MYD88: Difference between revisions

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==Discovery==
==Discovery==


MyD88 was originally discovered and cloned by Drs Dan A Liebermann and Barbara Hoffman in mice.<ref name="pmid2374694">{{cite journal |author=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 |year=1990 |pmid=2374694 |doi=}}</ref>
MyD88 was originally discovered and cloned by Drs Wwand Barbara Hoffman in mice.<ref name="pmid2374694">{{cite journal |author=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 |year=1990 |pmid=2374694 |doi=}}</ref>


==References==
==References==

Revision as of 01:59, 19 January 2009

Template:PBB Myeloid differentiation primary response gene (88) (MYD88) is a protein which in humans is encoded by the MYD88 gene.[1][2]

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, though available evidence suggests that MYD88 is dispensible 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 Wwand Barbara Hoffman in mice.[5]

References

  1. ^ "Entrez Gene: MYD88 Myeloid differentiation primary response gene (88)".
  2. ^ Bonnert TP, Garka KE, Parnet P, Sonoda G, Testa JR, Sims JE (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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. PMID 18064347.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ von Bernuth H, Picard C, Jin Z; et al. (2008). "Pyogenic bacterial infections in humans with MyD88 deficiency". Science (journal). 321 (5889): 691–6. doi:10.1126/science.1158298. PMID 18669862. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  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.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Further reading

External links

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