SignalSilence^® ADAM9 siRNA I inhibits human and monkey ADAM9 expression.

Monkey

SignalSilence^® ADAM9 siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit ADAM9 expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence^® siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis.

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).