This antibody is purified through a protein A column, followed by peptide affinity purification.
Immunogen
This F13B antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 151-179 amino acids from the N-terminal region of human F13B.
F13B
Reactivity: Human
ELISA
Host: Rabbit
Polyclonal
HRP
Application Notes
For WB starting dilution is: 1:1000
Restrictions
For Research Use only
Format
Liquid
Concentration
0.5 mg/mL
Buffer
Supplied in PBS with 0.09 % (W/V) sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C,-20 °C
Storage Comment
Store at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Target
F13B
(Coagulation Factor 13, B Polypeptide (F13B))
F13B antibody, coagulation factor XIII B chain antibody, LOC100347263 antibody
Background
This gene encodes coagulation factor XIII B subunit. 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 comprised only of 2 A subunits, which are identical to those of plasma origin. Upon activation by the 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.