Cerebral ischemia initiates a cascade of cytotoxic molecules responsible for the death of neural cells as well as the damage of the blood brain barrier (BBB) at the injury site (Doyle et al., 2008). In more than one decade, ischemia-associated neuronal injury has been a topic of intensive investigation, which leads to the identification of several mechanisms accounting for cerebral ischemia injury, such as apoptosis, oxidative damage, inflammatory injury, mitochondrial dysfunction and dysregulated protein degradation (Caldeira et al., 2014; Kalogeris et al., 2014; Palencia et al., 2015). The ubiquitin-proteasome system (UPS) is the major intracellular machinery for protein degradation, which is responsible for maintaining cellular homeostasis by regulating several important processes such as cell death, cell division, cell signal transduction, cell cycle progression and transmembrane transport (Wagner et al., 2011). Emerging evidence has suggested a role of suppressed proteasome activity in contributing to neuronal death in ischemic brain injury. However, little is known about the UPS components whose activities are suppressed under brain ischemia conditions (Caldeira et al., 2014).