[RANKL/RANK signaling-inhibitor].
Osteoclast differentiation requires the interaction of RANK (receptor activator of NF kappaB) and RANK ligand, conserved member of the TNF (tumor necrosis factor) receptor and TNF families, respectively. We tested the ability of a peptide mimic (WP9QY) of a critical contact site on the TNF receptor to inhibit RANK ligand induced osteoclastogenesis and discuss whether it could work as both TNF-alpha and RANKL antagonists, and the possibility of the drug development using the techniques in the structural biology.
Aoki
Kazuhiro
K
Department of Hard Tissue Engineering (Pharmacology), Tokyo Medical and Dental University, Graduate School.
Ohya
Keiichi
K
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D001862:Bone Resorption / Q000188:drug therapy; D002352:Carrier Proteins / Q000502:physiology*; D008562:Membrane Glycoproteins / Q000502:physiology*; D051379:Mice; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse; D014409:Tumor Necrosis Factor-alpha