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Recombinant Human F13a/Factor XIIIa Protein (His Tag) (PKSH033713)

Recombinant Human F13a/Factor XIIIa Protein (His Tag) - 1
  • Recombinant Human F13a/Factor XIIIa Protein (His Tag) - 1
  • Recombinant Human F13a/Factor XIIIa Protein (His Tag) - 2
All Size Price Qty
50μg $ 198.00
- +
10μg $ 88.00
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For research use only.

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
Form Liquid
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.
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.
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