A proteolytic system that compensates for loss of proteasome function

Inactivation of the proteasome in mammalian cells by covalent inhibitors has been shown to permit the outgrowth of inhibitor-resistant cells. The growth of these cells seems to be maintained by the induction of other proteolytic systems that balance out the loss of proteasomal activity. The reduced proteasomal activity in adapted cells was found to be caused by covalent modification of beta-subunits by NIPL3-VS, an amino-terminally modified tri-leucine vinyl sulphone.