Human PROZ (Vitamin K-dependent protein Z) ELISA Kit

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935106861
info@markelab.com
name
Human PROZ (Vitamin K-dependent protein Z) ELISA Kit
category
ELISA Kits
provider
FineTest
reference
EH1029
tested applications
ELISA

Documents del producto

Instrucciones
Descargar
Data sheet

Product specifications

Category
ELISA Kits
Reactivity
Human
Detection Method
Colorimetric
Assay Data
4 hours
Assay Type
Sandwich ELISA, Double Antibody
Test Range
0.156-10ng/ml
Sensitivity
0.094ng/ml
Size 1
96T
Tested Applications
ELISA
Sample Type
Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples
Availability
Shipped within 10-14 working days.
Storage
2-8 °C for 12 months
UniProt ID
P22891
Alias
PROZ, Vitamin K-dependent protein Z, protein Z
Background
Elisa kits for PROZ
Status
RUO

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abx016049

Vitamin K-Dependent Protein Z (PROZ) Antibody

PROZ protein Z, vitamin K-dependent plasma glycoprotein.It is 62 kDa large and 396 amino acids long.It has four domains: a gla-rich region, two EGF-like domains and a trypsin-like domain.It lacks the serine residue that would make it catalytically active as a serine protease.It is a member of the coagulation cascade, the group of blood proteins that leads to the formation of blood clots.It is vitamin K-dependent, and its functionality is therefore impaired in warfarin therapy.It is a glycoprotein.Although it is not enzymatically active, it is structurally related to several serine proteases of the coagulation cascade: factors VII, IX, X and protein C.The carboxyglutamate residues (which require vitamin K) bind protein Z to phospholipid surfaces.The main role of protein Z appears to be the degradation of factor Xa.This is done by protein Z-related protease inhibitor (ZPI), but the reaction is accelerated 1000-fold by the presence of protein Z.Oddly, ZPI also degrades factor XI, but this reaction does not require the presence of protein Z.In some studies, deficiency states have been associated with a propensity to thrombosis.Others, however, link it to bleeding tendency; there is no clear explanation for this, as it acts physiologically as an inhibitor, and deficiency would logically have led to a predisposition for thrombosis.

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