Human ADAM Metallopeptidase With Thrombospondin Type 1 Motif 13 / vWFCP (ADAMTS13) CLIA Kit

Product specifications

CLIA Kits

ADAM Metallopeptidase With Thrombospondin Type 1 Motif 13 / vWFCP (ADAMTS13)

Human

Chemiluminescent

Quantitative

Sandwich

0.312 ng/ml - 20 ng/ml

< 0.127 ng/ml

Optimal dilutions/concentrations should be determined by the end user.

96 tests

5 × 96 tests

10 × 96 tests

Lyophilized

CLIA

Serum, plasma and other biological fluids.

Shipped within 5-20 working days.

 Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual.

No

VWF-CP,VWFCP,Von Willebrand Factor-Cleaving Protease,ADAM-TS13,ADAMTS-13,A Disintegrin And Metalloproteinase With Thrombospondin Motifs 13

CLIA Kits ADAMTS13

RUO

The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request.   This product is for research use only.   The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments.   Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.

Descripción

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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