F13A1 Rabbit pAb- ABclonal,ABclonal,A1461

Reactivity

Human, Mouse, Rat

Application

WB, IF-P, ELISA

Conjugate

Unconjugated

Platform ID

BAB386626268

ABclonal

Headquarters

500W Cummings Park, Ste. 6500 Woburn, MA 01801

Contact

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Product Specifications
Scientific Background

Specifications

NameF13A1 Rabbit pAb- ABclonal
Cat. No.A1461
RRID#N/A
IsotypeIgG
ReactivityHuman, Mouse, Rat
ConjugationUnconjugated
ApplicationWB, IF-P, ELISA
Working DilutionsWB:1:1000 - 1:5000 | IF-P:1:500 - 1:1000 | ELISA:Recommended starting concentration is 1 μg/mL. Please optimize the concentration based on your specific assay requirements.
ImmunogenRecombinant protein (or fragment).This information is considered to be commercially sensitive.
PurityAffinity purification
Appearance/FormLiquid
StorageStore at -20℃. Avoid freeze / thaw cycles.; Buffer: Buffer: PBS containing 50% glycerol, preserved with proclin300 or sodium azide (as specified on the Certificate of Analysis), pH 7.3.
Regulatory StatusResearch Use Only

Scientific Background

This gene encodes the coagulation factor XIII A 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 plasma carrier molecules. Platelet factor XIII is comprised only of 2 A subunits, which are identical to those of plasma origin. Upon 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. It also crosslinks alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin. 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.

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