Product Pathways - Cytoskeletal Signaling
ADAM9 (D64B5) Rabbit mAb #4151
|4151S||100 µl (10 western blots)||---||In Stock||---|
|4151||carrier free and custom formulation / quantity||email request|
|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||100-115, 75-80||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Specificity / Sensitivity
ADAM9 (D64B5) Rabbit mAb detects endogenous levels of total ADAM9 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human ADAM9.
The ADAM (A Disintegrin and A Metalloprotease) family of multidomain membrane proteins influences cell signaling and adhesion by shedding cell surface proteins such as cytokines and growth factors, by influencing cell adhesion to the extracellular matrix (ECM), and by directly remodeling the ECM. Conserved domains in ADAM family members include a prodomain, a zinc-dependent metalloprotease domain, a disintegrin domain, a cysteine-rich domain, an EGF-like sequence, and a short cytoplasmic tail (1,2).
The prodomain is thought to aid in protein folding. Disintegrin and cysteine-rich domains mediate adhesion, at least in part, through binding to integrins. Phosphorylation of the cytoplasmic tail as well as its interaction with other signaling proteins may influence intra- and extracellular signaling (1). ADAM9 is widely distributed and has been shown to affect migration in skin keratinocytes (3,4). Research studies have shown that ADAM9 is overexpressed in prostate cancer (5), pancreatic cancer (6), gastric cancer (7), and has been linked to invasion and metastasis in small cell lung cancer (8). Research has also shown that an alternatively spliced short (50 kDa) form of ADAM9 containing protease activity is involved in tumor cell invasion (9).
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This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.
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