Correction to: Oncogene (2006) 25: 4744–4756. doi:10.1038/sj.onc.1209609 Published online 30 January 2006

Figure 1 of this paper contains a large portion of Figure 4 from an article by Paul S Brookes et al., published in the American Journal of Physiology-Cell-Physiology.

Figure 1
figure 1

The permeability transition pore (PTP) function. During apoptosis, many signals can converge on the mitochondrion to regulate the mitochondrial membrane permeability. In response to calcium (Ca2+), atractyloside, adenine nucleotide depletion, chemotherapeutics and pro-oxidant agents, the membrane permeabilization can result from the opening of PTP as a large unspecific channel and leads to the release of proapoptotic factors into the cytosol. In contrast, many agents (CsA, bongkrekic acid, Mg2+, high ADP/ATP) or conditions (pH<7) promote the closure of the PTP and prevent apoptosis. When available, PDB structure models for PTP members have been inserted.

The authors would like to apologize for not citing this originally.

The following should be added to the figure legend: ‘Adapted with permission from Brookes PS, Yoon Y, Robotham JL, Anders MW, Sheu S-SS. (2004). Calcium, ATP and ROS: a mitochondrial love–hate triangle. Am J Physiol Cell Physiol 287: C817–C833.’

Copyright (2005) National Academy of Sciences, USA.