Decay-accelerating factor

Decay-accelerating factor
CD55 molecule, decay accelerating factor for complement (Cromer blood group)

PDB rendering based on 1h03.
Identifiers
Symbols CD55; CR; CROM; DAF; TC
External IDs OMIM125240 MGI104850 HomoloGene479 GeneCards: CD55 Gene
RNA expression pattern
PBB GE CD55 201925 s at tn.png
PBB GE CD55 201926 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 1604 13136
Ensembl ENSG00000196352 ENSMUSG00000026399
UniProt P08174 Q3TU32
RefSeq (mRNA) NM_000574.3 NM_010016
RefSeq (protein) NP_000565.1 NP_034146
Location (UCSC) Chr 1:
207.49 – 207.53 Mb
Chr 1:
132.27 – 132.29 Mb
PubMed search [1] [2]

Complement decay-accelerating factor also known as CD55 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.

Contents

Pathology

DAF is not expressed on paroxysmal nocturnal hemoglobinuria III (markedly abnormal) RBCs; this, coupled with CD59 absence leads to PNH.

Infectious diseases

DAF is used as a receptor by some coxsackieviruses and other enteroviruses.[2] Recombinant soluble DAF-Fc has been tested in mice as an anti-enterovirus therapy for heart damage;[3] 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.[4] 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 (April 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=304572. 
  2. ^ Karnauchow TM, Tolson DL, Harrison BA, Altman E, Lublin DM, Dimock K (August 1996). "The HeLa cell receptor for enterovirus 70 is decay-accelerating factor (CD55)". J. Virol. 70 (8): 5143–52. PMC 190469. PMID 8764022. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=190469. 
  3. ^ Yanagawa B, Spiller OB, Choy J, Luo H, Cheung P, Zhang HM, Goodfellow IG, Evans DJ, Suarez A, Yang D, McManus BM (January 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. 
  4. ^ Spiller OB, Goodfellow IG, Evans DJ, Almond JW, Morgan BP (January 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. 

Further reading

  • Selinka HC, Wolde A, Sauter M, et al. (2004). "Virus-receptor interactions of coxsackie B viruses and their putative influence on cardiotropism.". Med. Microbiol. Immunol. 193 (2-3): 127–31. doi:10.1007/s00430-003-0193-y. PMID 12920584. 
  • Mikesch JH, Schier K, Roetger A, et al. (2007). "The expression and action of decay-accelerating factor (CD55) in human malignancies and cancer therapy.". Cell. Oncol. 28 (5-6): 223–32. PMID 17167176. 

External links



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