ELISA/assay

Human fibrinogen total antigen assay ELISA Kit

MBS135523

1 Kit

365 USD

ELISA Kit

Human fibrinogen total antigen assay ELISA Kit

[fibrinogen total antigen assay]

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

[FGA]

[FGA; FGA; Fib2]

FIBA_HUMAN

General

866

Pooled normal plasma from mouse, rat, pig, rabbit, sheep, canine, and guinea pig were assayed for cross-reactivity. No significant cross-reactivity was observed.

Complete Kit

Store at 4 degree C. Shelf Life: 12 months from manufacture, see label for expiration date

Typical Testing Data/Standard Curve (for reference only)

Samples: Human Plasma, Serum, Urine, Milk, Saliva And Cell Culture Samples.

Intra-assay Precision: Three samples of known concentration were tested twenty times on one plate to assess intra-assay precision. Inter-assay Precision: Three samples of known concentration were tested in ten independent assays to assess inter-assay precision.

Fibrinogen; Fibrinogen ELISA Kits

Intended Uses: This human complement component 3 antigen assay is intended for the quantitative determination of total complement component 3 antigen in human plasma, serum, urine, milk, saliva and cell culture samples. For research use only. Principle of the Assay: Human C3 will bind to the capture antibody coated on the microtiter plate. After appropriate washing steps, biotin labeled anti-human C3 primary antibody binds to the captured protein. Excess primary antibody is washed away and bound antibody is reacted with peroxidase conjugated streptavidin. Following an additional washing step, TMB substrate is used for color development at 450nm. A standard calibration curve is prepared along with the samples to be measured using dilutions of human C3. Color development is proportional to the concentration of total C3 in the samples!!Background/Introduction: Complement Component 3 (C3), the most abundant serum complement component, is a disulfide-linked 185kDa 1,637 amino acid glycoprotein which supports the classical, alternative, and lectin pathways of complement activation [1]. C3 is proteolytically activated by C3-convertase to the anaphylatoxin C3a and the opsonizing agent C3b [2]. Serum concentrations of C3 are increased during acute and chronic inflammation such as rheumatoid arthritis, and are decreased due to increased consumption or autoimmune disorders such as systemic lupus erythematosus [3].

4503689

NP_000499.1

NM_000508.3

P02671

94,973 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); Formation Of Fibrin Clot (Clotting Cascade) Pathway (106057); GRB2:SOS Provides Linkage To MAPK Signaling For Intergrins Pathway (106055); Hemostasis Pathway (106028); Integrin AlphaIIb Beta3 Signaling Pathway (106054)

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; cell-matrix adhesion; signal transduction; cellular protein complex assembly; platelet degranulation; positive regulation of protein secretion; positive regulation of vasoconstriction; innate immune response; blood coagulation; response to calcium ion; positive regulation of exocytosis. Disease: Amyloidosis, Familial Visceral; Afibrinogenemia, Congenital; Dysfibrinogenemia, Congenital

1 Kit

365 USD

5 Kits

1375