ADAM15抗体

ADAM15抗体产品信息

免疫原 :
Recombinant Human ADAM15 protein (Catalog#10517-H08H)
Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
克隆号 :
1B7G8
抗体宿主 :
Mouse IgG1
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 :
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human ADAM15 (rh ADAM15; Catalog#10517-H08H; NP_997074.1; Met 1-Thr 696). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
ADAM15抗体 Background
The adamalysin (ADAM) metalloproteinase disintegrins, also known as metalloprotease/disintegrin/cysteine-rich proteins, are a branch of the metzincin metalloproteinase superfamily that are related to snake venom metalloproteinases and integrin ligands. Human ADAM15 was first named metargidin, and uniquely, it carries an RGD binding motif in a position similar to that in snake venom disintegrins. ADAM15 is widely expressed in various tissues and cells, including human umbilical vein endothelial cells and smooth muscle cells, and its expression can be drived by Vascular endothelial (VE)-cadherin. Overexpression of ADAM15 in NIH3T3 cells appears to enhance cell-cell interactions, as suggested by decreased cell migration, altered cell morphology at the wound edge, decreased monolayer permeability, and increased cell adhesion to monolayers of cells expressing ADAM15 by retroviral transduction. ADAM15 plays a physiological roleas a natural binding partner of integrin αvβ3 thereby loosening tumor cell adhesion to the underlying matrix and regulating tumor cell migration and invasion, and functional interplay between ADAM15 and Src family PTKs may contribute to signaling in hematopoietic cells. Aslo, ADAM15 is believed to interact with integrins αvβ3, α5β1, and α9β1 through its disintegrin domain. ADAM15 has been shown to degrade collagens I and IV and to cleave the inflammatory cytokine CD23, thus influence ECM remodeling within rheumatoid synovial tissues and in atherosclerosis.The high expression levels of ADAM15 correlated with advanced metastatic diseases, and a clear association with clinical parameters was determined.
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