Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

ADAM9 Mouse, Unlabeled, Clone: 15, BD

Mouse Monoclonal Antibody

Manufacturer:  BD Biosciences 610750

Catalog No. BDB610750

This item has been discontinued by the manufacturer and is no longer available. Please call customer service for assistance: 1-800-766-7000.



MDC9 (metalloprotease/disintegrin/cysteine-rich protein 9) belongs to a family of cellular disintegrins known as ADAM (A Disintegrin And Metalloprotease domain). The ADAM proteins are involved in cell-cell and cell-matrix adhesion and, possibly, the degradation of the extracellular matrix. All members possess: 1) a prodomain; 2) a metalloprotease-, disintegrin-, and EGF-like region; 3) a cysteine-rich region; 4) a transmembrane domain; and 5) a cytoplasmic domain. In addition to these regions, MDC9 contains two cytoplasmic proline-rich sequences that may bind to the SH3 domains of cytoskeletal or signaling proteins. MDC9 also contains a membrane-bound metalloprotease and disintegrin domain, suggesting multifunctional activity. Immunofluorescence staining demonstrated that MDC9 is located at the plasma membrane. MDC9 human and mouse protein sequence share 82% identity and are ubiquitously expressed.

Immunofluorescence, Immunoprecipitation, Western Blotting



Human, Murine, Rat
Immunofluorescence, Western Blot
Affinity Purified
Human MDC9 aa. 86-227
Cell Biology
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit