Rat ADAMTS13/VWFCP (Von Willebrand Factor Cleaving Protease) ELISA Kit

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name
Rat ADAMTS13/VWFCP (Von Willebrand Factor Cleaving Protease) ELISA Kit
category
ELISA Kits
provider
FineTest
reference
ER1460
tested applications
ELISA
Documents del producto
Instrucciones
Data sheet
Product specifications
Category | ELISA Kits |
Reactivity | Rat |
Detection Method | Colorimetric |
Assay Data | 4 hours |
Assay Type | Sandwich ELISA, Double Antibody |
Test Range | 1.563-100ng/ml |
Sensitivity | 0.938ng/ml |
Size 1 | 96T |
Tested Applications | ELISA |
Sample Type | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
Availability | Shipped within 10-14 working days. |
Storage | 2-8 °C for 12 months |
UniProt ID | D4A0T9 |
Alias | VWF-CP,VWFCP,Von Willebrand Factor-Cleaving Protease,ADAM-TS13,ADAMTS-13,A Disintegrin And Metalloproteinase With Thrombospondin Motifs 13 |
Background | Elisa kits for ADAMTS13 |
Status | RUO |
ADAMTS13 (ADAM metallopeptidase with thrombospondin type 1 motif 13) is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. ADAMTS13 contains multiple domains, including a signal peptide, a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and multiple thrombospondin type 1 (TSP1) motifs. ADAMTS13 is primarily known for its role in cleaving VWF. VWF normally forms long multimeric strands, which are essential for platelet adhesion and aggregation during clot formation. However, excessively large VWF multimers can lead to thrombotic disorders. ADAMTS13 cleaves these large VWF multimers into smaller, less active forms, thereby regulating platelet aggregation and preventing excessive clot formation. Deficiency or dysfunction of ADAMTS13 can result in a rare but severe condition called thrombotic thrombocytopenic purpura (TTP). In TTP, the lack of functional ADAMTS13 leads to the buildup of large VWF multimers, which can cause widespread microvascular thrombosis and thrombocytopenia. ADAMTS13 may also have other physiological functions that are not fully understood. Some studies suggest potential involvement in angiogenesis, inflammation, and tissue remodeling. Autoantibodies inhibit ADAMTS13 activity, while in hereditary TTP, genetic mutations affect the production or function of ADAMTS13. Both conditions lead to the accumulation of large VWF multimers, resulting in microvascular thrombosis and associated complications. ADAMTS13 activity has also been implicated in other thrombotic disorders, such as arterial thrombosis and stroke.
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