Recombinant Human F13a/Factor XIIIa Protein (His Tag)
SKU: PKSH033713-50
Recombinant Human F13a/Factor XIIIa Protein (His Tag)
SKU # | PKSH033713 |
Expression Host | HEK293 Cells |
Description
Synonyms | Coagulation Factor XIII A Chain, Coagulation Factor XIIIa, F13A, F13A1, Protein-Glutamine Gamma-Glutamyltransferase A Chain, Transglutaminase A Chain |
Species | Human |
Expression Host | HEK293 Cells |
Sequence | Gly39-Met732 |
Accession | AAH27963.1 |
Calculated Molecular Weight | 80.3 kDa |
Observed Molecular Weight | 80-90 kDa |
Tag | C-His |
Bio-activity | Not validated for activity |
Properties
Purity | > 95 % as determined by reducing SDS-PAGE. |
Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
Storage | Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles. |
Shipping | This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C. |
Formulation | Supplied as a 0.2 μm filtered solution of 50 mM NaCl, 5% Sucrose, 0.3% Histidine, pH 8.0. |
Reconstitution | Not Applicable |
Background
Coagulation factor XIII is the last zymogen to become activated in the blood coagulation cascade. Plasma factor XIII is a heterotetramer composed of 2 A subunits and 2 B subunits. The A subunits have catalytic function, and the B subunits do not have enzymatic activity and may serve as plasma carrier molecules. Platelet factor XIII is composed of just 2 A subunits, which are identical to those of plasma origin. Upon cleavage of the activation peptide by thrombin and in the presence of calcium ion, the plasma factor XIII dissociates its B subunits and yields the same active enzyme, factor XIIIa, as platelet factor XIII. This enzyme acts as a transglutaminase to catalyze the formation of gamma-glutamyl-epsilon-lysine crosslinking between fibrin molecules, thus stabilizing the fibrin clot. Factor XIII deficiency is classified into two categories: type I deficiency, characterized by the lack of both the A and B subunits; and type II deficiency, characterized by the lack of the A subunit alone. These defects can result in a lifelong bleeding tendency, defective wound healing, and habitual abortion.