作者: Vladimir Marshansky , Xin Wang , Richard Bertrand , Hongyu Luo , William Duguid
DOI: 10.4049/JIMMUNOL.166.5.3130
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摘要: The mechanism underlying apoptosis induced by proteasome inhibition in leukemic Jurkat and Namalwa cells was investigated this study. inhibitor lactacystin differentially regulated the protein levels of proapoptotic Bcl-2 family members Bik accumulated at mitochondria. overexpression sufficed to induce these cells. Detailed examination along respiration chain showed that compromised a step after complex III, exogenous cytochrome c could overcome compromise. Probably as result, succinate-stimulated generation mitochondrial membrane potential significantly diminished. Bcl-x(L) interacted with cells, prevented leakage out mitochondria, corrected defect, protected from apoptosis. These results show proteasomes can modulate lymphocytes affecting half-life members, being one them.