miR-126 in human cancers: clinical roles and current perspectives.
Gold Coast, Australia. In Exp Mol Pathol, 2014
In addition, miR-126 can alter a multitude of cellular mechanisms in cancer pathogenesis via suppressing gene translation of numerous validated targets such as PI3K, KRAS, EGFL7, CRK, ADAM9, HOXA9, IRS-1, SOX-2, SLC7A5 and VEGF.
α-Cleavage of cellular prion protein.
Cleveland, United States. In Prion, 2012
The effect of ADAM10, ADAM17, and ADAM9 on N1 secretion clearly indicates their involvement in the α-cleavage of PrP (C) , but there has been no report of direct PrP (C) α-cleavage activity with any of the three ADAMs in a purified protein form.
Genomic and transcriptional aberrations linked to breast cancer pathophysiologies.
San Francisco, United States. In Cancer Cell, 2006
Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable.
ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23.
New York City, United States. In Nat Immunol, 2006
Here we used loss-of-function and gain-of-function experiments with cells lacking or overexpressing candidate CD23-releasing enzymes (ADAM8, ADAM9, ADAM10, ADAM12, ADAM15, ADAM17, ADAM19 and ADAM33), ADAM-knockout mice and a selective inhibitor to identify ADAM10 as the main CD23-releasing enzyme in vivo.