Human ADAMTS1(A disintegrin and metalloproteinase with thrombospondin motifs 1) ELISA Kit

Background

ADAMTS1 (ADAM metallopeptidase with thrombospondin type 1 motif 1) is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. ADAMTS1 contains several distinct domains, including a signal peptide, a propeptide region, a metalloproteinase domain, a disintegrin-like domain, a thrombospondin type 1 (TSP1) motif, and a spacer region. ADAMTS1 is expressed in various tissues during development and in adulthood. It is found in tissues such as the heart, lungs, kidneys, blood vessels, and skeletal tissues. Its expression is often regulated in response to physiological cues and pathological conditions. ADAMTS1 plays a crucial role in ECM remodeling by cleaving ECM proteins such as aggrecan, versican, and brevican. These proteolytic activities are essential for tissue development, maintenance, and repair. ADAMTS1 is also involved in angiogenesis, It can promote or inhibit angiogenesis depending on the context and interacting partners. ADAMTS1 influences endothelial cell migration, proliferation, and tube formation during blood vessel development and remodeling.ADAMTS1 has been implicated in modulating inflammation and immune responses. It can regulate the activity of cytokines, chemokines, and growth factors, influencing immune cell recruitment, activation, and function. ADAMTS1 expression is dysregulated in various cancers, including breast cancer, ovarian cancer, and prostate cancer. Its roles in ECM remodeling, angiogenesis, and inflammation contribute to tumor progression, invasion, metastasis, and angiogenesis.Dysregulation of ADAMTS1 activity has been associated with musculoskeletal disorders such as osteoarthritis and intervertebral disc degeneration. In these conditions, ADAMTS1 contributes to the degradation of ECM components within cartilage and intervertebral discs, leading to tissue degeneration and joint dysfunction. ADAMTS1 expression levels correlate with cancer progression and poor prognosis in several types of cancer. It promotes tumor growth, invasion, and metastasis by facilitating ECM remodeling, angiogenesis, and inflammation within the tumor microenvironment.