Mouse A disintegrin and metalloproteinase with thrombospondin motifs 12 (ADAMTS12) ELISA Kit

Background

ADAMTS12 (ADAM metallopeptidase with thrombospondin type 1 motif 12) is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. ADAMTS12 contains several domains typical of the ADAMTS family, including a signal peptide, a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and multiple thrombospondin type 1 (TSP1) motifs. ADAMTS12 is expressed in various tissues during development and in adulthood. It is found in tissues such as the heart, lungs, kidneys, and skeletal tissues. ADAMTS12 plays a significant role in ECM remodeling by cleaving ECM proteins such as aggrecan, versican, and brevican ADAMTS12 is implicated in various aspects of tissue development, particularly in skeletal development. It is involved in processes such as chondrogenesis and osteogenesis , where it regulates ECM composition and structure. ADAMTS12 has been associated with inflammation and immune responses. It can regulate the activity of cytokines, chemokines, and growth factors, influencing immune cell recruitment, activation, and function. ADAMTS12 expression or activity may contribute to inflammatory disorders. ADAMTS12 expression levels have been found to be dysregulated in various cancers, including breast cancer, ovarian cancer, and colorectal cancer. Its roles in ECM remodeling and tissue development suggest potential contributions to tumor progression, invasion, and metastasis.Dysregulation of ADAMTS12 activity has been associated with musculoskeletal disorders such as osteoarthritis and intervertebral disc degeneration. In these conditions, ADAMTS12 contributes to the degradation of ECM components within cartilage and intervertebral discs, leading to tissue degeneration and joint dysfunction. ADAMTS12 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 and inflammation within the tumor microenvironment.