ELISA/assay

Rabbit Fibrinopeptide A ELISA Kit

MBS725347

48-Strip-Wells

440 USD

ELISA Kit

Rabbit Fibrinopeptide A ELISA Kit

[Fibrinopeptide A]

[fibrinogen alpha chain isoform alpha preproprotein; Fibrinogen alpha chain; fibrinogen alpha chain; fibrinogen, A alpha polypeptide; fibrinogen alpha chain]

[FPA]

[FGA; FGA; Fib2]

FIBA_HUMAN

Rabbit

This assay has high sensitivity and excellent specificity for detection of FOXL2. No significant cross-reactivity or interference between FOXL2 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between FOXL2 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma, Cell Culture Supernatants, Body Fluid And Tissue Homogenate. Assay Type: Quantitative Competitive. Sensitivity: 0.1 ng/mL.

Cardiovascular

Intended Uses: This FOXL2 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human FOXL2. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: FOXL2 ELISA kit applies the competitive enzyme immunoassay technique utilizing a polyclonal anti-FOXL2 antibody and an FOXL2-HRP conjugate. The assay sample and buffer are incubated together with FOXL2-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 FOXL2 concentration since FOXL2 from samples and FOXL2-HRP conjugate compete for the anti-FOXL2 antibody binding site. Since the number of sites is limited, as more sites are occupied by FOXL2 from the sample, fewer sites are left to bind FOXL2-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The FOXL2 concentration in each sample is interpolated from this standard curve.

11761629

NP_068657.1

NM_021871.2

69,757 Da

Amyloids Pathway (366238); Blood Clotting Cascade Pathway (198840); Common Pathway (106060); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); Disease Pathway (530764); Extracellular Matrix Organization Pathway (576262); Formation Of Fibrin Clot (Clotting Cascade) Pathway (106057); GRB2:SOS Provides Linkage To MAPK Signaling For Integrins Pathway (106055); Hemostasis Pathway (106028)

The protein encoded by this gene is the alpha component of fibrinogen, a blood-borne glycoprotein comprised of three pairs of nonidentical polypeptide chains. Following vascular injury, fibrinogen is cleaved by thrombin to form fibrin which is the most abundant component of blood clots. In addition, various cleavage products of fibrinogen and fibrin regulate cell adhesion and spreading, display vasoconstrictor and chemotactic activities, and are mitogens for several cell types. Mutations in this gene lead to several disorders, including dysfibrinogenemia, hypofibrinogenemia, afibrinogenemia and renal amyloidosis. Alternative splicing results in two isoforms which vary in the carboxy-terminus. [provided by RefSeq, Jul 2008]

FGA: Fibrinogen has a double function: yielding monomers that polymerize into fibrin and acting as a cofactor in platelet aggregation. Defects in FGA are a cause of congenital afibrinogenemia (CAFBN). This is a rare autosomal recessive disorder characterized by bleeding that varies from mild to severe and by complete absence or extremely low levels of plasma and platelet fibrinogen. The majority of cases of afibrinogenemia are due to truncating mutations. Variations in position Arg-35 (the site of cleavage of fibrinopeptide a by thrombin) leads to alpha- dysfibrinogenemias. Defects in FGA are a cause of amyloidosis type 8 (AMYL8); also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 4q28. Cellular Component: extracellular space; cell surface; fibrinogen complex; plasma membrane; extracellular region; cell cortex; vesicle; external side of plasma membrane. Molecular Function: protein binding, bridging; protein binding; cell adhesion molecule binding; structural molecule activity; receptor binding. Biological Process: protein polymerization; platelet activation; extracellular matrix organization and biogenesis; positive regulation of heterotypic cell-cell adhesion; platelet degranulation; cellular protein complex assembly; positive regulation of protein secretion; cell-matrix adhesion; positive regulation of vasoconstriction; innate immune response; signal transduction; response to calcium ion; blood coagulation; positive regulation of exocytosis. Disease: Amyloidosis, Familial Visceral; Afibrinogenemia, Congenital; Dysfibrinogenemia, Congenital

48-Strip-Wells

440 USD

96-Strip-Wells

640

5x96-Strip-Wells

2895

10x96-Strip-Wells

5415