|  Help  |  About  |  Contact Us

Search our database by keyword

Examples

  • Search this entire website. Enter identifiers, names or keywords for genes, diseases, strains, ontology terms, etc. (e.g. Pax6, Parkinson, ataxia)
  • Use OR to search for either of two terms (e.g. OR mus) or quotation marks to search for phrases (e.g. "dna binding").
  • Boolean search syntax is supported: e.g. Balb* for partial matches or mus AND NOT embryo to exclude a term

Search results 2401 to 2500 out of 3085 for Myd88

0.032s

Categories

Hits by Pathway

Hits by Category

Hits by Strain

Type Details Score
Publication
First Author: Aviello G
Year: 2014
Journal: Am J Physiol Gastrointest Liver Physiol
Title: MyD88 adaptor-like (Mal) regulates intestinal homeostasis and colitis-associated colorectal cancer in mice.
Volume: 306
Issue: 9
Pages: G769-78
Publication
First Author: Strickson S
Year: 2017
Journal: Proc Natl Acad Sci U S A
Title: Roles of the TRAF6 and Pellino E3 ligases in MyD88 and RANKL signaling.
Volume: 114
Issue: 17
Pages: E3481-E3489
Publication
First Author: Kenny EF
Year: 2009
Journal: J Immunol
Title: MyD88 adaptor-like is not essential for TLR2 signaling and inhibits signaling by TLR3.
Volume: 183
Issue: 6
Pages: 3642-51
Publication  
First Author: Xie L
Year: 2016
Journal: J Natl Cancer Inst
Title: Targeting of MyD88 Homodimerization by Novel Synthetic Inhibitor TJ-M2010-5 in Preventing Colitis-Associated Colorectal Cancer.
Volume: 108
Issue: 4
Publication
First Author: Bosschaerts T
Year: 2010
Journal: PLoS Pathog
Title: Tip-DC development during parasitic infection is regulated by IL-10 and requires CCL2/CCR2, IFN-gamma and MyD88 signaling.
Volume: 6
Issue: 8
Pages: e1001045
Publication
First Author: Corr SC
Year: 2014
Journal: Mucosal Immunol
Title: MyD88 adaptor-like (Mal) functions in the epithelial barrier and contributes to intestinal integrity via protein kinase C.
Volume: 7
Issue: 1
Pages: 57-67
Interaction Experiment
Description: MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages.
Interaction Experiment
Description: SPOP promotes ubiquitination and degradation of MyD88 to suppress the innate immune response.
Publication
First Author: Popovic ZV
Year: 2011
Journal: J Immunol
Title: The proteoglycan biglycan enhances antigen-specific T cell activation potentially via MyD88 and TRIF pathways and triggers autoimmune perimyocarditis.
Volume: 187
Issue: 12
Pages: 6217-26
Publication
First Author: Semaan N
Year: 2008
Journal: J Immunol
Title: Etk/BMX, a Btk family tyrosine kinase, and Mal contribute to the cross-talk between MyD88 and FAK pathways.
Volume: 180
Issue: 5
Pages: 3485-91
Protein
Organism: Mus musculus/domesticus
Length: 241  
Fragment?: false
Publication
First Author: Guillamot M
Year: 2019
Journal: Nat Immunol
Title: The E3 ubiquitin ligase SPOP controls resolution of systemic inflammation by triggering MYD88 degradation.
Volume: 20
Issue: 9
Pages: 1196-1207
Publication
First Author: Lopez Kostka S
Year: 2022
Journal: J Invest Dermatol
Title: Exclusive Expression of MyD88 on Dendritic Cells Is Sufficient to Induce Protection against Experimental Leishmaniasis.
Volume: 142
Issue: 4
Pages: 1230-1233
Publication
First Author: Janssens S
Year: 2002
Journal: Trends Biochem Sci
Title: A universal role for MyD88 in TLR/IL-1R-mediated signaling.
Volume: 27
Issue: 9
Pages: 474-82
Protein
Organism: Mus musculus/domesticus
Length: 119  
Fragment?: false
Publication
First Author: Zhao Y
Year: 2018
Journal: Mol Cell
Title: OTUD4 Is a Phospho-Activated K63 Deubiquitinase that Regulates MyD88-Dependent Signaling.
Volume: 69
Issue: 3
Pages: 505-516.e5
Pathway
Pathway
Interaction Experiment
Description: Integrin CD11b negatively regulates TLR-triggered inflammatory responses by activating Syk and promoting degradation of MyD88 and TRIF via Cbl-b.
Publication
First Author: Lysakova-Devine T
Year: 2010
Journal: J Immunol
Title: 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 molecule.
Volume: 185
Issue: 7
Pages: 4261-71
Publication
First Author: Gravina HD
Year: 2016
Journal: J Biol Chem
Title: MyD88 Adapter-like (Mal)/TIRAP Is Required for Cytokine Production by Splenic Ly6CloTLR2hi but Not by Ly6ChiTLR2hi Monocytes during Trypanosoma cruzi Infection.
Volume: 291
Issue: 45
Pages: 23832-23841
GO Term
GO Term
Publication
First Author: Janssens S
Year: 2002
Journal: Curr Biol
Title: Regulation of interleukin-1- and lipopolysaccharide-induced NF-kappaB activation by alternative splicing of MyD88.
Volume: 12
Issue: 6
Pages: 467-71
HT Experiment
Series Id: GSE17438
Experiment Type: transcription profiling by array
Study Type: WT vs. Mutant
Source: ArrayExpress
Publication
First Author: Yu X
Year: 2018
Journal: Cancer Res
Title: MYD88 L265P Mutation in Lymphoid Malignancies.
Volume: 78
Issue: 10
Pages: 2457-2462
Publication
First Author: Muzio M
Year: 1997
Journal: Science
Title: IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling.
Volume: 278
Issue: 5343
Pages: 1612-5
Allele
Name: myeloid differentiation primary response gene 88; endonuclease-mediated mutation 2, Shanghai Model Organisms Center
Allele Type: Endonuclease-mediated
Attribute String: Null/knockout
Publication
First Author: Shi CS
Year: 2008
Journal: J Biol Chem
Title: MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages.
Volume: 283
Issue: 48
Pages: 33175-82
Publication
First Author: Li Q
Year: 2020
Journal: PLoS Pathog
Title: SPOP promotes ubiquitination and degradation of MyD88 to suppress the innate immune response.
Volume: 16
Issue: 5
Pages: e1008188
GO Term
GO Term
GO Term
Allele
Name: myeloid differentiation primary response gene 88; endonuclease-mediated mutation 1, Shanghai Model Organisms Center
Allele Type: Endonuclease-mediated
Attribute String: Conditional ready, No functional change
Strain
Attribute String: coisogenic, mutant strain, endonuclease-mediated mutation
DO Term
Publication
First Author: Loiarro M
Year: 2007
Journal: J Leukoc Biol
Title: Pivotal Advance: Inhibition of MyD88 dimerization and recruitment of IRAK1 and IRAK4 by a novel peptidomimetic compound.
Volume: 82
Issue: 4
Pages: 801-10
GO Term
Ontology Term
Publication
First Author: Choi KC
Year: 2006
Journal: Nat Immunol
Title: Smad6 negatively regulates interleukin 1-receptor-Toll-like receptor signaling through direct interaction with the adaptor Pellino-1.
Volume: 7
Issue: 10
Pages: 1057-65
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Allele
Name: transgene insertion 1, Lora Hooper
Allele Type: Transgenic
Attribute String: Inserted expressed sequence
Strain
Attribute String: coisogenic, endonuclease-mediated mutation, mutant strain
Publication
First Author: Pauls E
Year: 2013
Journal: J Immunol
Title: Two phases of inflammatory mediator production defined by the study of IRAK2 and IRAK1 knock-in mice.
Volume: 191
Issue: 5
Pages: 2717-30
Protein
Organism: Mus musculus/domesticus
Length: 622  
Fragment?: false
Allele
Name: myeloid differentiation primary response gene 88; targeted mutation 1, Anthony L DeFranco
Allele Type: Targeted
Attribute String: Conditional ready, No functional change
Strain
Attribute String: coisogenic, mutant strain, transgenic
Publication
First Author: Gantier MP
Year: 2008
Journal: J Immunol
Title: TLR7 is involved in sequence-specific sensing of single-stranded RNAs in human macrophages.
Volume: 180
Issue: 4
Pages: 2117-24
Publication
First Author: Alexopoulou L
Year: 2002
Journal: Nat Med
Title: Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice.
Volume: 8
Issue: 8
Pages: 878-84
Protein Domain
Type: Family
Description: Toll-like receptor 7 (TLR7) is a key component of innate and adaptive immunity. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. TLR7 is a nucleotide-sensing TLR, which is activated by single-stranded RNA, acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response [, ].
Protein Domain
Type: Family
Description: Toll-like receptor 1 (TLR1) participates in the innate immune response to microbial agents. TLR1 cooperates with TLR2 to mediate the innate immune response to bacterial lipoproteins or lipopeptides [, ]. It acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response.
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Strain
Attribute String: major histocompatibility congenic, congenic, mutant strain, spontaneous mutation, targeted mutation
Strain
Attribute String: targeted mutation, mutant strain, congenic
Strain
Attribute String: targeted mutation, mutant strain, congenic
Strain
Attribute String: congenic, targeted mutation
Genotype
Symbol: Myd88/Myd88
Background: B6.129P2(SJL)-Myd88/J
Zygosity: hm
Has Mutant Allele: true
Publication
First Author: Takeuchi O
Year: 2002
Journal: J Immunol
Title: Cutting edge: role of Toll-like receptor 1 in mediating immune response to microbial lipoproteins.
Volume: 169
Issue: 1
Pages: 10-4
Publication
First Author: Ferrao R
Year: 2012
Journal: Curr Opin Struct Biol
Title: Helical assembly in the death domain (DD) superfamily.
Volume: 22
Issue: 2
Pages: 241-7
Protein Domain
Type: Domain
Description: This entry represents the Death Domain (DD) of Myeloid Differentiation primary response protein 88 (MyD88). MyD88 is an adaptor protein involved in interleukin-1 receptor (IL-1R)- and Toll-like receptor (TLR)-induced activation of nuclear factor-kappaB (NF-kB) and mitogen activated protein kinase pathways that lead to the induction of proinflammatory cytokines []. It is a key component in the signaling pathway of pathogen recognition in the innate immune system. MyD88 contains an N-terminal DD and a C-terminal Toll/IL-1 Receptor (TIR) homology domain that mediates interaction with TLRs and IL-1R [].In general, DDs are protein-protein interaction domains found in a variety of domain architectures. Their common feature is that they form homodimers by self-association or heterodimers by associating with other members of the DD superfamily including CARD (Caspase activation and recruitment domain), DED (Death Effector Domain), and PYRIN []. They serve as adaptors in signaling pathways and can recruit other proteins into signaling complexes [].
Publication
First Author: Bauer S
Year: 2001
Journal: Proc Natl Acad Sci U S A
Title: Human TLR9 confers responsiveness to bacterial DNA via species-specific CpG motif recognition.
Volume: 98
Issue: 16
Pages: 9237-42
Publication
First Author: Chuang TH
Year: 2002
Journal: J Leukoc Biol
Title: Toll-like receptor 9 mediates CpG-DNA signaling.
Volume: 71
Issue: 3
Pages: 538-44
Publication
First Author: Anderson AE
Year: 2007
Journal: Eur J Immunol
Title: TLR9 polymorphisms determine murine lymphocyte responses to Helicobacter: results from a genome-wide scan.
Volume: 37
Issue: 6
Pages: 1548-61
Publication
First Author: Takeshita F
Year: 2001
Journal: J Immunol
Title: Cutting edge: Role of Toll-like receptor 9 in CpG DNA-induced activation of human cells.
Volume: 167
Issue: 7
Pages: 3555-8
Publication
First Author: Huang X
Year: 2010
Journal: Expert Opin Ther Targets
Title: Targeting the TLR9-MyD88 pathway in the regulation of adaptive immune responses.
Volume: 14
Issue: 8
Pages: 787-96
Publication
First Author: Nyman T
Year: 2008
Journal: J Biol Chem
Title: The crystal structure of the human toll-like receptor 10 cytoplasmic domain reveals a putative signaling dimer.
Volume: 283
Issue: 18
Pages: 11861-5
Publication
First Author: Hasan U
Year: 2005
Journal: J Immunol
Title: Human TLR10 is a functional receptor, expressed by B cells and plasmacytoid dendritic cells, which activates gene transcription through MyD88.
Volume: 174
Issue: 5
Pages: 2942-50
Protein Domain
Type: Family
Description: Toll-like receptor 10 (TLR10) participates in the innate immune response to microbial agents. The human TLR family consist of numerous members, which recognise a wide variety of pathogen-associated molecular patterns. No ligand has yet been reported for TLR10, thus it remains the only orphanfamily member []. It acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. TLR10 has been shown to form homodimers and to interact with TLRs 1 and 2 [].
Protein Domain
Type: Family
Description: Toll-like receptor 9 (TLR9) is a key component of innate and adaptive immunity [, ]. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. TLR9 is activated by unmethylated cytidine-phosphate-guanosine (CpG) dinucleotides, which is more abundant in bacterial genomes or viral DNA compared to the vertebrate genomes [, , , ]. It acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. TLR9 controls lymphocyte response to Helicobacter infection [].
Protein Domain
Type: Family
Description: Interleukin-1 receptor-associated kinase-like 2 (IRAK2) is a critical mediator of TLR/IL1-R signalling [, ]. It is required for production of pro-inflammatory cytokines [, ].All IRAKs are multidomain proteins, consisting of a conserved N-terminal death domain (DD) and a central kinase domain (KD). The DD is a protein interaction motif implicated in binding to the adaptor protein MyD88 []. IRAK2 lacks an active kinase domain, as a critical residue in the kinase domain has changed [].
HT Experiment
Series Id: GSE17344
Experiment Type: transcription profiling by array
Study Type: WT vs. Mutant
Source: ArrayExpress
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein Coding Gene
Type: protein_coding_gene
Organism: mouse, laboratory
Protein
Organism: Mus musculus/domesticus
Length: 435  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 457  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 1493  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 445  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 419  
Fragment?: false
Publication
First Author: Govindaraj RG
Year: 2011
Journal: PLoS One
Title: Comparative analysis of species-specific ligand recognition in Toll-like receptor 8 signaling: a hypothesis.
Volume: 6
Issue: 9
Pages: e25118
Publication
First Author: Peng G
Year: 2005
Journal: Science
Title: Toll-like receptor 8-mediated reversal of CD4+ regulatory T cell function.
Volume: 309
Issue: 5739
Pages: 1380-4
Publication
First Author: Jurk M
Year: 2002
Journal: Nat Immunol
Title: Human TLR7 or TLR8 independently confer responsiveness to the antiviral compound R-848.
Volume: 3
Issue: 6
Pages: 499
Publication
First Author: Melchjorsen J
Year: 2005
Journal: J Virol
Title: Activation of innate defense against a paramyxovirus is mediated by RIG-I and TLR7 and TLR8 in a cell-type-specific manner.
Volume: 79
Issue: 20
Pages: 12944-51
Publication
First Author: Droemann D
Year: 2003
Journal: Histochem Cell Biol
Title: Toll-like receptor 2 is expressed by alveolar epithelial cells type II and macrophages in the human lung.
Volume: 119
Issue: 2
Pages: 103-8
Publication
First Author: Sheedy FJ
Year: 2007
Journal: J Leukoc Biol
Title: The Troll in Toll: Mal and Tram as bridges for TLR2 and TLR4 signaling.
Volume: 82
Issue: 2
Pages: 196-203
Publication
First Author: Bochud PY
Year: 2008
Journal: J Infect Dis
Title: Toll-like receptor 2 (TLR2) polymorphisms are associated with reversal reaction in leprosy.
Volume: 197
Issue: 2
Pages: 253-61
Publication
First Author: Aliprantis AO
Year: 1999
Journal: Science
Title: Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2.
Volume: 285
Issue: 5428
Pages: 736-9
Publication
First Author: Takeuchi O
Year: 2001
Journal: Int Immunol
Title: Discrimination of bacterial lipoproteins by Toll-like receptor 6.
Volume: 13
Issue: 7
Pages: 933-40
Publication
First Author: Bochud PY
Year: 2003
Journal: J Immunol
Title: Cutting edge: a Toll-like receptor 2 polymorphism that is associated with lepromatous leprosy is unable to mediate mycobacterial signaling.
Volume: 170
Issue: 7
Pages: 3451-4
Publication
First Author: Schröder NW
Year: 2003
Journal: J Biol Chem
Title: Lipoteichoic acid (LTA) of Streptococcus pneumoniae and Staphylococcus aureus activates immune cells via Toll-like receptor (TLR)-2, lipopolysaccharide-binding protein (LBP), and CD14, whereas TLR-4 and MD-2 are not involved.
Volume: 278
Issue: 18
Pages: 15587-94
Publication
First Author: Kirschning CJ
Year: 2001
Journal: Int J Med Microbiol
Title: Toll-like receptors: cellular signal transducers for exogenous molecular patterns causing immune responses.
Volume: 291
Issue: 4
Pages: 251-60
Publication
First Author: Bulut Y
Year: 2001
Journal: J Immunol
Title: Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling.
Volume: 167
Issue: 2
Pages: 987-94
Publication
First Author: Takeda K
Year: 2002
Journal: J Endotoxin Res
Title: Recognition of lipopeptides by Toll-like receptors.
Volume: 8
Issue: 6
Pages: 459-63
Protein Domain
Type: Family
Description: Toll-like receptor 6 (TLR6) participates in the innate immune response to Gram-positive bacteria and fungi. TLRs recognize specific molecular patterns present only in micro-organisms. TLR1 and TLR6 are involved in the discrimination of a subtle difference between triacyl and diacyl lipopeptides through interaction with TLR2 []. Cooperatively with TLR2, TLR6 recognises mycoplasmal macrophage-activating lipopeptide-2 (MALP-2), soluble tuberculosis factor (STF), phenol-soluble modulin (PSM) and Borrelia burgdorferi outer surface protein A lipoprotein (OspA-L) []. TLR6 acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response [].
Protein Domain
Type: Family
Description: Toll-like receptor 2 (TLR2) is a member of the Toll-like receptor (TLR) family, which plays a role in activation of innate immunity and pathogen recognition []. It helps mediate the innate immune response to bacterial lipoproteins and other microbial cell wall components, acting via MyD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response [, , , ]. TLR2 in association with TLR1 or TLR6 is essential for recognising bacterial lipoproteins and lipopeptides [, ]. It also promotes apoptosis in response to lipoproteins [].Genetic variations in TLR2 are associated with susceptibility to leprosy, a chronic disease associated with depressed cellular (but not humoral) immunity [, ].
Protein Domain
Type: Family
Description: Toll-like receptor 8 (TLR8) is a key component of innate and adaptive immunity [, , ]. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. It acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response []. TLR8 has been shown to recognise different types of ligands such as viral or bacterial ssRNA, as well as small synthetic molecules. Activation by ligands is species-specific, varying among non-rodents and rodents [, ].