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Zinc metalloproteinase-disintegrin-like jararhagin

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Snake venom zinc metalloproteinase-disintegrin-like jararhagin: causes hemorrhage. This is the result of the degradation of sub-endothelial matrix proteins leading to the disruption of the blood vessel endothelium, with accompanying disturbances in platelet function. It is able to degrade von Willebrand factor (vWF) and it hydrolyzes the alpha-chain of fibrinogen (FGA) while leaving the beta and gamma chains unaffected. It inhibits collagen-induced platelet aggregation through the binding to alpha-2/beta-1 integrin (ITGA2/ITGB1) (collagen receptor), and it cleaves the beta-1 subunit of the same integrin, inhibiting platelet interaction and ultimately causing impairment of signal transduction. It has inability to be affected by the plasma inhibitor alpha(2)-macroglobulin. In fibroblasts, it functions as a collagen-mimetic substrate and, in endothelial cells, it causes apoptosis and indirectly inhibits cell proliferation by release of angiostatin-like compounds. It induces a strong pro-inflammatory response characterized by intense leukocyte accumulation and release of cytokines at the site of the injection. Although hemorrhage and edema are a response to the direct effect of this toxin, jararhagin-induced inflammation and necrosis are dependent on macrophages and key pro-inflammatory cytokines or their receptors. It also possesses anti-tumorgenic properties.; Disintegrin jararhagin-C: the monomeric form inhibits collagen- and ADP-induced platelet aggregation, but has no effect on glycoprotein Ib-IX-dependent (GP1BA/GP5/GP9) platelet agglutination. Locally activates the early events of an acute inflammatory response as leukocyte rolling and pro-inflammatory cytokine release.; Disintegrin jararhagin-C: the dimeric form jaracetin may be a dimeric form of jararhagin-C. It binds to von Willebrand factor (VWF) and induces its interaction with GPIbalpha (GP1BA) (via the vWF A1 domain), resulting in platelet aggregation. Also binds the alpha-2 subunit of the alpha-2/beta-1 (ITGA2/ITGB1) integrin. It potently induces platelet aggregation in citrated platelet-rich plasma.

Below are the list of possible Zinc metalloproteinase-disintegrin-like jararhagin products. If you cannot find the target and/or product is not available in our catalog, please click here to contact us and request the product or submit your request for custom elisa kit production, custom recombinant protein production or custom antibody production. Custom ELISA Kits, Recombinant Proteins and Antibodies can be designed, manufactured and produced according to the researcher's specifications.
 

Zinc metalloproteinase-disintegrin-like jararhagin

 Zinc metalloproteinase-disintegrin-like jararhagin ELISA Kit
 Zinc metalloproteinase-disintegrin-like jararhagin Recombinant
 Zinc metalloproteinase-disintegrin-like jararhagin Antibody
Also known as Zinc metalloproteinase-disintegrin-like jararhagin (HF2-proteinase) (JG) (Jararafibrase I) (JF I) (Snake venom metalloproteinase) (SVMP).
Snake venom zinc metalloproteinase-disintegri
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n-like jararhagin: causes hemorrhage. This is the result of the degradation of sub-endothelial matrix proteins leading to the disruption of the blood vessel endothelium, with accompanying disturbances in platelet function. It is able to degrade von Willebrand factor (vWF) and it hydrolyzes the alpha-chain of fibrinogen (FGA) while leaving the beta and gamma chains unaffected. It inhibits collagen-induced platelet aggregation through the binding to alpha-2/beta-1 integrin (ITGA2/ITGB1) (collagen receptor), and it cleaves the beta-1 subunit of the same integrin, inhibiting platelet interaction and ultimately causing impairment of signal transduction. It has inability to be affected by the plasma inhibitor alpha(2)-macroglobulin. In fibroblasts, it functions as a collagen-mimetic substrate and, in endothelial cells, it causes apoptosis and indirectly inhibits cell proliferation by release of angiostatin-like compounds. It induces a strong pro-inflammatory response characterized by intense leukocyte accumulation and release of cytokines at the site of the injection. Although hemorrhage and edema are a response to the direct effect of this toxin, jararhagin-induced inflammation and necrosis are dependent on macrophages and key pro-inflammatory cytokines or their receptors. It also possesses anti-tumorgenic properties.
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