Description
Key facts
Detection method:Colorimetric,
Sample types:Cell culture media, Cerebral Spinal Fluid, Citrate plasma, EDTA Plasma, Heparin Plasma, Serum,
Reacts with:Human,
Assay type:Sandwich (quantitative),
Sensitivity:= 27.522 pg/mL,
Range:125 - 8000 pg/mL,
Assay time:1h 30m,
Assay Platform:Pre-coated microplate (12 x 8 well strips)
Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C, Storage information-+4°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
The C1QA protein is one part of the complement component 1q (C1q) molecule also called C1Q-A. This protein plays an important role in the immune system. The C1q complex consists of three polypeptide chains: C1QA C1QB and C1QC. C1QA alone has a mass of around 26 kDa. These proteins mainly express in immune cells like macrophages dendritic cells and B cells. It forms part of the extracellular matrix where it participates in immune functions.
Biological function summary
C1QA interacts with pathogens and modified host cells to trigger the complement cascade. This starts the activation of the classical pathway which enhances immune responses. C1QA together with C1QB and C1QC binds to Fc regions of antibodies attached to antigens. This binding leads to the subsequent activation of C1r and C1s proteases facilitating opsonization and clearance of immune complexes and apoptotic cells.
Pathways
The synthesis of C1QA plays an important role in the classical complement pathway and is part of the innate immunity. C1QA collaborates with proteins like C1QB and C1QC in this pathway. This pathway bridges innate and adaptive immunity by assisting in the removal of pathogens and cell debris. It also relates to the coagulation pathway where its activity can influence inflammation and tissue repair processes.
Impaired C1QA function links to conditions like systemic lupus erythematosus (SLE) and rheumatoid arthritis. These diseases often associate with inappropriate activation or regulation of the complement system. C1QA mutations or deficiencies can result in a higher susceptibility to SLE and interactions with C1QB and C1QC are also implicated in this disease. Moreover C1QA influences the pathogenesis of rheumatoid arthritis by modulating inflammation responses.
