F13B
Reactivity: Human
ELISA, IHC, IF
Host: Rabbit
Polyclonal
unconjugated
Application Notes
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,IHC: 1:100-1:300,ELISA 1:10000,IF 1:50-200
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % 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
-20 °C
Storage Comment
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Expiry Date
12 months
Target
F13B
(Coagulation Factor 13, B Polypeptide (F13B))
Alternative Name
Factor XIII B
Background
F13B, Coagulation factor XIII B chain, Fibrin-stabilizing factor B subunit, Protein-glutamine gamma-glutamyltransferase B chain, Transglutaminase B chainF13B (coagulation factor XIII B chain) 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.