Rabbit anti-Mouse Complement Factor H (CFH) Polyclonal Antibody | anti-CFH antibody

Polyclonal Antibody to Complement Factor H (CFH)

Cat. Num. AAA2111951

• Gene Names: Cfh; NOM; Sas1; Mud-1; Sas-1
• Reactivity: Mouse
• Applications: Western Blot, Immunohistochemistry, Immunocytochemistry, Immunoprecipitation
• Purity: Antigen-specific affinity chromatography followed by Protein A affinity chromatography
• Synonyms: Complement Factor H (CFH); Polyclonal Antibody; Polyclonal Antibody to Complement Factor H (CFH); CF-H; FH; FHL1; ARMD4; ARMS1; CFHL3; HF1; HF2; HUS; H Factor 2; Age-Related Maculopathy Susceptibility 1; Adrenomedullin binding protein; anti-CFH antibody

• Host: Rabbit
• Reactivity: Mouse
• Clonality: Polyclonal
• Specificity: The antibody is a rabbit polyclonal antibody raised against CFH. It has been selected for its ability to recognize CFH in immunohistochemical staining and western blotting.
• Purity/Purification: Antigen-specific affinity chromatography followed by Protein A affinity chromatography
• Form/Format: Liquid; PBS, pH7.4, containing 0.02% NaN3, 50% glycerol.
• Concentration: 1mg/ml (varies by lot)

• Applicable Applications for anti-CFH antibody: Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunoprecipitation (IP)
• Application Notes: WB: 0.5-2ug/mL; 1:500-2000; IHC: 5-20ug/mL; 1:50-200; ICC: 5-20ug/mL; 1:50-200
• Cross Reactivity: Mouse
• Conjugation: None
• Preparation and Storage: Store at 4 degree C for frequent use. Aliquot and store at -20 degree C for 12 months.; Avoid repeated freeze/thaw cycles.; The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37 degree C for 48h, and no obvious degradation and precipitation were observed. The loss rate is less than 5% within the expiration date under appropriate storage condition.

Western Blot (WB)

(Western Blot; Sample: Lane1: Mouse Serum; Lane2: Mouse Plasma; Lane3: Mouse Liver lysate Primary Ab:)

Product Categories/Family for anti-CFH antibody

Metabolic Pathway; Infection Immunity; Immune Molecule

NCBI and Uniprot Product Information

• NCBI GI #: 109627652
• NCBI GeneID: 12628
• NCBI Accession #: NP_034018.2
• NCBI GenBank Nucleotide #: NM_009888.3
• UniProt Accession #: P06909; Q6NZK3
• Molecular Weight: 139,138 Da
• NCBI Official Full Name: complement factor H
• NCBI Official Synonym Full Names: complement component factor h
• NCBI Official Symbol: Cfh
• NCBI Official Synonym Symbols: NOM; Sas1; Mud-1; Sas-1
• NCBI Protein Information: complement factor H
• UniProt Protein Name: Complement factor H
• Protein Family: Complement factor
• UniProt Gene Name: Cfh
• UniProt Synonym Gene Names: Hf1
• UniProt Entry Name: CFAH_MOUSE

Uniprot Description

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; Secreted, signal peptide

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