Product nameAnti-Factor XII antibody - C-terminal
See all Factor XII primary antibodies
DescriptionRabbit polyclonal to Factor XII - C-terminal
Tested applicationsSuitable for: IHC-P, WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Recombinant fragment corresponding to Human Factor XII (C terminal).
Database link: P00748
- HepG2, MCF7, SW480 and mouse liver extracts; Rat kidney tissue.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 50% Glycerol, 0.87% Sodium chloride
PBS without Mg2+ and Ca2+.
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab196670 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/50 - 1/100.|
|WB||1/500 - 1/2000. Predicted molecular weight: 68 kDa.|
FunctionFactor XII is a serum glycoprotein that participates in the initiation of blood coagulation, fibrinolysis, and the generation of bradykinin and angiotensin. Prekallikrein is cleaved by factor XII to form kallikrein, which then cleaves factor XII first to alpha-factor XIIa and then trypsin cleaves it to beta-factor XIIa. Alpha-factor XIIa activates factor XI to factor XIa.
Involvement in diseaseDefects in F12 are the cause of factor XII deficiency (FA12D) [MIM:234000]; also known as Hageman factor deficiency. This trait is an asymptomatic anomaly of in vitro blood coagulation. Its diagnosis is based on finding a low plasma activity of the factor in coagulating assays. It is usually only accidentally discovered through pre-operative blood tests. F12 deficiency is divided into two categories, a cross-reacting material (CRM)-negative group (negative F12 antigen detection) and a CRM-positive group (positive F12 antigen detection).
Defects in F12 are the cause of hereditary angioedema type 3 (HAE3) [MIM:610618]; also known as estrogen-related HAE or hereditary angioneurotic edema with normal C1 inhibitor concentration and function. HAE is characterized by episodic local subcutaneous edema, and submucosal edema involving the upper respiratory and gastrointestinal tracts. HAE3 occurs exclusively in women and is precipitated or worsened by high estrogen levels (e.g., during pregnancy or treatment with oral contraceptives). It differs from HAE types 1 and 2 in that both concentration and function of C1 inhibitor are normal.
Sequence similaritiesBelongs to the peptidase S1 family.
Contains 2 EGF-like domains.
Contains 1 fibronectin type-I domain.
Contains 1 fibronectin type-II domain.
Contains 1 kringle domain.
Contains 1 peptidase S1 domain.
modificationsFactor XII is activated by kallikrein in alpha-factor XIIa, which is then further converted by trypsin into beta-factor XIIa. Alpha-factor XIIa is composed of the NH2-terminal heavy chain (Coagulation factor XIIa heavy chain) and the COOH-terminal light chain (Coagulation factor XIIa light chain), connected by a disulfide bond. Beta-factor XIIa is composed of 2 chains linked by a disulfide bond, a light chain (Beta-factor XIIa part 2), corresponding to the COOH-terminal light chain (Coagulation factor XIIa light chain) and a nonapeptide (Beta-factor XIIa part 1).
O- and N-glycosylated. The O-linked polysaccharides were not identified, but are probably the mucin type linked to GalNAc.
- Information by UniProt
- Factor XII antibody
- Beta factor XIIa part 1 antibody
- Beta factor XIIa part 2 antibody
All lanes : Anti-Factor XII antibody - C-terminal (ab196670) at 1/500 dilution
Lane 1 : HepG2 cell extract
Lane 2 : MCF7 cell extract
Lane 3 : SW480 cell extract
Lane 4 : Mouse liver extract
Predicted band size: 68 kDa
Immunohistochemical analysis of paraffin-embedded rat kidney tissue labeling Factor XII with ab196670 at 1/50 dilution.
This product has been referenced in:
- Tabit CE et al. Elevated Angiopoietin-2 Level in Patients With Continuous-Flow Left Ventricular Assist Devices Leads to Altered Angiogenesis and Is Associated With Higher Nonsurgical Bleeding. Circulation 134:141-52 (2016). Read more (PubMed: 27354285) »