|Application ||WB, IF|
|Calculated MW||55928 Da|
|Other Names||Fibrinogen beta chain, Fibrinopeptide B, Fibrinogen beta chain, FGB|
|Target/Specificity||A synthetic peptide corresponding to residues near the C-terminus of in human Fibrinogen beta chain was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Fibrinogen beta Antibody chain is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Cleaved by the protease thrombin to yield monomers which, together with fibrinogen alpha (FGA) and fibrinogen gamma (FGG), polymerize to form an insoluble fibrin matrix. Fibrin has a major function in hemostasis as one of the primary components of blood clots. In addition, functions during the early stages of wound repair to stabilize the lesion and guide cell migration during re-epithelialization. Was originally thought to be essential for platelet aggregation, based on in vitro studies using anticoagulated blood. However subsequent studies have shown that it is not absolutely required for thrombus formation in vivo. Enhances expression of SELP in activated platelets. Maternal fibrinogen is essential for successful pregnancy. Fibrin deposition is also associated with infection, where it protects against IFNG-mediated hemorrhage. May also facilitate the antibacterial immune response via both innate and T-cell mediated pathways.|
|Tissue Location||Detected in blood plasma (at protein level).|
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Provided below are standard protocols that you may find useful for product applications.
Fibrinogen beta chain yields monomers that polymerize into fibrin and acting as a cofactor in platelet aggregation. 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. Defects in FGB are a cause of thrombophilia. Defects in FGB are a cause of congenital afibrinogenemia. This rare autosomal recessive disorder is characterized by bleeding that varies from mild to severe and by complete absence or extremely low levels of plasma and platelet fibrinogen (1).
1. The UniProt Consortium, The Universal Protein source (UniProt), Nucleic Acids Res. 36:D190-D195 (2008)
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