|Recombinant Human F13B / Coagulation factor XIII B chain protein (Catalog#11510-H08H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Human F13B / Coagulation factor XIII B chain (rh F13B / Coagulation factor XIII B chain; Catalog#11510-H08H; P05160; Met 1-Thr 661). Total IgG was purified by Protein A affinity chromatography.|
ELISA: 0.5-1 μg/mL
This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human F13B. The detection limit for Human F13B is approximately 0.00245 ng/well.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Coagulation factor XIII B chain, also known as Fibrin-stabilizing factor B subunit, Protein-glutamine gamma-glutamyltransferase B chain, Transglutaminase B chain and F13B, is a secreted protein which contains 10 Sushi ( CCP / SCR ) domains. 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 a plasma carrier molecules. Platelet factor XIII is composed of just 2 A subunits, which are identical to those of plasma origin. The B chain of factor XIII is not catalytically active, but is thought to stabilize the A subunits and regulate the rate of transglutaminase formation by thrombin. Factor XIII 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. Defects in F13B are the cause of factor XIII subunit B deficiency ( FA13BD ) which is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.