Complement decay-accelerating factor (CD55)

The protein contains 381 amino acids for an estimated molecular weight of 41400 Da.

 

This protein recognizes C4b and C3b fragments that condense with cell-surface hydroxyl or amino groups when nascent C4b and C3b are locally generated during C4 and c3 activation. Interaction of daf with cell-associated C4b and C3b polypeptides interferes with their ability to catalyze the conversion of C2 and factor B to enzymatically active C2a and Bb and thereby prevents the formation of C4b2a and C3bBb, the amplification convertases of the complement cascade (PubMed:7525274). Inhibits complement activation by destabilizing and preventing the formation of C3 and C5 convertases, which prevents complement damage (PubMed:28657829).', '(Microbial infection) Acts as a receptor for Coxsackievirus A21, coxsackieviruses B1, B3 and B5.', '(Microbial infection) Acts as a receptor for Human enterovirus 70 and D68 (Probable).', '(Microbial infection) Acts as a receptor for Human echoviruses 6, 7, 11, 12, 20 and 21. (updated: March 28, 2018)

Protein identification was indicated in the following studies:

  1. Goodman and co-workers. (2013) The proteomics and interactomics of human erythrocytes. Exp Biol Med (Maywood) 238(5), 509-518.
  2. Lange and co-workers. (2014) Annotating N termini for the human proteome project: N termini and Nα-acetylation status differentiate stable cleaved protein species from degradation remnants in the human erythrocyte proteome. J Proteome Res. 13(4), 2028-2044.
  3. Hegedűs and co-workers. (2015) Inconsistencies in the red blood cell membrane proteome analysis: generation of a database for research and diagnostic applications. Database (Oxford) 1-8.
  4. Wilson and co-workers. (2016) Comparison of the Proteome of Adult and Cord Erythroid Cells, and Changes in the Proteome Following Reticulocyte Maturation. Mol Cell Proteomics. 15(6), 1938-1946.
  5. Bryk and co-workers. (2017) Quantitative Analysis of Human Red Blood Cell Proteome. J Proteome Res. 16(8), 2752-2761.
  6. D'Alessandro and co-workers. (2017) Red blood cell proteomics update: is there more to discover? Blood Transfus. 15(2), 182-187.

Methods

The following articles were analysed to gather the proteome content of erythrocytes.

The gene or protein list provided in the studies were processed using the ID mapping API of Uniprot in September 2018. The number of proteins identified and mapped without ambiguity in these studies is indicated below.
Only Swiss-Prot entries (reviewed) were considered for protein evidence assignation.

PublicationIdentification 1Uniprot mapping 2Not mapped /
Obsolete
TrEMBLSwiss-Prot
Goodman (2013)2289 (gene list)227853205992269
Lange (2014)123412347281224
Hegedus (2015)2638262202352387
Wilson (2016)165815281702911068
d'Alessandro (2017)18261817201815
Bryk (2017)20902060101081942
Chu (2018)18531804553621387

1 as available in the article and/or in supplementary material
2 uniprot mapping returns all protein isoforms as one entry

The compilation of older studies can be retrieved from the Red Blood Cell Collection database.

The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.

No sequence conservation computed yet.

This protein is annotated as membranous in Gene Ontology, is annotated as membranous in UniProt.


Interpro domains
Total structural coverage: 100%
Model score: 100

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VariantDescription
Tc(b) antigen
Tc(c) antigen
WES(a) antigen
Dr(a-) antigen
Cr(a-) antigen
GUTI(-) antigen
CHAPLE

The reference OMIM entry for this protein is 125240

Cd55 antigen; cd55
Decay-accelerating factor for complement; daf

DESCRIPTION

The major isoform of DAF, or CD55, is a 70-kD plasma membrane protein that is widely distributed on all blood cells and on endothelial and epithelial tissues. The physiologic role of DAF is to inhibit the complement cascade at the level of the critical C3 (120700) convertase step. By this mechanism, DAF protects autologous cells and tissues from complement-mediated damage and thereby plays a role in preventing or modulating autoimmune disease and inflammation. DAF also serves as a receptor for certain strains of E. coli and certain types of enteroviruses. Variation in DAF forms the basis of the Cromer blood group system (CROM; 613793) (review by Lublin, 2005). In addition to the major membrane-bound isoform of DAF, several other minor soluble and membrane-bound DAF isoforms are produced by alternative splicing (Osuka et al., 2006)

CLONING

Avoidance by host tissues of attack by autologous complement proteins is dependent in part on the activities of membrane regulatory factors. One molecule involved in this control is a 70-kD glycoprotein termed decay-accelerating factor (DAF). Interruption by DAF of the complement sequence at an early step in activation effectively halts progression of the cascade and prevents consequent cell injury. In man, a glycolipid-anchored form of DAF is expressed on the plasma membrane of all cell types that are in intimate contact with plasma complement proteins. DAF is also found on the surfaces of epithelial cells lining extracellular compartments, and variants of DAF are present in body fluids and in extracellular matrix. Medof et al. (1987) cloned cDNAs for human DAF. The deduced 376-amino acid protein contains a 29-amino acid N-terminal leader peptide, followed by 4 approximately 61-amino acid repeats of internal homology, a 70-amino acid serine- and threonine-rich segment with multiple potential O-glycosylation sites, and a C-terminal hydrophobic segment. However, the sequence lacks an initiation codon, indicating it is incomplete. Northern blot analysis of HeLa cells and myeloid leukemia cells detected transcripts of 3.1, 2.7, and 2.0 kb. Osuka et al. (2006) noted that glycosylphosphatidylinositol (GPI)-anchored DAF (gDAF) and soluble DAF (sDAF) are generated by alternative splicing. Insertion of a unique exon (exon 10) into the sDAF cDNA causes a frameshift that results in a unique C-terminal sequence lacking the GPI-anchored portion of gDAF. By RT-PCR of a lung cDNA library, Osuka et al. (2006) cloned 5 additional minor DAF variants. Three of the variants, vDAF1, vDAF2, and vDAF3, include novel exons (exons 11, 12, and 13, respectively) compared with gDAF and, like sDAF, encode proteins lacking the GPI-anchored portion in the C terminus. Variants vDAF4 and vDAF5 include part or all of intron 7, respectively, and encode proteins that retain the GPI-anchored portion of the C terminus but have expanded central STP-rich regions. PCR analysis detected expression of the DAF variants in almost all tissues examined, with higher expression of all variants in lung, liver, and peripheral blood compared with colon and stomach. The main band was derived from gDAF. Transfection of vDAF1, vDAF2, and vDAF3 into Chinese hamster ovary cells resulted in the secretion of these isoforms into the culture medium. Each was highly O-glycosylated prior to secretion. vDAF4 was expressed as a highly O-glycosylated membrane-bound protein.

GENE FUNCTION

CD55 is deficient in red blood cel ... More on the omim web site

The reference OMIM entry for this protein is 613793

Blood group, cromer system; crom
Cromer blood group system

A number sign (#) is used with this entry because the Cromer blood group system is based on variation in the CD55 gene (CD55; 125240).

DESCRIPTION

The Cromer blood group system (CROM) consists of 12 high-prevalence and 3 low-prevalence antigens that reside on decay-accelerating factor (DAF, or CD55; 125240), a regulator of complement activation. Nearly all Cromer antigens result from SNPs in the DAF gene. The red blood cells (RBCs) of people with the Cromer-null phenotype, Inab, lack DAF but do not appear to show increased susceptibility to hemolysis. Antibodies to Cromer antigens are rarely encountered, although evidence suggests that the antibodies may cause accelerated destruction of transfused RBCs. Cromer system antibodies are not associated with hemolytic disease of the newborn, because placenta is a rich source of fetally derived DAF, which is thought to absorb the antibodies (review by Storry et al., 2010).

CLINICAL FEATURES

Reid et al. (1996) studied 2 cases in which strongly reactive Cromer system antibodies, anti-Cr(a) and anti-Dr(a), became undetectable during the second and third trimesters of pregnancy.

MOLECULAR GENETICS

- Inab Phenotype The Inab phenotype, or Cromer null, in which RBCs lack all Cromer system antigens, is very rare. The RBCs of individuals with Inab phenotype have a deficiency of DAF, but they are not known to have any associated hematologic or other abnormalities. In the individual in which the Inab phenotype was first detected, Lublin et al. (1994) demonstrated a nonsense mutation in exon 2 of the DAF gene (125240.0001). The mutation truncated DAF near the N terminus, explaining the complete absence of surface DAF in the red cells of the individual. In a 28-year-old Japanese woman, Wang et al. (1998) demonstrated that the Cromer Inab phenotype was due to homozygosity for a 1579C-A transversion at the position 24 bp upstream of the 3-prime end of exon 2 of the CD55 gene (125240.0002). This substitution resulted in an mRNA with a 26-bp deletion, which introduced a frameshift and created a stop codon immediately downstream of the deletion. Translation of the mRNA would be terminated at the first amino acid of the second short consensus repeat (SCR2) domain of DAF. The woman and her brother, who also had the Cromer-null phenotype, had no history of intestinal disease. ... More on the omim web site

The reference OMIM entry for this protein is 226300

Enteropathy, protein-losing

Sheba et al. (1968) and Shani et al. (1974) described a family in which inheritance appeared clearly to be autosomal recessive. Intestinal lymphangiectasia was initially suspected but was later shown not to be present. See lymphangiectasia, intestinal (152800). The kindred was from an inbred Christian Arab group living in Israel. Eight of 28 children in 2 sibships were affected. The parents were in each case related as first cousins once removed, and the 2 affected sibships were first cousins through their mothers and second cousins through their fathers. Affected children showed edema, growth retardation, diarrhea, abdominal pain, and clubbing. Ascites and death occurred in 4; autopsies, performed in 2 of these, showed hepatic vein stenosis which caused a Budd-Chiari syndrome (600880). Lymphocyte counts were normal. Iron-deficiency anemia and hypoproteinemia were shown by all 8. ... More on the omim web site

Subscribe to this protein entry history

July 2, 2021: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 2, 2021: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 2, 2021: Protein entry updated
Automatic update: OMIM entry 613793 was added.

April 11, 2021: Protein entry updated
Automatic update: OMIM entry 125240 was added.

April 11, 2021: Protein entry updated
Automatic update: OMIM entry 226300 was added.

April 11, 2021: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Feb. 17, 2021: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Feb. 17, 2021: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Feb. 17, 2021: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Oct. 21, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Oct. 21, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Oct. 21, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Aug. 25, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Aug. 25, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Aug. 25, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

June 30, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

June 30, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

June 30, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

April 26, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

April 26, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

April 26, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

March 4, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

March 4, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

March 4, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Jan. 23, 2020: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Jan. 23, 2020: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Jan. 23, 2020: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Dec. 3, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Dec. 3, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Dec. 3, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Oct. 28, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Oct. 28, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Oct. 28, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Sept. 22, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Sept. 22, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Sept. 22, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Aug. 20, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Aug. 20, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Aug. 20, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 4, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 4, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 4, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

June 7, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

June 7, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

June 7, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

May 12, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

May 12, 2019: Protein entry updated
Automatic update: model status changed

May 12, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

May 12, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Jan. 21, 2019: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Jan. 21, 2019: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Jan. 21, 2019: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Nov. 17, 2018: Protein entry updated
Automatic update: model status changed

Nov. 17, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Nov. 17, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Nov. 17, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

Oct. 19, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Oct. 19, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

Oct. 19, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 6, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 6, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 6, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 5, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 4, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 4, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 4, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

July 2, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

July 2, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

July 2, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

May 27, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

May 27, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

May 27, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

April 27, 2018: Protein entry updated
Automatic update: OMIM entry 125240 was added.

April 27, 2018: Protein entry updated
Automatic update: OMIM entry 226300 was added.

April 27, 2018: Protein entry updated
Automatic update: OMIM entry 613793 was added.

April 12, 2018: Protein entry updated
Automatic update: Entry updated from uniprot information.

Feb. 10, 2018: Protein entry updated
Automatic update: Entry updated from uniprot information.

Feb. 2, 2018: Protein entry updated
Automatic update: Uniprot description updated

Dec. 19, 2017: Protein entry updated
Automatic update: Uniprot description updated

Nov. 23, 2017: Protein entry updated
Automatic update: Uniprot description updated

Oct. 26, 2017: Protein entry updated
Automatic update: model status changed

March 16, 2016: Protein entry updated
Automatic update: OMIM entry 125240 was added.

Jan. 24, 2016: Protein entry updated
Automatic update: model status changed