Key features and details
- Expression system: Insect cells
- Purity: > 95% SDS-PAGE
- Active: Yes
- Suitable for: SDS-PAGE
Product nameRecombinant rat Factor alpha XIIa protein
See all Factor alpha XIIa proteins and peptides
Activity is determined via complementation in an APTT clotting assay using Factor XII immuno-deficient human plasma.
Purity> 95 % SDS-PAGE.
Recombinant rat Factor XII is activated (to produce Factor XIIa) by human Kallikein followed by removal of the activator. >95percent activation is observed on SDS-PAGE.
Expression systemInsect cells
Protein lengthFull length protein
Amino acids20 to 595
Our Abpromise guarantee covers the use of ab229835 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Concentration information loading...
Preparation and Storage
Stability and Storage
Shipped on Dry Ice. Store at -80°C.
Constituents: 0.03% Sodium acetate, 0.87% Sodium chloride
This product is an active protein and may elicit a biological response in vivo, handle with caution.
- Coagulation factor XII
- coagulation factor XIIa heavy chain
- Coagulation factor XIIa light chain
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
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab229835 has not yet been referenced specifically in any publications.