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Mouse Monoclonal Fibrinogen gamma antibody [4H9] (STJ98072)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, IF, FC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
Recommended protocols: check protocols
Click or hover above images to see image description for Fibrinogen gamma Monoclonal Antibody.
Check alternative names for the antibodyExpand
FGG antibody, PRO2061 antibody,|FGG antibody|FIBG_HUMAN antibody|Fibrinogen gamma chain antibody|Fibrinogen gamma polypeptide antibody|fibrinogen gamma-b chain antibody|Anti-Fibrinogen gamma chain antibody [5A6] (ab119948)
SCBT cat No: sc-81620|sc-133157|sc-18032|sc-133226|sc-133156|sc-33582|
Fibrinogen gamma Monoclonal Antibody
|Catalogue No.|| |
Fibrinogen gamma Monoclonal Antibody detects endogenous levels of Fibrinogen gamma protein.
Purified recombinant fragment of human Fibrinogen gamma expressed in E Coli
WB, IHC, IF, FC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
Fibrinogen gamma Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
Fibrinogen gamma Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Fibrinogen gamma chain antibody
|Protein names|| |
Fibrinogen gamma chain
|Protein function|| |
Together with fibrinogen alpha (FGA) and fibrinogen beta (FGB), polymerizes to form an insoluble fibrin matrix. 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 via an ITGB3-dependent pathway. 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.
|Protein tissue specificity|| |
Detected in blood plasma (at protein level).
|Involvement in disease|| |
Congenital afibrinogenemia (CAFBN) [MIM:202400]: 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. . Note: The disease is caused by mutations affecting the gene represented in this entry. Patients with congenital fibrinogen abnormalities can manifest different clinical pictures. Some cases are clinically silent, some show a tendency toward bleeding and some show a predisposition for thrombosis with or without bleeding.; Dysfibrinogenemia, congenital (DYSFIBRIN) [MIM:616004]: A disorder characterized by qualitative abnormalities (dysfibrinogenemia) of the circulating fibrinogen. Affected individuals are frequently asymptomatic, but some patients have bleeding diathesis, thromboembolic complications, or both. In some cases, dysfibrinogenemia is associated with low circulating fibrinogen levels (hypodysfibrinogenemia). . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and 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. / Contains 1 fibrinogen C-terminal domain.
|Protein post-translational modifications|| |
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. / Sulfation of C-terminal tyrosines increases affinity for thrombin.
|Protein cellular localization|| |
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St John’s Laboratory Ltd.
|Product type|| |
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