Version 5.4
Bos taurus Protein: MYD88
Summary
InnateDB Protein IDBP-696932.2
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol MYD88
Protein Name Myeloid differentiation primary response protein MyD88
Synonyms
Species Bos taurus
Ensembl Protein ENSBTAP00000000735
InnateDB Gene IDBG-644299 (MYD88)
Protein Structure
UniProt Annotation
Function Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine. {ECO:0000269PubMed:17936907, ECO:0000269PubMed:18760477}.
Subcellular Localization Cytoplasm {ECO:0000250}.
Disease Associations
Tissue Specificity
Comments
Interactions
Number of Interactions This gene and/or its encoded proteins are associated with 0 experimentally validated interaction(s) in this database.
They are also associated with 116 interaction(s) predicted by orthology.
Predicted by orthology
Total 116 [view]
Gene Ontology

Molecular Function
Accession GO Term
GO:0005515 protein binding
GO:0042802 identical protein binding
GO:0070976 TIR domain binding
Biological Process
GO:0002238 response to molecule of fungal origin
GO:0002376 immune system process
GO:0002755 MyD88-dependent toll-like receptor signaling pathway
GO:0006954 inflammatory response
GO:0007165 signal transduction
GO:0007166 cell surface receptor signaling pathway
GO:0009615 response to virus
GO:0016064 immunoglobulin mediated immune response
GO:0031663 lipopolysaccharide-mediated signaling pathway
GO:0032494 response to peptidoglycan
GO:0032496 response to lipopolysaccharide
GO:0032740 positive regulation of interleukin-17 production
GO:0032747 positive regulation of interleukin-23 production
GO:0032755 positive regulation of interleukin-6 production
GO:0032760 positive regulation of tumor necrosis factor production
GO:0042127 regulation of cell proliferation
GO:0043123 positive regulation of I-kappaB kinase/NF-kappaB signaling
GO:0044130 negative regulation of growth of symbiont in host
GO:0045080 positive regulation of chemokine biosynthetic process
GO:0045087 innate immune response
GO:0045351 type I interferon biosynthetic process
GO:0046330 positive regulation of JNK cascade
GO:0050671 positive regulation of lymphocyte proliferation
GO:0050727 regulation of inflammatory response
GO:0050830 defense response to Gram-positive bacterium
GO:0051092 positive regulation of NF-kappaB transcription factor activity
GO:0070555 response to interleukin-1
GO:0070935 3'-UTR-mediated mRNA stabilization
GO:0071260 cellular response to mechanical stimulus
GO:0090557 establishment of endothelial intestinal barrier
Cellular Component
GO:0005737 cytoplasm
GO:0005829 cytosol
GO:0005886 plasma membrane
Protein Structure and Domains
PDB ID
InterPro IPR000157 Toll/interleukin-1 receptor homology (TIR) domain
IPR000488 Death domain
IPR011029 Death-like domain
IPR017281 Myeloid differentiation primary response protein MyD88
PFAM PF01582
PF13676
PF00531
PRINTS
PIRSF PIRSF037756
SMART SM00255
SM00005
TIGRFAMs
Post-translational Modifications
Modification
Cross-References
SwissProt Q599T9
PhosphoSite PhosphoSite-
TrEMBL
UniProt Splice Variant
Entrez Gene 444881
UniGene Bt.48995
RefSeq NP_001014404
HUGO
OMIM
CCDS
HPRD
IMGT
EMBL AJ853453 AY634627 AY934808 AY937381 BC102851
GenPept AAI02852 AAT48485 AAY16578 AAY22119 CAH68521

If you use InnateDB for your research, please cite the following publication:

Breuer et al., InnateDB: systems biology of innate immunity and beyond - recent updates and continuing curation. Nucl. Acids Res. (2013) 41 (D1) 

InnateDB is being developed jointly by the Brinkman Laboratory (Simon Fraser University, British Columbia, Canada), the Hancock Laboratory (University of British Columbia, Vancouver, British Columbia) and the Lynn EMBL Australia Group (South Australian Health & Medical Research Institute and Flinders University, Adelaide, Australia).

Funding is currently provided by Allergen and EMBL Australia. Previous funding has been provided by Genome Canada, the Foundation for the National Institutes of Health through the Grand Challenges in Global Health initiative and by Teagasc. InnateDB curated interactions are licensed under the Design Science License. All other data is licensed under the terms of the originating database. Contact: innatedb-mail@sfu.ca