A Disintegrin And Metalloproteinase With Thrombospondin 10 (ADAMTS10) Antibody

Product specifications

Primary Antibodies

A Disintegrin And Metalloproteinase With Thrombospondin 10 (ADAMTS10)

Rabbit

Human

WB: 0.01-2 µg/ml, IHC: 5-20 µg/ml, IF/ICC: 5-20 µg/ml. Optimal dilutions/concentrations should be determined by the end user.

Polyclonal

Unconjugated

Purified by antigen-specific affinity chromatography, followed by Protein A affinity chromatography.

100 µl

200 µl

1 ml

Liquid

WB, IHC, IF/ICC

0.01 M PBS, pH 7.4, containing 0.05% Proclin-300, 50% glycerol.

Shipped within 5-7 working days.

Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.

No

Type 1 Motif 10,A Disintegrin And Metalloproteinase With Thrombospondin Motifs 10,WMS,WMS1,ADAMTS-10,ADAM-TS10

Antibody anti-ADAMTS10

RUO

Descripción

ADAMTS10 (ADAM metallopeptidase with thrombospondin type 1 motif 10) is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. ADAMTS10 contains several domains, including a signal peptide, a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and multiple thrombospondin type 1 (TSP1) motifs. ADAMTS10 plays a crucial role in ECM remodeling by cleaving ECM proteins such as aggrecan, versican, and brevican. ADAMTS10 is implicated in embryonic development, particularly in skeletal development. It is involved in processes such as chondrogenesis and osteogenesis , where it regulates ECM composition and structure. Mutations in the ADAMTS10 gene have been associated with human genetic disorders such as Weill-Marchesani syndrome (WMS) and geleophysic dysplasia (GD). These disorders are characterized by skeletal abnormalities, short stature, and other connective tissue abnormalities. ADAMTS10 gene mutations can also cause GD, another rare connective tissue disorder characterized by short stature, joint contractures, and cardiac abnormalities. Like in WMS, mutations in ADAMTS10 disrupt normal ECM remodeling and tissue development, leading to the characteristic features of GD.ADAMTS10 expression levels have been found to be dysregulated in various cancers, including breast cancer, colon cancer, and gastric cancer. Its roles in ECM remodeling and tissue development suggest potential contributions to tumor progression, invasion, and metastasis

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