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Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul 151-742, KoreaReceived January 14, 2013, Accepted February 13, 2013The proteasome, which is highly evolutionarily conserved, is responsible for the degradation of most short-lived proteins in cells. Small-molecule inhibitors targeting the proteasome's degradative activity have beenextensively developed as lead compounds for various human diseases. An exemplified molecule is bortezomib,which was approved by FDA in 2003 for the treatment of multiple myeloma. Here, using transiently and stablyexpressed N-end rule model substrates in mammalian cells, we evaluated and identified that salinosporamideA and salinosporamide B effectively inhibited the proteasomal degradation. Considering that a variety ofproteasome substrates are implicated in the pathogenesis of many diseases, they have the potential to beclinically applicable as therapeutic agents. Key Words : Degradation, Ubiquitin, Proteasome, Inhibitor, N-end ruleIntroductionMost intracellular protein degradation in cells are mediatedby the ubiquitin-proteasome system (UPS), where proteinsare modified with multiple ubiquitin (Ub) moieties anddegraded by proteasomes.

Salinosporamides A and B Inhibit Proteasome Activity and Delay the Degradation of N-end Rule Model Substrates