ELISA/assay

Canine Coagulation Factor VII ELISA Kit

MBS734934

48-Strip-Wells

470 USD

ELISA Kit

Canine Coagulation Factor VII ELISA Kit

Coagulation Factor VII

coagulation factor VII, partial; Coagulation factor VII; coagulation factor VII; eptacog alfa; proconvertin; FVII coagulation protein; coagulation factor VII (serum prothrombin conversion accelerator); Proconvertin; Serum prothrombin conversion accelerator; SPCA; INN: Eptacog alfaCleaved into the following 2 chains:Factor VII light chain; Factor VII heavy chain

F7

F7; F7; SPCA; SPCA

FA7_HUMAN

Canine

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 ng/mL.

Intended Uses: This F7 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Canine F7. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cardiovascular

Principle of the Assay: F7 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-F7 antibody and an F7-HRP conjugate. The assay sample and buffer are incubated together with F7-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the F7 concentration since F7 from samples and F7-HRP conjugate compete for the anti-F7 antibody binding site. Since the number of sites is limited, as more sites are occupied by F7 from the sample, fewer sites are left to bind F7-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The F7 concentration in each sample is interpolated from this standard curve.

12750767

AAC50211.2

49,320 Da

BMAL1:CLOCK,NPAS2 Activates Circadian Gene Expression Pathway (477138); Blood Clotting Cascade Pathway (198840); Circadian Clock Pathway (187173); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); Extrinsic Pathway (106058); Formation Of Fibrin Clot (Clotting Cascade) Pathway (106057); Gamma-carboxylation Of Protein Precursors Pathway (106233); Gamma-carboxylation, Transport, And Amino-terminal Cleavage Of Proteins Pathway (106232)

This gene encodes coagulation factor VII which is a vitamin K-dependent factor essential for hemostasis. This factor circulates in the blood in a zymogen form, and is converted to an active form by either factor IXa, factor Xa, factor XIIa, or thrombin by minor proteolysis. Upon activation of the factor VII, a heavy chain containing a catalytic domain and a light chain containing 2 EGF-like domains are generated, and two chains are held together by a disulfide bond. In the presence of factor III and calcium ions, the activated factor then further activates the coagulation cascade by converting factor IX to factor IXa and/or factor X to factor Xa. Defects in this gene can cause coagulopathy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, May 2012]

F7: Initiates the extrinsic pathway of blood coagulation. Serine protease that circulates in the blood in a zymogen form. Factor VII is converted to factor VIIa by factor Xa, factor XIIa, factor IXa, or thrombin by minor proteolysis. In the presence of tissue factor and calcium ions, factor VIIa then converts factor X to factor Xa by limited proteolysis. Factor VIIa will also convert factor IX to factor IXa in the presence of tissue factor and calcium. Defects in F7 are the cause of factor VII deficiency (FA7D). A hemorrhagic disease with variable presentation. The clinical picture can be very severe, with the early occurrence of intracerebral hemorrhages or repeated hemarthroses, or, in contrast, moderate with cutaneous-mucosal hemorrhages (epistaxis, menorrhagia) or hemorrhages provoked by a surgical intervention. Finally, numerous subjects are completely asymptomatic despite very low factor VII levels. Belongs to the peptidase S1 family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: EC 3.4.21.21; Secreted; Protease; Apoptosis; Secreted, signal peptide; Motility/polarity/chemotaxis. Chromosomal Location of Human Ortholog: 13q34. Cellular Component: extracellular space; Golgi lumen; endoplasmic reticulum lumen; plasma membrane; extracellular region; vesicle. Molecular Function: protein binding; serine-type peptidase activity; serine-type endopeptidase activity; calcium ion binding; glycoprotein binding; receptor binding. Biological Process: circadian rhythm; organ regeneration; positive regulation of blood coagulation; positive regulation of positive chemotaxis; positive regulation of leukocyte chemotaxis; post-translational protein modification; proteolysis; peptidyl-glutamic acid carboxylation; positive regulation of protein kinase B signaling cascade; blood coagulation, extrinsic pathway; cellular protein metabolic process; response to vitamin K; response to estrogen stimulus; blood coagulation; positive regulation of cell migration. Disease: Myocardial Infarction, Susceptibility To; Factor Vii Deficiency

48-Strip-Wells

470 USD

96-Strip-Wells

675