Product nameAnti-Factor H antibody [OX-24]
See all Factor H primary antibodies
DescriptionMouse monoclonal [OX-24] to Factor H
Specificityab118820 recognizes the Human serum complement protein factor H and a 43-49kD truncated form of factor H present at.
Tested applicationsSuitable for: WB, IP, ELISA, IHC-P, Flow Cyt, ICC/IFmore details
Species reactivityReacts with: Human
Full length native protein (purified) corresponding to Human Factor H.
- WB: Human plasma, Human serum, Purified Factor H protein
ab118820 has switched from ascites to TCS on 19th September 2019.
This antibody clone is manufactured by Abcam. If you require a custom buffer formulation or conjugation for your experiments, please contact firstname.lastname@example.org.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.02% Sodium azide
Concentration information loading...
PurityProtein G purified
Purification notesPurified from TCS.
Light chain typekappa
Our Abpromise guarantee covers the use of ab118820 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use at an assay dependent concentration. Predicted molecular weight: 139 kDa.|
|IP||Use at an assay dependent concentration.|
|ELISA||Use at an assay dependent concentration.|
|IHC-P||Use a concentration of 20 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
|Flow Cyt||Use at an assay dependent concentration.
ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.
|ICC/IF||Use at an assay dependent concentration. PubMed: 25254972|
FunctionFactor 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.
Tissue specificityExpressed by the liver and secreted in plasma.
Involvement in diseaseGenetic variations in CFH are associated with basal laminar drusen (BLD) [MIM:126700]; 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 (CFH deficiency) [MIM:609814]. CFH deficiency determines uncontrolled activation of the alternative complement pathway with consumption of C3 and often other terminal complement components. It is associated with a number of renal diseases with variable clinical presentation and progression, including membranoproliferative glomerulonephritis and atypical hemolytic uremic syndrome. CFH deficiency patients may show increased susceptibility to meningococcal infections.
Defects in CFH are a cause of susceptibility to hemolytic uremic syndrome atypical type 1 (AHUS1) [MIM:235400]. 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. Note=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) [MIM:610698]. 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.
Sequence similaritiesContains 20 Sushi (CCP/SCR) domains.
- Information by UniProt
- adrenomedullin binding protein antibody
- age related maculopathy susceptibility 1 antibody
- AHUS 1 antibody
All lanes : Anti-Factor H antibody [OX-24] (ab118820) at 1 µg/ml
Lane 1 : Human serum diluted 1/1000 at 10 µl
Lane 2 : Human plasma diluted 1/1000 at 10 µl
Lane 3 : Purified Factor H protein at 0.5 µg
Lane 4 : Purified Factor H protein at 0.1 µg
Performed under reducing conditions.
Predicted band size: 139 kDa
Observed band size: 170 kDa why is the actual band size different from the predicted?
This blot was produced using a 4-12% Bis-tris under the MOPS buffer system. The gel was run at 200V for 55 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 3% milk before being incubated with ab118820 overnight at 4°C at a 1ug/ml concentration. Antibody binding was detected using Goat anti-Mouse IgG H&L (IRDye® 800CW) preadsorbed (ab216772) at 1/20000 dilution for 1 hour at room temperature before imaging.
This product has been referenced in:
- Liu J & Hoh J Loss of Complement Factor H in Plasma Increases Endothelial Cell Migration. J Cancer 8:2184-2190 (2017). WB ; Mouse . Read more (PubMed: 28819420) »
- Popek S et al. IL-6 and IL-8 enhance factor H binding to the cell membranes. Mol Med Rep 13:3886-94 (2016). IF . Read more (PubMed: 27035765) »