PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 3384397

[Structure and function of a cell-associated complement regulatory protein, membrane cofactor protein (MCP)].

T Seya
View original source ↗Export metadata ↓

Abstract

Based on evidence suggesting that human leukocytes have factor I cofactor activity that is distinct from C3b/C4b receptor (CR1), we purified the cofactor protein from several human leukocyte cell-lines, and its structural and functional properties assessed. This protein migrates Mr 45,000-70,000 dalton region with a broad singlet or doublet on SDS-PAGE, specifically binds to C3b and C4b, has an acidic pI around pH 4, is rich in proline in amino acid analysis, possesses both N-linked and O-linked oligosaccharides, generates iC3b by acting as a cofactor for I-mediated C3b cleavage, and does not disassemble the C3 convertases. This protein therefore shares some common properties characteristic to complement regulatory proteins, CR1, H, and C4b-binding protein (C4bp). In addition, the functional profile of this protein is complementary to that of decay-accelerating factor (DAF) that has been known to be a protective protein for complement-mediated cell damage. We named this protein membrane cofactor protein (MCP), and suspect that the reason DAF and MCP are widely distributed on human peripheral blood cells relates to their synergistic activity profile such that complement activation on autologous tissue is inhibited.

Explore related subjects

Antigens, CDComplement System ProteinsHumansLeukocytesMembrane Cofactor ProteinMembrane GlycoproteinsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T Seya. 1988. [Structure and function of a cell-associated complement regulatory protein, membrane cofactor protein (MCP)].. https://pubmed.ncbi.nlm.nih.gov/3384397/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Autophagic-like cell death in neutrophils induced by autoantibodies.

Human neutrophils undergo autophagic-like cell death following Sialic acid binding immunoglobulin-like lectin-9 (Siglec-9) ligation and concurrent stimulation with certain, but not all, neutrophil survival cytokines. Caspase inhibition by these cytokines is required, but is not sufficient, to trigger this particular form of cell death. Additional mechanisms may involve reactive oxygen species (ROS), and blocking of ROS or prevention of ROS production prevents autophagic-like neutrophil death. Interestingly, human intravenous immunoglobulin (IVIg) preparations contain natural anti-Siglec-9 autoantibodies, which are able to ligate Siglec-9 on neutrophils and induce autophagic-like cell death in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and some other survival cytokines. Here, we discuss the pathophysiological and therapeutic implications of these recent findings.

Antigens, CD↗
PubMed2007

Bias in association studies of systemic lupus erythematosus susceptibility due to geographical variation in the frequency of a programmed cell death 1 polymorphism across Europe.

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 x 10(-6)) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.

Antigens, CD↗