ELISA/assay

Mouse Complement factor H ELISA Kit

MBS2883304

48-Strip-Wells

355 USD

ELISA Kit

Mouse Complement factor H ELISA Kit

[Complement factor H]

[Complement factor H; Protein beta-1-H; Cfh; Hf1]

[complement factor H; Complement factor H; complement factor H; complement component factor h; Protein beta-1-H]

[Cfh]

[Cfh; Cfh; NOM; Sas1; Mud-1; Sas-1; Hf1]

CFAH_MOUSE

Mouse

1252

Recombinant and natural Mouse Complement factor H

For long term storage, please store the entire kit at -20 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, plasma, tissue homogenates, cell culture supernates or other biological fluids. Detection Range: 3.12ng/mL - 200 ng/mL

Intra-assay Precision: Intra-Assay CV: <5.5%. Inter-assay Precision: Inter-Assay CV: <7.9%

Intended Uses: This immunoassay kit allows for the in vitro quantitative determination of target antigen concentrations in serum, plasma, tissue homogenates, cell culture supernates or other biological fluids. Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to target antigen. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific for target antigen and then avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. Then a TMB substrate solution is added to each well. Only those wells that contain target antigen, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The concentration of target antigen in the samples is then determined by comparing the O.D. of the samples to the standard curve.

109627652

NP_034018.2

NM_009888.3

P06909

139,138 Da

Complement And Coagulation Cascades Pathway (198335); Complement And Coagulation Cascades Pathway (83270); Complement And Coagulation Cascades Pathway (484); Complement Cascade Pathway (1323708); Immune System Pathway (1323639); Innate Immune System Pathway (1323671); PodNet: Protein-protein Interactions In The Podocyte Pathway (755428); Regulation Of Complement Cascade Pathway (1323715); Staphylococcus Aureus Infection Pathway (172855); Staphylococcus Aureus Infection Pathway (171867)

CFH: Factor H functions as a cofactor in the inactivation of C3b by factor I and also increases the rate of dissociation of the C3bBb complex (C3 convertase) and the (C3b)NBB complex (C5 convertase) in the alternative complement pathway. Genetic variations in CFH are associated with basal laminar drusen (BLD); also known as drusen of Bruch membrane or cuticular drusen or grouped early adult-onset drusen. Drusen are extracellular deposits that accumulate below the retinal pigment epithelium on Bruch membrane. Basal laminar drusen refers to an early adult-onset drusen phenotype that shows a pattern of uniform small, slightly raised yellow subretinal nodules randomly scattered in the macula. In later stages, these drusen often become more numerous, with clustered groups of drusen scattered throughout the retina. In time these small basal laminar drusen may expand and ultimately lead to a serous pigment epithelial detachment of the macula that may result in vision loss. Defects in CFH are the cause of complement factor H deficiency (CFHD). A disorder that can manifest as several different phenotypes, including asymptomatic, recurrent bacterial infections, and renal failure. Laboratory features usually include decreased serum levels of factor H, complement component C3, and a decrease in other terminal complement components, indicating activation of the alternative complement pathway. It is associated with a number of renal diseases with variable clinical presentation and progression, including membranoproliferative glomerulonephritis and atypical hemolytic uremic syndrome. Defects in CFH are a cause of susceptibility to hemolytic uremic syndrome atypical type 1 (AHUS1). An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype. Genetic variation in CFH is associated with age-related macular degeneration type 4 (ARMD4). ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid (known as drusen) that lie beneath the retinal pigment epithelium and within an elastin- containing structure known as Bruch membrane. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted, signal peptide; Secreted. Cellular Component: cytoplasm; extracellular region; extracellular space; nucleus; plasma membrane. Molecular Function: complement component C3b binding; heparan sulfate proteoglycan binding; heparin binding. Biological Process: complement activation, alternative pathway; immune system process; innate immune response; regulation of complement activation

48-Strip-Wells

355 USD

96-Strip-Wells

475

5x96-Strip-Wells

2030

10x96-Strip-Wells

3700