The course of etoposide-induced apoptosis in jurkat cells lacking p53 and Bax

Natalie O. Karpinich, Marco Tafani, Timothy Schneider, Matteo A. Russo, John L. Farber

Research output: Contribution to journalArticlepeer-review


Jurkat T-lymphocytes lack p53 and Bax but contain p73 and Bid and are killed by etoposide (ETO). With ETO c-abl is phosphorylated and phosphorylated p73 increased. Translocation of full-length Bid to mitochondria follows, with induction of the mitochondrial permeability transition (MPT) and release of cytochrome c into the cytosol. Pronounced swelling of mitochondria was evident ultrastructurally, and the MPT inhibitor cyclosporin A prevented the release of cytochrome c. Overexpression of Bcl-2 prevented the translocation of Bid, the release of cytochrome c, and cell death. The pan-caspase inhibitor ZVAD-FMK prevented the cell killing, but not the initial release of cytochrome c. An accumulation of tBid occurred at later times in association with Bid degradation. A sequence is proposed that couples DNA damage to Bid translocation via activation of c-abl and p73. Bid translocation induces the MPT, the event that causes release of cytochrome c, activation of caspases, and cell death.

Original languageEnglish
Pages (from-to)55-63
Number of pages9
JournalJournal of Cellular Physiology
Issue number1
Publication statusPublished - Jul 2006

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology


Dive into the research topics of 'The course of etoposide-induced apoptosis in jurkat cells lacking p53 and Bax'. Together they form a unique fingerprint.

Cite this