ELISA/assay

Human Coagulation Factor V/Plasma Factor V ELISA Kit

MBS765920

48-Strip-Wells

300 USD

ELISA Kit

Human Coagulation Factor V/Plasma Factor V ELISA Kit

[Coagulation Factor V/Plasma Factor V]

[F5 (Coagulation Factor V/Plasma Factor V)/Activated protein C cofactor/PCCF/Proaccelerin; labile factor]

[coagulation factor V preproprotein; Coagulation factor V; coagulation factor V; coagulation factor V; Activated protein C cofactor; Proaccelerin, labile factor]

[F5]

[F5; F5; FVL; PCCF; THPH2; RPRGL1]

FA5_HUMAN

Human

2224

This assay has high sensitivity and excellent specificity for detection of F5. No significant crossreactivity or interference between F5 and analogues was observed.

Store at 4 degree C if kit is to be used within 1 week. Stable for 6 months (if micro ELISA Plate, Lyophilized Standard and Concentrated Biotinylated Detection Protein stored at-20 degree C. Other components at 2-8 degree C). Stable for 12 months (if the entire kit is stored at-20 degree C).

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, plasma, tissue homogenates and other biological fluids. Detection Range: 15.625-1000pg/ml. Sensitivity: <9.375pg/ml

Intra-assay Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level F5 were tested 20 times on one plate, respectively. Intra-Assay: CV<8%. Inter-assay Precision: Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level F5 were tested on 3 different plates, 8 replicates in each plate. CV (%) = SD/meanX100. Inter-Assay: CV<10%

Principle of the Assay: This kit was based on sandwich enzyme-linked immune-sorbent assay technology. Anti- F5 antibody was pre-coated onto 96-well plates. And the biotin conjugated anti- F5 antibody was used as detection antibodies. The standards, test samples and biotin conjugated detection antibody were added to the wells subsequently, and washed with wash buffer. HRP-Streptavidin was added and unbound conjugates were washed away with wash buffer. TMB substrates were used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the F5 amount of sample captured in plate. Read the O.D. absorbance at 450nm in a microplate reader, and then the concentration of F5 can be calculated.

105990535

NP_000121.2

NM_000130.4

251,703 Da

Asparagine N-linked Glycosylation Pathway (1268714); Blood Clotting Cascade Pathway (198840); COPII (Coat Protein 2) Mediated Vesicle Transport Pathway (1268727); Cargo Concentration In The ER Pathway (1309087); Common Pathway Of Fibrin Clot Formation (1269371); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); ER To Golgi Anterograde Transport Pathway (1268726); Formation Of Fibrin Clot (Clotting Cascade) Pathway (1269368)

This gene encodes an essential cofactor of the blood coagulation cascade. This factor circulates in plasma, and is converted to the active form by the release of the activation peptide by thrombin during coagulation. This generates a heavy chain and a light chain which are held together by calcium ions. The activated protein is a cofactor that participates with activated coagulation factor X to activate prothrombin to thrombin. Defects in this gene result in either an autosomal recessive hemorrhagic diathesis or an autosomal dominant form of thrombophilia, which is known as activated protein C resistance. [provided by RefSeq, Oct 2008]

factor V: Central regulator of hemostasis. It serves as a critical cofactor for the prothrombinase activity of factor Xa that results in the activation of prothrombin to thrombin. Defects in F5 are the cause of factor V deficiency (FA5D); also known as Owren parahemophilia. It is an hemorrhagic diastesis. Defects in F5 are the cause of thrombophilia due to activated protein C resistance (THPH2). THPH2 is a hemostatic disorder due to defective degradation of factor Va by activated protein C. It is characterized by a poor anticoagulant response to activated protein C resulting in tendency to thrombosis. Defects in F5 are a cause of susceptibility to Budd- Chiari syndrome (BDCHS). A syndrome caused by obstruction of hepatic venous outflow involving either the hepatic veins or the terminal segment of the inferior vena cava. Obstructions are generally caused by thrombosis and lead to hepatic congestion and ischemic necrosis. Clinical manifestations observed in the majority of patients include hepatomegaly, right upper quadrant pain and abdominal ascites. Budd-Chiari syndrome is associated with a combination of disease states including primary myeloproliferative syndromes and thrombophilia due to factor V Leiden, protein C deficiency and antithrombin III deficiency. Budd-Chiari syndrome is a rare but typical complication in patients with polycythemia vera. Defects in F5 may be a cause of susceptibility to ischemic stroke (ISCHSTR); also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors. Defects in F5 are associated with susceptibility to pregnancy loss, recurrent, type 1 (RPRGL1). RPRGL1 is a common complication of pregnancy, resulting in spontaneous abortion before the fetus has reached viability. The term includes all miscarriages from the time of conception until 24 weeks of gestation. Recurrent pregnancy loss is defined as 3 or more consecutive spontaneous abortions. Belongs to the multicopper oxidase family. Protein type: Secreted, signal peptide; Secreted; Protease. Chromosomal Location of Human Ortholog: 1q23. Cellular Component: endoplasmic reticulum lumen; ER to Golgi transport vesicle; ER-Golgi intermediate compartment membrane; extracellular region; extracellular space; Golgi membrane; membrane; plasma membrane. Molecular Function: copper ion binding; protein binding. Biological Process: blood circulation; blood coagulation; cellular protein metabolic process; COPII coating of Golgi vesicle; ER to Golgi vesicle-mediated transport; platelet activation; platelet degranulation; post-translational protein modification; protein amino acid N-linked glycosylation via asparagine. Disease: Budd-chiari Syndrome; Factor V Deficiency; Pregnancy Loss, Recurrent, Susceptibility To, 1; Stroke, Ischemic; Thrombophilia Due To Activated Protein C Resistance

48-Strip-Wells

300 USD

96-Strip-Wells

415

5x96-Strip-Wells

1825

10x96-Strip-Wells

3425