All Factor XIII reagents are produced in house and quality controlled, including 3 Factor XIII Antibody, 1 Factor XIII ELISA, 24 Factor XIII Gene, 1 Factor XIII Lysate, 1 Factor XIII Protein, 1 Factor XIII qPCR. All Factor XIII reagents are ready to use.
Recombinant Factor XIII proteins are expressed by HEK293 Cells with fusion tags as C-His.
Factor XIIIantibodies are validated with different applications, which are ELISA, ELISA(Cap).
Factor XIIIcDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each Factor XIII of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
Factor XIIIELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
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.