Key features and details
- FITC Rabbit polyclonal to Fibrinogen
- Suitable for: IHC-P
- Reacts with: Human
- Conjugation: FITC. Ex: 493nm, Em: 528nm
- Isotype: IgG
Product nameFITC Anti-Fibrinogen antibody
See all Fibrinogen primary antibodies
DescriptionFITC Rabbit polyclonal to Fibrinogen
ConjugationFITC. Ex: 493nm, Em: 528nm
SpecificityThis antibody reacts with native fibrinogen as well as with the fibrinogen fragments D, E, X and Y.
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Fibrinogen isolated from human plasma.
Fluorescein isothiocyanate (FITC) isomer 1.
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Storage instructionsShipped at 4°C. Store at +4°C.
Storage bufferPreservative: 0.05% Sodium azide
Constituent: 1% BSA
Concentration information loading...
Purification notesTraces of contaminating antibodies have been removed by solid phase absorption with human plasma proteins.
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Our Abpromise guarantee covers the use of ab4217 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration.
Use at an assay dependent concentration.
FunctionFibrinogen has a double function: yielding monomers that polymerize into fibrin and acting as a cofactor in platelet aggregation.
Involvement in diseaseDefects in FGA are a cause of congenital afibrinogenemia (CAFBN) [MIM:202400]. 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. Note=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) [MIM:105200]; 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.
Sequence similaritiesContains 1 fibrinogen C-terminal domain.
DomainA long coiled coil structure formed by 3 polypeptide chains connects the central nodule to the C-terminal domains (distal nodules). The long C-terminal ends of the alpha chains fold back, contributing a fourth strand to the coiled coil structure.
modificationsThe alpha chain is not glycosylated.
Forms F13A-mediated cross-links between a glutamine and the epsilon-amino group of a lysine residue, forming fibronectin-fibrinogen heteropolymers.
About one-third of the alpha chains in the molecules in blood were found to be phosphorylated.
Conversion of fibrinogen to fibrin is triggered by thrombin, which cleaves fibrinopeptides A and B from alpha and beta chains, and thus exposes the N-terminal polymerization sites responsible for the formation of the soft clot. The soft clot is converted into the hard clot by factor XIIIA which catalyzes the epsilon-(gamma-glutamyl)lysine cross-linking between gamma chains (stronger) and between alpha chains (weaker) of different monomers.
Phosphorylation sites are present in the extracellular medium.
- Information by UniProt
- FGA antibody
- FGB antibody
- FGG antibody
ab4217 has been referenced in 1 publication.
- Jiménez JM et al. Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression. J R Soc Interface 11:20131079 (2014). PubMed: 24554575