catalog number :
MBS009559
products type :
ELISA Kit
products full name :
Mouse Coagulation Factor VII ELISA Kit
products short name :
Coagulation Factor VII
other names :
coagulation factor VII; Coagulation factor VII; coagulation factor VII; eptacog alfa; proconvertin; FVII coagulation protein; coagulation factor VII (serum prothrombin conversion accelerator); Proconvertin; Serum prothrombin conversion accelerator
other gene names :
F7; F7; SPCA; SPCA
uniprot entry name :
FA7_HUMAN
specificity :
No significant cross-reactivity or interference between Mouse F7 and analogues was observed.
storage stability :
Store all reagents at 2-8 degree C
other info1 :
Samples: Serum, Plasma, Tissue Homogenate, Feces, Urine and Body Fluids. Assay Type: Sandwich. Detection Range: 0.625 ug/ml - 20 ug/ml. Sensitivity: 0.1 ug/ml.
other info2 :
Intended Uses: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated F7 concentrations in Mouse serum, plasma and other body fluids. Using Purified Mouse F7 antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add F7 and F7 antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of F7 in the samples is then determined by comparing the O.D. of the samples to the standard curve. Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean x100]
products description :
Background/Introduction: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated F7 concentrations in Mouse serum, plasma and other body fluids. Using Purified Mouse F7 antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add F7 and F7 antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of F7 in the samples is then determined by comparing the O.D. of the samples to the standard curve.
ncbi acc num :
AAC50211.2
ncbi mol weight :
51,594 Da
ncbi pathways :
BMAL1:CLOCK/NPAS2 Activates Circadian 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)
ncbi summary :
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]
uniprot summary :
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: Secreted, signal peptide; Protease; EC 3.4.21.21; Secreted; Apoptosis; Motility/polarity/chemotaxis. Chromosomal Location of Human Ortholog: 13q34. Cellular Component: extracellular space; endoplasmic reticulum lumen; Golgi lumen; extracellular region; plasma membrane; vesicle. Molecular Function: protein binding; serine-type peptidase activity; serine-type endopeptidase activity; calcium ion binding; glycoprotein binding; receptor binding. Biological Process: circadian rhythm; positive regulation of protein kinase B signaling cascade; organ regeneration; blood coagulation, extrinsic pathway; positive regulation of positive chemotaxis; cellular protein metabolic process; positive regulation of blood coagulation; response to vitamin K; response to estrogen stimulus; positive regulation of leukocyte chemotaxis; proteolysis; blood coagulation; post-translational protein modification; peptidyl-glutamic acid carboxylation; positive regulation of cell migration. Disease: Myocardial Infarction, Susceptibility To; Factor Vii Deficiency