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Decay-accelerating factor

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This is an old revision of this page, as edited by Scray (talk | contribs) at 01:38, 21 February 2013 (Pathology: "type III" is not a modifier of PNH - it is a description of RBCs within an individual with GPI mutation; refactoring section and adding source). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Template:PBB Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene.[1]

Decay accelerating factor is a 70 kDa membrane protein that regulates the complement system on the cell surface. It prevents the assembly of the C3bBb complex (the C3-convertase of the alternative pathway) or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.

This glycoprotein is broadly distributed among hematopoietic and non-hematopoietic cells. It is a determinant for the Cromer blood group system.

Pathology

Paroxysmal nocturnal hemoglobinuria

Because DAF is a GPI-anchored protein, its expression is reduced in persons with mutations that reduce GPI levels such as those with paroxysmal nocturnal hemoglobinuria; in that disorder, RBCs with very low levels of DAF and CD59 undergo complement-mediated hemolysis.[2]

Infectious diseases

DAF is used as a receptor by some coxsackieviruses and other enteroviruses.[3] Recombinant soluble DAF-Fc has been tested in mice as an anti-enterovirus therapy for heart damage;[4] however, the human enterovirus that was tested binds much more strongly to human DAF than to mouse or rat DAF. Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF.[5] and DAF-Fc has yet to be tested in humans.

See also

References

  1. ^ Medof ME, Lublin DM, Holers VM, Ayers DJ, Getty RR, Leykam JF, Atkinson JP, Tykocinski ML (1987). "Cloning and characterization of cDNAs encoding the complete sequence of decay-accelerating factor of human complement". Proc. Natl. Acad. Sci. U.S.A. 84 (7): 2007–11. doi:10.1073/pnas.84.7.2007. PMC 304572. PMID 2436222. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  2. ^ Parker C, Omine M, Richards S; et al. (2005). "Diagnosis and management of paroxysmal nocturnal hemoglobinuria". Blood. 106 (12): 3699–709. doi:10.1182/blood-2005-04-1717. PMC 1895106. PMID 16051736. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  3. ^ Karnauchow TM, Tolson DL, Harrison BA, Altman E, Lublin DM, Dimock K (1996). "The HeLa cell receptor for enterovirus 70 is decay-accelerating factor (CD55)". J. Virol. 70 (8): 5143–52. PMC 190469. PMID 8764022. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  4. ^ Yanagawa B, Spiller OB, Choy J, Luo H, Cheung P, Zhang HM, Goodfellow IG, Evans DJ, Suarez A, Yang D, McManus BM (2003). "Coxsackievirus B3-associated myocardial pathology and viral load reduced by recombinant soluble human decay-accelerating factor in mice". Lab. Invest. 83 (1): 75–85. PMID 12533688. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ Spiller OB, Goodfellow IG, Evans DJ, Almond JW, Morgan BP (2000). "Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF". J. Infect. Dis. 181 (1): 340–3. doi:10.1086/315210. PMID 10608785. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

Further reading

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