Abcam, ab222864, Human Complement Factor P ELISA Kit

Size: 1 x 96Tests
Human Complement Factor P ELISA Kit is a Sandwich (quantitative) ELISA for the measurement of Human Complement Factor P in Human in Biofluids samples.
Key facts
Detection method:Colorimetric,
Sample types:Cerebral Spinal Fluid, Saliva, Urine, Plasma, Serum,
Reacts with:Human,
Assay type:Sandwich (quantitative),
Sensitivity:= 0.26 ng/mL,
Range:0.156 - 10 ng/mL,
Assay time:4h,
Assay Platform:Pre-coated microplate (12 x 8 well strips)

Product details:
The Human Complement Factor P (CFP) ELISA (Enzyme-Linked Immunosorbent Assay) Kit (ab222864) is designed for detection of Complement Factor P in human plasma, serum, urine, saliva, CSF, and cell culture samples.
This assay employs a quantitative sandwich enzyme immunoassay technique that measures human Complement Factor P in approximately 4 hours. A polyclonal antibody specific for human Complement Factor P has been pre-coated onto a 96-well microplate with removable strips. Complement Factor P in standards and samples is sandwiched by the immobilized antibody and a biotinylated polyclonal antibody specific for human Complement Factor P, which is recognized by a streptavidin-peroxidase (SP) conjugate. All unbound material is washed away and a peroxidase enzyme substrate is added. The color development is stopped and the intensity of the color is measured.
The entire kit may be stored at -20°C for long term storage before reconstitution - Avoid repeated freeze-thaw cycles.
Complement factor P (CFP), also known as properdin, is a plasma glycoprotein that positively regulates the alternative complement pathway convertases (C3bBb) of the innate immune system. CFP consists of 442-amino acids with a molecular weight of 53 kDa and is composed of multiple identical protein subunits. The subunits bind to each other in a head to tail manner to form cyclic dimers, trimers, tetramers, pentamers, and higher cyclic oligomers. It is mainly produced by neutrophils but also by monocytes, T cells, and bone marrow progenitor cells. CFP binds to many microbial surfaces and apoptotic cells. Complement factor P also stabilizes the C3- and C5-convertase enzyme complexes in a feedback loop that ultimately leads to formation of the membrane attack complex and lysis of the target cell.

Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions-Multi, Storage information-Please refer to protocols

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Complement Factor P also known as Properdin or P protein is a glycoprotein with a mass of approximately 53 kDa. It stabilizes the alternative pathway convertase complexes C3bBb prolonging their activity in the complement system. Factor P is expressed in various tissues prominently in circulating polymorphonuclear leukocytes monocytes and T cells. Through its expression and mechanical action Factor P acts independently not requiring other proteins for initial activation.
Biological function summary
Factor P enhances the opsonization and clearance of pathogens by promoting the deposition of C3b on microbial surfaces. It acts as a properdin complex binding with target surfaces and interacting with complement components C3 and C5 leading to the production of critical immune responses. This makes Factor P key to solving immunological imbalances. The expression ensures rapid response against infections supporting the immune system’s efficiency in pathogen elimination.
Pathways
Factor P integrates into the alternative complement pathway and elevates the immune response by increasing the potency of complement-mediated pathogen destruction. Factor P directly binds to C3b enhancing the formation of the C3/C5 convertase which leads to a cascade that enhances membrane attack complex (MAC) assembly. This pathway also relates Factor P to proteins such as C3 and C5 which represent integral parts of complement activation sequences.
Factor P deficiency or dysregulation links to increased vulnerability to Neisseria infections and atypical hemolytic uremic syndrome (aHUS). Neisseria infections occur due to impaired opsonophagocytosis where Factor P ensures effective destruction of bacteria. In aHUS abnormalities in Factor P can exacerbate underlying issues leading to severe kidney problems. Factor P's interactions with complement regulators such as factor H illustrate its important involvement in these pathological conditions.