antibody

Rabbit CD55 Antibody

MBS001568

0.05 ml

270 USD

polyclonal

rabbit

nonconjugated

western blot, ELISA, enzyme immunoassay

Antibody

Rabbit CD55 Antibody

CD55

complement decay-accelerating factor isoform 1 preproprotein; Complement decay-accelerating factor; complement decay-accelerating factor; CD55 antigen; CD55 molecule, decay accelerating factor for complement (Cromer blood group)

CD55

CD55; CD55; CR; TC; DAF; CROM; CR; DAF

DAF_HUMAN

Rabbit

Human

381

Phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol

1 mg/ml

ELISA (EIA), Western Blot (WB)

10835143

NP_000565.1

NM_000574.3

P08174

41,400 Da

Class B/2 (Secretin Family Receptors) Pathway 106378!!Complement Activation, Classical Pathway 198823!!Complement And Coagulation Cascades Pathway 83073!!Complement And Coagulation Cascades Pathway 484!!Complement Cascade Pathway 106405!!GPCR Ligand Binding Pathway 161020!!Hematopoietic Cell Lineage Pathway 83078!!Hematopoietic Cell Lineage Pathway 489!!Immune System Pathway 106386!!Innate Immune System Pathway 106387

This gene encodes a protein involved in the regulation of the complement cascade. The encoded glycoprotein is also known as the decay-accelerating factor (DAF); binding of DAF to complement proteins accelerates their decay, disrupting the cascade and preventing damage to host cells. Antigens present on the DAF glycoprotein constitute the Cromer blood group system (CROM). Two alternatively spliced transcripts encoding different proteins have been identified. The predominant transcript encodes a membrane-bound protein expressed on cells exposed to plasma component proteins but an alternatively spliced transcript produces a soluble protein present at much lower levels. Additional, alternatively spliced transcript variants have been described, but their biological validity has not been determined. [provided by RefSeq, Jul 2008]

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. Ref.14. Subunit structure: Monomer (major form) and non-disulfide-linked, covalent homodimer (minor form). Binds to coxsackievirus A21, coxsackieviruses B1, B3 and B5, human enterovirus 70, human echoviruses 6, 7, 11, 12, 20 and 21 capsid proteins and acts as a receptor for these viruses. Ref.13 Ref.15 Ref.16 Ref.17 Ref.18 Ref.21. Subcellular location: Isoform 1: Cell membrane; Single-pass type I membrane protein. Isoform 2: Cell membrane; Lipid-anchor GPI-anchor. Tissue specificity: Expressed on the plasma membranes of all cell types that are in intimate contact with plasma complement proteins. It is also found on the surfaces of epithelial cells lining extracellular compartments, and variants of the molecule are present in body fluids and in extracellular matrix. Domain: The first Sushi domain (SCR1) is not necessary for function. SCR2 and SCR4 provide the proper conformation for the active site on SCR3 . By similarity. Ref.13. Post-translational modification: The Ser/Thr-rich domain is heavily O-glycosylated. Polymorphism: Responsible for the Cromer blood group system (CROM) [. MIM:613793]. It consists of at least 8 high-incidence (Cr(a), Tc(a), Dr(a), Es(a), WES(b), UMC, IFC and GUTI) and three low-incidence (Tc(b), Tc(c) and WES(a)) antigens that reside on DAF. In the Cromer phenotypes Dr(a-) and Inab there is reduced or absent expression of DAF, respectively. In the case of the Dr(a-) phenotype, a single nucleotide substitution within exon 5 accounts for two changes: a simple amino acid substitution, Leu-199 that is the basis of the antigenic variation, and an alternative splicing event that underlies the decreased expression of DAF in this phenotype. The Inab phenotype is a very rare one in which the red blood cells lack all Cromer system antigens. The red blood cells of individuals with Inab phenotype have a deficiency of DAF, but these individuals are not known to have any associated hematologic or other abnormalities. Sequence similarities: Belongs to the receptors of complement activation (RCA) family.Contains 4 Sushi (CCP/SCR) domains.

0.05 ml

270 USD