FIBRINOGEN

ArtNr	11-783-79539
Hersteller	GENWAY
Menge	25 mg
Kategorie	Peptides & Proteins Recombinant Proteins Cell Biology Cell Movement Cell Adhesion ELISA
Typ	Proteins
Applikationen	ELISA
Specific against	other
ECLASS 10.1	32160409
ECLASS 11.0	32160409
UNSPSC	12352202
Alias	GWB-D76AF7
Similar products	11-783-79539
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Genway ID:	GWB-D76AF7
Specificity:	FIBRINOGEN
Preparation:	Protein purified by precipitation
Buffer Solution:	Contains sodium citrate & sodium chloride
Function:	Fibrinogen has a double
Function:	yielding monomers that polymerize into fibrin and acting as a cofactor in platelet aggregation.
Subunit:	Heterohexamer; disulfide linked. Contains 2 sets of 3 non-identical chains (alpha beta and gamma). The 2 heterotrimers are in head to head conformation with the N-termini in a small central domain.
Subcellular Location:	Secreted.
Domain:	A 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.
Ptm:	The alpha chain is not glycosylated.
Ptm:	Forms F13A-mediated cross-links between a glutamine and the epsilon-amino group of a lysine residue forming fibronectin-fibrinogen heteropolymers.
Ptm:	About one-third of the alpha chains in the molecules in blood were found to be phosphorylated.
Ptm:	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.
Disease:	Defects in FGA are a cause of congenital afibrinogenemia [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. The majority of cases of afibrinogenemia are due to truncating mutations.
Disease:	Variations in position Arg-35 (the site of cleavage of fibrinopeptide a by thrombin) leads to alpha-dysfibrinogenemias.
Disease:	Defects in FGA are a cause of amyloidois 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.
Similarity:	Contains 1 fibrinogen C-terminal domain.

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Menge: 25 mg

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