CD55
CD55 (CD55 Molecule (Cromer Blood Group)) is a Protein Coding gene. Diseases associated with CD55 include Complement Hyperactivation, Angiopathic Thrombosis, And Protein-Losing Enteropathy and Blood Group, Cromer System. Among its related pathways are Creation of C4 and C2 activators and Transport to the Golgi and subsequent modification. Gene Ontology (GO) annotations related to this gene include lipid binding and virus receptor activity. An important paralog of this gene is C4BPA.
Full Name
CD55 Molecule (Cromer Blood Group)
Function
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.
Biological Process
Complement activation, classical pathway Source: UniProtKB-KW
Endoplasmic reticulum to Golgi vesicle-mediated transport Source: Reactome
Innate immune response Source: UniProtKB-KW
Negative regulation of complement activation Source: UniProtKB
Neutrophil degranulation Source: Reactome
Positive regulation of CD4-positive, alpha-beta T cell activation Source: UniProtKB
Positive regulation of CD4-positive, alpha-beta T cell proliferation Source: UniProtKB
Positive regulation of cytosolic calcium ion concentration Source: UniProtKB
Positive regulation of T cell cytokine production Source: UniProtKB
Regulation of complement activation Source: MGI
Regulation of complement-dependent cytotoxicity Source: MGI
Regulation of lipopolysaccharide-mediated signaling pathway Source: UniProtKB
Respiratory burst Source: UniProtKB
Cellular Location
Isoform 1&2&6&7: Cell membrane
Isoform 3&4&5: Secreted
Involvement in disease
Complement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy (CHAPLE): An autosomal recessive disease characterized by abdominal pain and diarrhea, primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease. Patients' T lymphocytes show increased complement activation causing surface deposition of complement and the generation of soluble C5a.
PTM
The Ser/Thr-rich domain is heavily O-glycosylated.