Human ADAMTS10 (A disintegrin and metalloproteinase with thrombospondin motifs 10) ELISA Kit

Este producto es parte de ADAMTS10 - ADAM metallopeptidase with thrombospondin type 1 motif 10
Human ADAMTS10 (A disintegrin and metalloproteinase with thrombospondin motifs 10) ELISA Kit
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Name
Human ADAMTS10 (A disintegrin and metalloproteinase with thrombospondin motifs 10) ELISA Kit
Category
ELISA Kits
Provider
FineTest
Reference
EH4922
Tested Applications
ELISA

Documentos del producto

Instrucciones
Descargar
Data sheet

Especificaciones del producto

Category
ELISA Kits
Reactivity
Human
Detection Method
Colorimetric
Assay Data
4 hours
Assay Type
Sandwich ELISA, Double Antibody
Test Range
0.156-10ng/ml
Sensitivity
0.094ng/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
Q9H324
Alias
Type 1 Motif 10,A Disintegrin And Metalloproteinase With Thrombospondin Motifs 10,WMS,WMS1,ADAMTS-10,ADAM-TS10
Background
Elisa kits for ADAMTS10
Status
RUO

Background

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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