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
Reaktivität: Human
ELISA
Wirt: Kaninchen
Polyclonal
HRP
Applikationshinweise
For WB starting dilution is: 1:1000
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
0.5 mg/mL
Buffer
Supplied in PBS with 0.09 % (W/V) sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
4 °C,-20 °C
Informationen zur Lagerung
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 antikoerper, coagulation factor XIII B chain antikoerper, LOC100347263 antikoerper
Hintergrund
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.