A Disintegrin And Metalloproteinase With Thrombospondin 2 (ADAMTS2), Monoclonal

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

Mouse

500ug/ml (lot specific)

Manufactured in an ISO 9001:2008 and ISO 13485:2003 Certified Laboratory.

Manufactured in a lab with traceable raw materials. Bulk orders can typically be prepared to the customer’s specifications, please inquire.

Small volumes of anti-ADAMTS2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Western Blot (WB), Immunocytochemistry (ICC), Immunohistochemistry (IHC), Immunoprecipitation (IP), ELISA (EIA)

61,756 Da

ADAM metallopeptidase with thrombospondin type 1 motif 2

A disintegrin and metalloproteinase with thrombospondin motifs 2

A disintegrin and metalloproteinase with thrombospondin motifs 2

PCINP; PCPNI; ADAM-TS 2; ADAM-TS2; ADAMTS-2; PC I-NP; pNPI  [Similar Products]

This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. Members of the family share several distinct protein modules, including a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and a thrombospondin type 1 (TS) motif. Individual members of this family differ in the number of C-terminal TS motifs, and some have unique C-terminal domains. The encoded preproprotein is proteolytically processed to generate the mature procollagen N-proteinase. This proteinase excises the N-propeptide of the fibrillar procollagens types I-III and type V. Mutations in this gene cause Ehlers-Danlos syndrome type VIIC, a recessively inherited connective-tissue disorder. Alternative splicing results in multiple transcript variants, at least one of which encodes an isoform that is proteolytically processed. [provided by RefSeq, Feb 2016]

ADAMTS2: Cleaves the propeptides of type I and II collagen prior to fibril assembly. Does not act on type III collagen. May also play a role in development that is independent of its role in collagen biosynthesis. Defects in ADAMTS2 are the cause of Ehlers-Danlos syndrome type 7C (EDS7C). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7C is marked by extremely fragile tissues, hyperextensible skin and easy bruising. Facial skin contains numerous folds, as in the cutis laxa syndrome. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: EC 3.4.24.14; Extracellular matrix; Motility/polarity/chemotaxis; Protease; Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 5q35.3

Cellular Component: extracellular region

Molecular Function: metalloendopeptidase activity; metallopeptidase activity

Disease: Ehlers-danlos Syndrome, Type Vii, Autosomal Recessive

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