Baculovirus P35 Inhibits the Glucocorticoid-mediated Pathway of Cell Death

摘要: Recent evidence suggests that members of the interleukin-1-β-converting enzyme (ICE)/Ced-3 family are key mediators mammalian apoptosis. The known ICE/Ced-3 cysteine protease synthesized as proenzymes and require proteolytic processing to produce active, heterodimeric enzymes. baculovirus protein P35 has recently been shown inhibit several family. importance proteases in programmed cell death prompted us investigate role apoptotic mediator, CPP32, glucocorticoid-mediated pathway. Glucocorticoids induce growth inhibition apoptosis sensitive leukemic lines, immature thymocytes, eosinophils. In this report, we demonstrate enzymatic cleavage proCPP32 its active subunits cells undergoing glucocorticoid-induced death. Concurrently, cells, PARP, a 116-kilodalton (kDa) human poly(ADP-ribose) polymerase, is proteolytically cleaved signature 85-kDa fragment. PARP (the nuclear DNA repair be association with apoptosis) catalyzed by Importantly, stable transfection antiapoptotic inhibits death, proCPP32, 116-kDa PARP. We conclude activation CPP32 critical event pathway inhibited at or upstream P35. These data occurs during show process blocked expression P35, supporting for ICE/Ced-3-like