MYD88

Myeloid differentiation primary response gene (88)

Signaling pathway of toll-like receptors. Dashed grey lines represent unknown associations
Identifiers
Symbols MYD88;
External IDs OMIM602170 MGI108005 HomoloGene1849 GeneCards: MYD88 Gene
RNA expression pattern
PBB GE MYD88 209124 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 4615 17874
Ensembl ENSG00000172936 ENSMUSG00000032508
UniProt Q99836 Q0PM15
RefSeq (mRNA) NM_001172566.1 NM_010851.2
RefSeq (protein) NP_001166037.1 NP_034981.1
Location (UCSC) Chr 3:
38.18 – 38.18 Mb
Chr 9:
119.25 – 119.25 Mb
PubMed search [1] [2]

Myeloid differentiation primary response gene (88) (MYD88) is a protein that, in humans, is encoded by the MYD88 gene.[1][2]

Contents

Function

In mice, MyD88 is a universal adapter protein as it is used by all TLRs (except TLR 3) to activate the transcription factor NF-κB. Mal (also known as TIRAP) is necessary to recruit Myd88 to TLR 2 and TLR 4, and MyD88 then signals through IRAK.[3] The human ortholog MYD88 seems to function similarly, since the immunological phenotype of human cells deficient in MYD88 is similar to cells from MyD88 deficient mice. However, available evidence suggests that MYD88 is dispensable for human resistance to common viral infections and to all but a few pyogenic bacterial infections, demonstrating a major difference between mouse and human immune responses.[4]

Discovery

MyD88 was originally discovered and cloned by Drs Dan A Liebermann and Barbara Hoffman in mice.[5]

Interactions

Myd88 has been shown to interact with TLR 4,[6][7][8][9] Interleukin 1 receptor, type I,[10][11] RAC1,[12] IRAK2[9][11][13] and IRAK1.[9][13][14][15] It also interacts functionally with amyloid formation and behavior in a transgenic mouse model of Alzheimer's disease.[16]

References

  1. ^ "Entrez Gene: MYD88 Myeloid differentiation primary response gene (88)". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=4615. 
  2. ^ Bonnert TP, Garka KE, Parnet P, Sonoda G, Testa JR, Sims JE (January 1997). "The cloning and characterization of human MyD88: a member of an IL-1 receptor related family". FEBS letters 402 (1): 81–4. doi:10.1016/S0014-5793(96)01506-2. PMID 9013863. 
  3. ^ Arancibia SA, Beltrán CJ, Aguirre IM, Silva P, Peralta AL, Malinarich F, Hermoso MA. (2007). "Toll-like receptors are key participants in innate immune responses". Biological research 40 (2): 97–112. doi:10.4067/S0716-97602007000200001. PMID 18064347. 
  4. ^ von Bernuth H, Picard C, Jin Z, et al. (August 2008). "Pyogenic Bacterial Infections in Humans with MyD88 Deficiency". Science 321 (5889): 691–6. doi:10.1126/science.1158298. PMC 2688396. PMID 18669862. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2688396. 
  5. ^ Lord KA, Hoffman-Liebermann B, Liebermann DA (1990). "Nucleotide sequence and expression of a cDNA encoding MyD88, a novel myeloid differentiation primary response gene induced by IL6". Oncogene 5 (7): 1095–7. PMID 2374694. 
  6. ^ Chuang, Tsung-Hsien; Ulevitch Richard J (May. 2004). "Triad3A, an E3 ubiquitin-protein ligase regulating Toll-like receptors". Nat. Immunol. (United States) 5 (5): 495–502. doi:10.1038/ni1066. ISSN 1529-2908. PMID 15107846. 
  7. ^ Doyle, Sean E; O'Connell Ryan, Vaidya Sagar A, Chow Edward K, Yee Kathleen, Cheng Genhong (Apr. 2003). "Toll-like receptor 3 mediates a more potent antiviral response than Toll-like receptor 4". J. Immunol. (United States) 170 (7): 3565–71. ISSN 0022-1767. PMID 12646618. 
  8. ^ Rhee, S H; Hwang D (Nov. 2000). "Murine TOLL-like receptor 4 confers lipopolysaccharide responsiveness as determined by activation of NF kappa B and expression of the inducible cyclooxygenase". J. Biol. Chem. (UNITED STATES) 275 (44): 34035–40. doi:10.1074/jbc.M007386200. ISSN 0021-9258. PMID 10952994. 
  9. ^ a b c Fitzgerald, K A; Palsson-McDermott E M, Bowie A G, Jefferies C A, Mansell A S, Brady G, Brint E, Dunne A, Gray P, Harte M T, McMurray D, Smith D E, Sims J E, Bird T A, O'Neill L A (Sep. 2001). "Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction". Nature (England) 413 (6851): 78–83. doi:10.1038/35092578. ISSN 0028-0836. PMID 11544529. 
  10. ^ Burns, K; Clatworthy J, Martin L, Martinon F, Plumpton C, Maschera B, Lewis A, Ray K, Tschopp J, Volpe F (Jun. 2000). "Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor". Nat. Cell Biol. (ENGLAND) 2 (6): 346–51. doi:10.1038/35014038. ISSN 1465-7392. PMID 10854325. 
  11. ^ a b Muzio, M; Ni J, Feng P, Dixit V M (Nov. 1997). "IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling". Science (UNITED STATES) 278 (5343): 1612–5. doi:10.1126/science.278.5343.1612. ISSN 0036-8075. PMID 9374458. 
  12. ^ Jefferies, C; Bowie A, Brady G, Cooke E L, Li X, O'Neill L A (Jul. 2001). "Transactivation by the p65 Subunit of NF-κB in Response to Interleukin-1 (IL-1) Involves MyD88, IL-1 Receptor-Associated Kinase 1, TRAF-6, and Rac1". Mol. Cell. Biol. (United States) 21 (14): 4544–52. doi:10.1128/MCB.21.14.4544-4552.2001. ISSN 0270-7306. PMC 87113. PMID 11416133. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=87113. 
  13. ^ a b Wesche, H; Gao X, Li X, Kirschning C J, Stark G R, Cao Z (Jul. 1999). "IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family". J. Biol. Chem. (UNITED STATES) 274 (27): 19403–10. doi:10.1074/jbc.274.27.19403. ISSN 0021-9258. PMID 10383454. 
  14. ^ Chen, Bing-Chang; Wu Wen-Tung, Ho Feng-Ming, Lin Wan-Wan (Jul. 2002). "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 MyD88". J. Biol. Chem. (United States) 277 (27): 24169–79. doi:10.1074/jbc.M106014200. ISSN 0021-9258. PMID 11976320. 
  15. ^ Li, Shyun; Strelow Astrid, Fontana Elizabeth J, Wesche Holger (Apr. 2002). "IRAK-4: A novel member of the IRAK family with the properties of an IRAK-kinase". Proc. Natl. Acad. Sci. U.S.A. (United States) 99 (8): 5567–72. doi:10.1073/pnas.082100399. ISSN 0027-8424. PMC 122810. PMID 11960013. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=122810. 
  16. ^ Lim, JE; Kou J, Song M, Pattanayak A, Jin J, Lalonde R, Fukuchi K (Sept. 2011). "MyD88 Deficiency Ameliorates β-Amyloidosis in an Animal Model of Alzheimer's Disease". Am. J. Pathol. (United States) 179 (3): 1095–103. doi:10.1016/j.ajpath.2011.05.045. PMC 3157279. PMID 21763676. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3157279. 

Further reading

External links



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