will be used to determine whether these mechanisms are TLR2/MyD88 dependent, active against other bacteria,..
- SHERVIN RABIZADEH; Fiscal Year: 2014..address the role of the innate immune signaling pathways, in particular the NOD/Rip2 and toll like receptor (TLR)/MyD88, in the ETBF-induced colitis model...
- Role of Glia and Inflammation in Altered Synapse Development in SchizophreniaSHINICHI KANO; Fiscal Year: 2012..Finally, we will address the role of innate immune signaling in microglia by using microglia-specific deletion of MyD88, a molecule that plays a central role in innate immune signaling...
- Regulated expression of B. burgdorferi virulence genesFELIPE CARDENAS CABELLO; Fiscal Year: 2010..2) Characterize B. burgdorferi genes relevant to colonization of the extracellular matrix in chronically infected MyD88 knockout mice using a global genomic approach involving saturated B...
- The Role of Toll-like Receptor 4 Positive T Cells in Intestinal Immune RegulationMIRAC NEDIM INCE; Fiscal Year: 2013..or colitic animals and in mice genetically deficient for proteins that participate in TLR4 signaling pathway, like MyD88-/- or TRIF-/- mouse strains...
- Ruxana T Sadikot; Fiscal Year: 2016..1 inhibits the expression of TREM-1 in response to LPS. Second, we have shown that MyD88 dependent and independent signaling determines the expression of TREM-1 in response to specific TLR ligands (2)...
- Innate immunity in Alzheimer's disease: Role of toll-like receptor signalingKen Ichiro Fukuchi; Fiscal Year: 2013..We hypothesize that these protective functions are mediated by MyD88-dependent pathways and that A[unreadable] load in the brain can be modulated by TLR4 signaling...
- Regulation of Toll-like receptor signaling by complementWenchao Song; Fiscal Year: 2012..of all TLRs? With a given TLR, is the effect of complement ligand-specific? Does complement regulate both MyD88-dependent and - independent pathways of TLR activation? Specific aim 2 To determine the specificity and site of ..
- Alexander V Chervonsky; Fiscal Year: 2016..In preliminary studies we have established that: a. non-obese diabetic (NOD) mice lacking MyD88 adaptor were resistant to spontaneous T1D when housed in conventional specific-pathogen-free (SPF) conditions;b...
- Role of MyD88-5 in the pathogenesis of Parkinson's diseaseBobby Thomas; Fiscal Year: 2012..We have cloned a neuron-specific mitochondrial protein, called MyD88-5, which is enriched in Lewy bodies from brains of postmortem PD patients and in pathologically affected regions ..
- Nejat K Egilmez; Fiscal Year: 2014..potential regulators of post-therapy tDC differentiation and activity, including IRF-8, SOCS-1, IDO-1/2, GCN-2 and MyD88 as well as additional candidates that are identified in Aim 1, are targeted via siRNA/gold nanorod complexes and ..
- Delays and variability in single-cell NFkB signalingLev S Tsimring; Fiscal Year: 2013..The third aim will address the role of two parallel pathways (MyD88 and TRIF) initiated by pathogen-derived lipopolysaccharide (LPS) signals...
- MyD88-bearing tumors in immune-regulation and chemo-resistanceGIL G MOR; Fiscal Year: 2012..a sub-population of epithelial ovarian cancer (EOC) cells that express Myeloid Differentiation Protein 88 (MyD88)...
- MARIO TOMAS PHILIPP; Fiscal Year: 2014..Thus far we have demonstrated that the adaptor molecule myeloid differentiation primary response gene 88 (MyD88), and the receptors Toll-like receptor 1 (TLR1), and TLR2 are directly involved in the activation of macrophage/..
- Age-associated Toll-like receptor dysfunction in the lungsCarlos J Orihuela; Fiscal Year: 2010..and FACs analysis we will determine if mRNA and protein levels of TLRs 1-9, and the TLR cell signaling molecules Myd88, IRAK-1, and IRAK-4 are decreased in alveolar macrophages and type II pneumocytes (lung mucosal epithelial cells) ..
- Toll-Like Receptor Signaling in Alzheimer's DiseaseKathryn J Moore; Fiscal Year: 2013..This hypothesis is based on preliminary findings that targeted deletion of the TLR signaling adaptor MyD88 abrogates microglial inflammatory responses to AB in vitro and in vivo...
- The Role of Direct Pathogen Detection by Sensory Neurons in Combating Bacterial IISAAC MING CHENG CHIU; Fiscal Year: 2012..neuron deficient mice, which lack the ability to produce neuropeptides, and neuronal conditional knockout mice for MyD88, the downstream signaling adaptor for all Toll-like Receptors...
- Novel DNA-Launched Attenuated Vaccine for VEE VirusPETER M PUSHKO; Fiscal Year: 2012..Recombinant i-DNA clones produced in bacteria contains CpG motifs that activate TLR9 and MyD88-dependent signaling pathways resulting in robust production of cyto- and chemokines, which induce strong priming ..
- Mechanisms of innate immune response modulation by mechanical ventilationWilliam A Altemeier; Fiscal Year: 2012..combination of highly specific toll-like receptor agonists and genetically modified mice, which lack either the MyD88 or TRIF adapter protein necessary for specific TLR signaling...
- Identification Of Proteins Responsible For Peanut AllergenicityFred Finkelman; Fiscal Year: 2009..platelet activating factor (PAF) and, to a lesser extent, histamine contribute to PE-induced shock;4) TLR2, TLR4, MyD88, and the adaptive immune system are not required for PE-induced shock;5) PE acts synergistically with IgE-mediated ..
- Innate Immune Response Genes and P. GingivalisJenny Ting; Fiscal Year: 2009..TLR activation requires a host of intracellular adaptor proteins proximal to the TLRs, including MyD88, TRAF6, MD-2 and TRAM...
- Structural biology of Toll like receptor/IL 1R signalingLiang Tong; Fiscal Year: 2005..The signaling pathway of the TLRs and IL-1RS involves many molecules, such as the adapter molecule MyD88, the protein kinase IRAK, TRAF6, and other down-stream mediators...
- Redox Mediated Signaling in the Toll-like Receptor FamilyFREDRICK OAKLEY; Fiscal Year: 2010..IL-1R1 and TLR-4 share many similar effectors (MyD88, IRAK, TRAF6), but also have unique effectors (TIRAP/Mal, TRAM, TRIP), that specify unique biological properties ..
- IRAK Family Function in Bacterial InfectionJames Thomas; Fiscal Year: 2001..This conserved signaling cascade consists of the proteins MyD88, the interleukin-1 receptor-associated kinase (IRAK) family of molecules (IRAK, IRAK2, and IRAK-M) and the tumor ..
- TLR Signaling in CD8 T Cell Response to Vaccinia VirusYiping Yang; Fiscal Year: 2010..We have shown that innate immune recognition of VV is mediated by Toll-like receptor 2 (TLR2) and dependent on MyD88 (a common adaptor for TLR signaling) and that the activation of TLR2-MyD88 pathway is critical for adaptive CD8 T ..
- IRAK Family Function in Bacterial InfectionJames Thomas; Fiscal Year: 2006..This conserved signaling cascade consists of the proteins MyD88, the interleukin-1 receptor-associated kinase (IRAK) family of molecules (IRAK, IRAK2, and IRAK-M) and the tumor ..