CRMP-2 peptide mediated decrease of high and low voltage-activated calcium channels attenuation of nociceptor excitability and anti-nociception in a model of AIDS therapy-induced painful peripheral neuropathy

摘要

BackgroundThe ubiquity of protein-protein interactions in biological signaling offers ample opportunities for therapeutic intervention. We previously identified a peptide, designated CBD3, that suppressed inflammatory and neuropathic behavioral hypersensitivity in rodents by inhibiting the ability of collapsin response mediator protein 2 (CRMP-2) to bind to N-type voltage-activated calcium channels (CaV2.2) [Brittain et al. Nature Medicine 17:822–829 (2011)].