MYD88

2017-09-07T18:40:29Z

86.58.143.146: deleted "gene" from name as only the gene for this protein should include the word "gene"

{{Infobox_gene}}
'''Myeloid differentiation primary response 88 (MYD88)''' is a [[protein]] that, in humans, is encoded by the ''MYD88'' [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: MYD88 Myeloid differentiation primary response gene (88)| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=4615| accessdate =}}</ref><ref name="pmid9013863">{{cite journal | vauthors = Bonnert TP, Garka KE, Parnet P, Sonoda G, Testa JR, Sims JE | title = The cloning and characterization of human MyD88: a member of an IL-1 receptor related family | journal = FEBS Letters | volume = 402 | issue = 1 | pages = 81–4 | date = Jan 1997 | pmid = 9013863 | doi = 10.1016/S0014-5793(96)01506-2 }}</ref>

==Model organisms==
[[Model organism]]s have been used in the study of MYD88 function. The gene was originally discovered and cloned by Dan Liebermann and Barbara Hoffman in mice.<ref name="pmid2374694">{{cite journal | vauthors = Lord KA, Hoffman-Liebermann B, Liebermann DA | title = Nucleotide sequence and expression of a cDNA encoding MyD88, a novel myeloid differentiation primary response gene induced by IL6 | journal = Oncogene | volume = 5 | issue = 7 | pages = 1095–7 | date = Jul 1990 | pmid = 2374694 | doi = }}</ref> In that species it is a universal [[Signal transducing adaptor protein|adapter protein]] as it is used by almost all [[toll-like receptor|TLR]]s (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 [[Interleukin-1 receptor-associated kinase|IRAK]].<ref name="pmid18064347">{{cite journal | vauthors = Arancibia SA, Beltrán CJ, Aguirre IM, Silva P, Peralta AL, Malinarich F, Hermoso MA | title = Toll-like receptors are key participants in innate immune responses | journal = Biological Research | volume = 40 | issue = 2 | pages = 97–112 | year = 2007 | pmid = 18064347 | doi = 10.4067/S0716-97602007000200001 }}</ref> It also interacts functionally with amyloid formation and behavior in a transgenic mouse model of [[Alzheimer's disease]].<ref name=pmid21763676>{{cite journal | vauthors = Lim JE, Kou J, Song M, Pattanayak A, Jin J, Lalonde R, Fukuchi K | title = MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease | journal = The American Journal of Pathology | volume = 179 | issue = 3 | pages = 1095–103 | date = Sep 2011 | pmid = 21763676 | pmc = 3157279 | doi = 10.1016/j.ajpath.2011.05.045 }}</ref>

{| class="wikitable sortable collapsible collapsed" border="1" cellpadding="2" style="float: right;" |
|+ ''Myd88'' knockout mouse phenotype
|-
! Characteristic!! Phenotype
|-
| [[Homozygote]] viability || bgcolor="#488ED3"|Normal
|-
| Fertility || bgcolor="#488ED3"|Normal
|-
| Body weight || bgcolor="#488ED3"|Normal
|-
| [[Open Field (animal test)|Anxiety]] || bgcolor="#488ED3"|Normal
|-
| Neurological assessment || bgcolor="#488ED3"|Normal
|-
| Grip strength || bgcolor="#488ED3"|Normal
|-
| [[Hot plate test|Hot plate]] || bgcolor="#488ED3"|Normal
|-
| [[Dysmorphology]] || bgcolor="#488ED3"|Normal
|-
| [[Indirect calorimetry]] || bgcolor="#488ED3"|Normal
|-
| [[Glucose tolerance test]] || bgcolor="#488ED3"|Normal
|-
| [[Auditory brainstem response]] || bgcolor="#488ED3"|Normal
|-
| [[Dual-energy X-ray absorptiometry|DEXA]] || bgcolor="#488ED3"|Normal
|-
| [[Radiography]] || bgcolor="#488ED3"|Normal
|-
| Body temperature || bgcolor="#488ED3"|Normal
|-
| Eye morphology || bgcolor="#488ED3"|Normal
|-
| [[Clinical chemistry]] || bgcolor="#488ED3"|Normal
|-
| [[Haematology]] || bgcolor="#488ED3"|Normal
|-
| [[Peripheral blood lymphocyte]]s || bgcolor="#488ED3"|Normal
|-
| [[Micronucleus test]] || bgcolor="#488ED3"|Normal
|-
| Heart weight || bgcolor="#488ED3"|Normal
|-
| ''[[Salmonella]]'' infection || bgcolor="#C40000"|Abnormal<ref name="''Salmonella'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MAVS/salmonella-challenge/ |title=''Salmonella'' infection data for Myd88 |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite journal | doi = 10.1111/j.1755-3768.2010.4142.x | title = The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice | year = 2010 | author = Gerdin AK | journal = Acta Ophthalmologica | volume = 88 | pages = 925–7 }}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
|}
A conditional [[knockout mouse]] line, called ''Myd88<sup>tm1a(EUCOMM)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Myd88 |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4434029 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{cite journal | vauthors = Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A | title = A conditional knockout resource for the genome-wide study of mouse gene function | journal = Nature | volume = 474 | issue = 7351 | pages = 337–42 | date = Jun 2011 | pmid = 21677750 | pmc = 3572410 | doi = 10.1038/nature10163 }}</ref><ref name="mouse_library">{{cite journal | vauthors = Dolgin E | title = Mouse library set to be knockout | journal = Nature | volume = 474 | issue = 7351 | pages = 262–3 | date = Jun 2011 | pmid = 21677718 | doi = 10.1038/474262a }}</ref><ref name="mouse_for_all_reasons">{{cite journal | vauthors = Collins FS, Rossant J, Wurst W | title = A mouse for all reasons | journal = Cell | volume = 128 | issue = 1 | pages = 9–13 | date = Jan 2007 | pmid = 17218247 | doi = 10.1016/j.cell.2006.12.018 }}</ref> Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal | vauthors = van der Weyden L, White JK, Adams DJ, Logan DW | title = The mouse genetics toolkit: revealing function and mechanism | journal = Genome Biology | volume = 12 | issue = 6 | pages = 224 | year = 2011 | pmid = 21722353 | pmc = 3218837 | doi = 10.1186/gb-2011-12-6-224 }}</ref> Twenty-one tests were carried out on [[homozygous]] [[mutant]] animals, revealing one abnormality: male mutants had an increased susceptibility to [[bacterial infection]].

== Function ==

The human [[Ortholog#Orthology|ortholog]] MYD88 seems to function similarly to mice, 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.<ref name="pmid18669862">{{cite journal | vauthors = von Bernuth H, Picard C, Jin Z, Pankla R, Xiao H, Ku CL, Chrabieh M, Mustapha IB, Ghandil P, Camcioglu Y, Vasconcelos J, Sirvent N, Guedes M, Vitor AB, Herrero-Mata MJ, Aróstegui JI, Rodrigo C, Alsina L, Ruiz-Ortiz E, Juan M, Fortuny C, Yagüe J, Antón J, Pascal M, Chang HH, Janniere L, Rose Y, Garty BZ, Chapel H, Issekutz A, Maródi L, Rodriguez-Gallego C, Banchereau J, Abel L, Li X, Chaussabel D, Puel A, Casanova JL | title = Pyogenic bacterial infections in humans with MyD88 deficiency | journal = Science | volume = 321 | issue = 5889 | pages = 691–6 | date = Aug 2008 | pmid = 18669862 | pmc = 2688396 | doi = 10.1126/science.1158298 }}</ref> Mutation in MYD88 at position 265 leading to a change from leucine to proline have been identified in many human lymphomas including ABC subtype of [[diffuse large B-cell lymphoma]]<ref name="pmid21179087">{{cite journal | vauthors = Ngo VN, Young RM, Schmitz R, Jhavar S, Xiao W, Lim KH, Kohlhammer H, Xu W, Yang Y, Zhao H, Shaffer AL, Romesser P, Wright G, Powell J, Rosenwald A, Muller-Hermelink HK, Ott G, Gascoyne RD, Connors JM, Rimsza LM, Campo E, Jaffe ES, Delabie J, Smeland EB, Fisher RI, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Staudt LM | title = Oncogenically active MYD88 mutations in human lymphoma | journal = Nature | volume = 470 | issue = 7332 | pages = 115–9 | year = 2011 | pmid = 21179087 | doi = 10.1038/nature09671 | pmc=5024568}}</ref> and [[Waldenstrom's macroglobulinemia]].<ref name="pmid22931316">{{cite journal | vauthors = Treon SP, Xu L, Yang G, Zhou Y, Liu X, Cao Y, Sheehy P, Manning RJ, Patterson CJ, Tripsas C, Arcaini L, Pinkus GS, Rodig SJ, Sohani AR, Harris NL, Laramie JM, Skifter DA, Lincoln SE, Hunter ZR | title = MYD88 L265P somatic mutation in Waldenström's macroglobulinemia | journal = N. Engl. J. Med. | volume = 367 | issue = 9 | pages = 826–33 | year = 2012 | pmid = 22931316 | doi = 10.1056/NEJMoa1200710 }}</ref>

== Interactions ==

Myd88 has been shown to [[Protein-protein interaction|interact]] with:
{{div col|colwidth=20em}}
* [[IRAK1]]<ref name = pmid11544529/><ref name = pmid10383454/><ref name = pmid11976320>{{cite journal | vauthors = Chen BC, Wu WT, Ho FM, Lin WW | title = 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 | journal = The Journal of Biological Chemistry | volume = 277 | issue = 27 | pages = 24169–79 | date = Jul 2002 | pmid = 11976320 | doi = 10.1074/jbc.M106014200 }}</ref><ref name = pmid11960013>{{cite journal | vauthors = Li S, Strelow A, Fontana EJ, Wesche H | title = IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 99 | issue = 8 | pages = 5567–72 | date = Apr 2002 | pmid = 11960013 | pmc = 122810 | doi = 10.1073/pnas.082100399 }}</ref>
* [[IRAK2]]<ref name = pmid11544529/><ref name = pmid9374458/><ref name = pmid10383454>{{cite journal | vauthors = Wesche H, Gao X, Li X, Kirschning CJ, Stark GR, Cao Z | title = IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family | journal = The Journal of Biological Chemistry | volume = 274 | issue = 27 | pages = 19403–10 | date = Jul 1999 | pmid = 10383454 | doi = 10.1074/jbc.274.27.19403}}</ref>
* [[Interleukin 1 receptor, type I]]<ref name = pmid10854325>{{cite journal | vauthors = Burns K, Clatworthy J, Martin L, Martinon F, Plumpton C, Maschera B, Lewis A, Ray K, Tschopp J, Volpe F | title = Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor | journal = Nature Cell Biology | volume = 2 | issue = 6 | pages = 346–51 | date = Jun 2000 | pmid = 10854325 | doi = 10.1038/35014038 }}</ref><ref name = pmid9374458>{{cite journal | vauthors = Muzio M, Ni J, Feng P, Dixit VM | title = IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling | journal = Science | volume = 278 | issue = 5343 | pages = 1612–5 | date = Nov 1997 | pmid = 9374458 | doi = 10.1126/science.278.5343.1612}}</ref>
* [[RAC1]]<ref name = pmid11416133>{{cite journal | vauthors = Jefferies C, Bowie A, Brady G, Cooke EL, Li X, O'Neill LA | title = 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 Rac1 | journal = Molecular and Cellular Biology | volume = 21 | issue = 14 | pages = 4544–52 | date = Jul 2001 | pmid = 11416133 | pmc = 87113 | doi = 10.1128/MCB.21.14.4544-4552.2001 }}</ref>
* [[TLR 4]]<ref name = pmid15107846>{{cite journal | vauthors = Chuang TH, Ulevitch RJ | title = Triad3A, an E3 ubiquitin-protein ligase regulating Toll-like receptors | journal = Nature Immunology | volume = 5 | issue = 5 | pages = 495–502 | date = May 2004 | pmid = 15107846 | doi = 10.1038/ni1066 }}</ref><ref name = pmid12646618>{{cite journal | vauthors = Doyle SE, O'Connell R, Vaidya SA, Chow EK, Yee K, Cheng G | title = Toll-like receptor 3 mediates a more potent antiviral response than Toll-like receptor 4 | journal = Journal of Immunology | volume = 170 | issue = 7 | pages = 3565–71 | date = Apr 2003 | pmid = 12646618 | doi = 10.4049/jimmunol.170.7.3565}}</ref><ref name = pmid10952994>{{cite journal | vauthors = Rhee SH, Hwang D | title = Murine TOLL-like receptor 4 confers lipopolysaccharide responsiveness as determined by activation of NF kappa B and expression of the inducible cyclooxygenase | journal = The Journal of Biological Chemistry | volume = 275 | issue = 44 | pages = 34035–40 | date = Nov 2000 | pmid = 10952994 | doi = 10.1074/jbc.M007386200 }}</ref><ref name = pmid11544529>{{cite journal | vauthors = Fitzgerald KA, Palsson-McDermott EM, Bowie AG, Jefferies CA, Mansell AS, Brady G, Brint E, Dunne A, Gray P, Harte MT, McMurray D, Smith DE, Sims JE, Bird TA, O'Neill LA | title = Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction | journal = Nature | volume = 413 | issue = 6851 | pages = 78–83 | date = Sep 2001 | pmid = 11544529 | doi = 10.1038/35092578 }}</ref>
{{Div col end}}

== Gene polymorphisms ==

Various single nucleotide polymorphisms (SNPs) of the MyD88 have been identified. and for some of them an association with susceptibility to various infectious diseases<ref name=" pmid = 22610250 ">{{cite journal | vauthors = Netea MG, Wijmenga C, O'Neill LA | title = Genetic variation in Toll-like receptors and disease susceptibility | journal = Nature Immunology | volume = 13 | issue = 6 | pages = 535–42 | date = Jun 2012 | pmid = 22610250 | doi = 10.1038/ni.2284 | url = http://www.nature.com/ni/journal/v13/n6/full/ni.2284.html }}</ref> and to some autoimmune diseases like [[ulcerative colitis]] was found.<ref name=" pmid = 24189845 ">{{cite journal | vauthors = Matsunaga K, Tahara T, Shiroeda H, Otsuka T, Nakamura M, Shimasaki T, Toshikuni N, Kawada N, Shibata T, Arisawa T | title = The *1244 A>G polymorphism of MyD88 (rs7744) is closely associated with susceptibility to ulcerative colitis | journal = Molecular Medicine Reports | volume = 9 | issue = 1 | pages = 28–32 | date = Jan 2014 | pmid = 24189845 | doi = 10.3892/mmr.2013.1769 | url = http://www.spandidos-publications.com/mmr/9/1/28 }}</ref>
{{-}}

== References ==
{{reflist|33em}}

== Further reading ==
{{refbegin|33em}}
* {{cite journal | vauthors = Hardiman G, Rock FL, Balasubramanian S, Kastelein RA, Bazan JF | title = Molecular characterization and modular analysis of human MyD88 | journal = Oncogene | volume = 13 | issue = 11 | pages = 2467–75 | date = Dec 1996 | pmid = 8957090 | doi = }}
* {{cite journal | vauthors = Bonnert TP, Garka KE, Parnet P, Sonoda G, Testa JR, Sims JE | title = The cloning and characterization of human MyD88: a member of an IL-1 receptor related family | journal = FEBS Letters | volume = 402 | issue = 1 | pages = 81–4 | date = Jan 1997 | pmid = 9013863 | doi = 10.1016/S0014-5793(96)01506-2 }}
* {{cite journal | vauthors = Hardiman G, Jenkins NA, Copeland NG, Gilbert DJ, Garcia DK, Naylor SL, Kastelein RA, Bazan JF | title = Genetic structure and chromosomal mapping of MyD88 | journal = Genomics | volume = 45 | issue = 2 | pages = 332–9 | date = Oct 1997 | pmid = 9344657 | doi = 10.1006/geno.1997.4940 }}
* {{cite journal | vauthors = Muzio M, Ni J, Feng P, Dixit VM | title = IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling | journal = Science | volume = 278 | issue = 5343 | pages = 1612–5 | date = Nov 1997 | pmid = 9374458 | doi = 10.1126/science.278.5343.1612 }}
* {{cite journal | vauthors = Jaunin F, Burns K, Tschopp J, Martin TE, Fakan S | title = Ultrastructural distribution of the death-domain-containing MyD88 protein in HeLa cells | journal = Experimental Cell Research | volume = 243 | issue = 1 | pages = 67–75 | date = Aug 1998 | pmid = 9716450 | doi = 10.1006/excr.1998.4131 }}
* {{cite journal | vauthors = Lan X, Han X, Li Q, Li Q, Gao Y, Cheng T, Wan J, Zhu W, Wang J | title = Pinocembrin protects hemorrhagic brain primarily by inhibiting toll-like receptor 4 and reducing M1 phenotype microglia | journal = Brain, behavior, and immunity | volume = 61 | pages = 326–339 | date = March 2017 | pmid = 28007523 | doi = 10.1016/j.bbi.2016.12.012 }}
* {{cite journal | vauthors = Wesche H, Gao X, Li X, Kirschning CJ, Stark GR, Cao Z | title = IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family | journal = The Journal of Biological Chemistry | volume = 274 | issue = 27 | pages = 19403–10 | date = Jul 1999 | pmid = 10383454 | doi = 10.1074/jbc.274.27.19403 }}
* {{cite journal | vauthors = Burns K, Clatworthy J, Martin L, Martinon F, Plumpton C, Maschera B, Lewis A, Ray K, Tschopp J, Volpe F | title = Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor | journal = Nature Cell Biology | volume = 2 | issue = 6 | pages = 346–51 | date = Jun 2000 | pmid = 10854325 | doi = 10.1038/35014038 }}
* {{cite journal | vauthors = Aliprantis AO, Yang RB, Weiss DS, Godowski P, Zychlinsky A | title = The apoptotic signaling pathway activated by Toll-like receptor-2 | journal = The EMBO Journal | volume = 19 | issue = 13 | pages = 3325–36 | date = Jul 2000 | pmid = 10880445 | pmc = 313930 | doi = 10.1093/emboj/19.13.3325 }}
* {{cite journal | vauthors = Rhee SH, Hwang D | title = Murine TOLL-like receptor 4 confers lipopolysaccharide responsiveness as determined by activation of NF kappa B and expression of the inducible cyclooxygenase | journal = The Journal of Biological Chemistry | volume = 275 | issue = 44 | pages = 34035–40 | date = Nov 2000 | pmid = 10952994 | doi = 10.1074/jbc.M007386200 }}
* {{cite journal | vauthors = Fitzgerald KA, Palsson-McDermott EM, Bowie AG, Jefferies CA, Mansell AS, Brady G, Brint E, Dunne A, Gray P, Harte MT, McMurray D, Smith DE, Sims JE, Bird TA, O'Neill LA | title = Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction | journal = Nature | volume = 413 | issue = 6851 | pages = 78–83 | date = Sep 2001 | pmid = 11544529 | doi = 10.1038/35092578 }}
* {{cite journal | vauthors = Tauszig-Delamasure S, Bilak H, Capovilla M, Hoffmann JA, Imler JL | title = Drosophila MyD88 is required for the response to fungal and Gram-positive bacterial infections | journal = Nature Immunology | volume = 3 | issue = 1 | pages = 91–7 | date = Jan 2002 | pmid = 11743586 | doi = 10.1038/ni747 }}
* {{cite journal | vauthors = Bannerman DD, Tupper JC, Kelly JD, Winn RK, Harlan JM | title = The Fas-associated death domain protein suppresses activation of NF-kappa B by LPS and IL-1 beta | journal = The Journal of Clinical Investigation | volume = 109 | issue = 3 | pages = 419–25 | date = Feb 2002 | pmid = 11828002 | pmc = 150862 | doi = 10.1172/JCI14774 }}
* {{cite journal | vauthors = Tamai R, Sakuta T, Matsushita K, Torii M, Takeuchi O, Akira S, Akashi S, Espevik T, Sugawara S, Takada H | title = Human gingival CD14(+) fibroblasts primed with gamma interferon increase production of interleukin-8 in response to lipopolysaccharide through up-regulation of membrane CD14 and MyD88 mRNA expression | journal = Infection and Immunity | volume = 70 | issue = 3 | pages = 1272–8 | date = Mar 2002 | pmid = 11854210 | pmc = 127773 | doi = 10.1128/IAI.70.3.1272-1278.2002 }}
* {{cite journal | vauthors = Radons J, Gabler S, Wesche H, Korherr C, Hofmeister R, Falk W | title = Identification of essential regions in the cytoplasmic tail of interleukin-1 receptor accessory protein critical for interleukin-1 signaling | journal = The Journal of Biological Chemistry | volume = 277 | issue = 19 | pages = 16456–63 | date = May 2002 | pmid = 11880380 | doi = 10.1074/jbc.M201000200 }}
* {{cite journal | vauthors = Janssens S, Burns K, Tschopp J, Beyaert R | title = Regulation of interleukin-1- and lipopolysaccharide-induced NF-kappaB activation by alternative splicing of MyD88 | journal = Current Biology | volume = 12 | issue = 6 | pages = 467–71 | date = Mar 2002 | pmid = 11909531 | doi = 10.1016/S0960-9822(02)00712-1 }}
* {{cite journal | vauthors = Li S, Strelow A, Fontana EJ, Wesche H | title = IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 99 | issue = 8 | pages = 5567–72 | date = Apr 2002 | pmid = 11960013 | pmc = 122810 | doi = 10.1073/pnas.082100399 }}
* {{cite journal | vauthors = Medvedev AE, Lentschat A, Wahl LM, Golenbock DT, Vogel SN | title = Dysregulation of LPS-induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor-associated kinase 1 activation in endotoxin-tolerant cells | journal = Journal of Immunology | volume = 169 | issue = 9 | pages = 5209–16 | date = Nov 2002 | pmid = 12391239 | doi = 10.4049/jimmunol.169.9.5209 }}
* {{cite journal | vauthors = Raschi E, Testoni C, Bosisio D, Borghi MO, Koike T, Mantovani A, Meroni PL | title = Role of the MyD88 transduction signaling pathway in endothelial activation by antiphospholipid antibodies | journal = Blood | volume = 101 | issue = 9 | pages = 3495–500 | date = May 2003 | pmid = 12531807 | doi = 10.1182/blood-2002-08-2349 }}
* {{cite journal | vauthors = Doyle SE, O'Connell R, Vaidya SA, Chow EK, Yee K, Cheng G | title = Toll-like receptor 3 mediates a more potent antiviral response than Toll-like receptor 4 | journal = Journal of Immunology | volume = 170 | issue = 7 | pages = 3565–71 | date = Apr 2003 | pmid = 12646618 | doi = 10.4049/jimmunol.170.7.3565 }}
{{refend}}

== External links ==
* {{MeshName|MyD88+Protein}}

{{Adaptor proteins}}
{{TLR signaling pathway}}

[[Category:Immune system]]
[[Category:Human proteins]]
[[Category:Genes mutated in mice]]

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MYD88