ADAM15 Antibody ( FITC )

ADAM15 Antibody Datasheet

ADAM15 Antibody Product Information

• Immunogen: Recombinant Human ADAM15 protein (Catalog#10517-H08H)
• Reagents: FITC-conjugated mouse monoclonal antibody
• Clone ID: 05
• Ig Type: Mouse IgG1
• Concentration: 10 μl/Test, 0.1 mg/ml
• Formulation: Aqueous solution containing 0.5% BSA and 0.09% sodium azide
• Preparation: 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) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.

ADAM15 Antibody Usage Guide

• Specificity: Human ADAM15
• Flow Cytometry:
  

  Profile of anti-ADAM15 reactivity on HeLa cells analyzed by flow cytometry.

  Flow cytometry was performed on a BD FACSCalibur flow cytometry system

  Please refer to www.sinobiological.com/Flow-Cytometry-FACS-Protocols-a-750.html for technical protocols.

• Storage: This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
  Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.

ADAM15 Antibody 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.

References

1. Barbara Herren, et al., 2001, Experimental Cell Research, Volume 271, Issue 1: 152-160.
2. Zaruhi Poghosyan, et al., 2002, Journal of Biologica Chemistry, Vol. 277, No. 7: 4999-5007.
3. Claire Ham, et al., 2002, Experimental Cell Research, Volume 279, Issue 2: 239-247.
4. Veronika Beck, et al., 2005, The International Journal of Biochemistry & Cell Biology, Volume 37, Issue 3: 590-603.
5. Jean-Francois Mosnier, et al., 2006, Laboratory Investigation, 86,1064-1073.
6. Barbara Herren, et al., 1997, FASEB J., 11: 173-180.
7. Xi-Ping Zhang, et al., 1998, THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 273, No. 13: 7345-7350.
8. Rainer Kuefer, et al., 2006, Neoplasia. Vol. 8, No. 4: 319-329.