The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Mitochondrial permeability transition is a central coordinating event of apoptosis.
Open accessAbstract
In a number of experimental systems, the early stage of the apoptotic process, i.e., the stage that precedes nuclear disintegration, is characterized by the breakdown of the inner mitochondrial transmembrane potential (delta psi m). This delta psi m disruption is mediated by the opening of permeability transition (PT) pores and appears to be critical for the apoptotic cascade, since it is directly regulated by Bcl-2 and since mitochondria induced to undergo PT in vitro become capable of inducing nuclear chromatinolysis in a cell-free system of apoptosis. Here, we addressed the question of which apoptotic events are secondary to mitochondrial PT. We tested the effect of a specific inhibitor of PT, bongkrekic acid (BA), a ligand of the mitochondrial adenine nucleotide translocator, on a prototypic model of apoptosis glucocorticoid-induced thymocyte death. In addition to abolishing the apoptotic delta psi m disruption, BA prevents a number of phenomena linked to apoptosis: depletion of nonoxidized glutathione, generation of reactive oxygen species, translocation of NF kappa B, exposure of phosphatidylserine residues on the outer plasma membrane, cytoplasmic vacuolization, chromatin condensation, and oligonucleosomal DNA fragmentation. BA is also an efficient inhibitor of p53-dependent thymocyte apoptosis induced by DNA damage. These data suggest that a number of apoptotic phenomena are secondary to PT. In addition, we present data indicating that apoptotic delta psi m disruption is secondary to transcriptional events. These data connect the PT control point to the p53- and ICE/ Ced 3-regulated control points of apoptosis and place PT upstream of nuclear and plasma membrane features of PCD.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
p53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Martin, S. J., Reutelingsperger, C. P., McGahon, A. J., Rader, J. A., van Schie, R. C., LaFace, D. M., & Green, D. R. (1995) · The Journal of experimental medicine · doi:10.1084/jem.182.5.1545 · Cited by 2,824
Cited by
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Self-citationTwo CD95 (APO‐1/Fas) signaling pathways
Scaffidi, C., Fulda, S., Srinivasan, A., Friesen, C., Li, F., Tomaselli, K. J., Debatin, K., Krammer, P. H., & Peter, M. E. (1998) · The EMBO Journal · doi:10.1093/emboj/17.6.1675 · Cited by 3,000
The mitochondrial permeability transition pore and its role in cell death
CROMPTON, M. (1999) · Biochemical Journal · doi:10.1042/bj3410233 · Cited by 2,432
Cai, J., & Jones, D. P. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.19.11401 · Cited by 765
Eskes, R., Antonsson, B., Osen-Sand, A., Montessuit, S., Richter, C., Sadoul, R., Mazzei, G., Nichols, A., & Martinou, J.-C. (1998) · The Journal of Cell Biology · doi:10.1083/jcb.143.1.217 · Cited by 651
Madesh, M., & Hajnóczky, G. (2001) · The Journal of Cell Biology · doi:10.1083/jcb.200105057 · Cited by 538
Cadet, J. L., Jayanthi, S., & Deng, X. (2003) · The FASEB Journal · doi:10.1096/fj.03-0073rev · Cited by 286
Costantini, P., Belzacq, A.-S., Vieira, H. L., Larochette, N., de Pablo, M. A., Zamzami, N., Susin, S. A., Brenner, C., & Kroemer, G. (2000) · Oncogene · doi:10.1038/sj.onc.1203299 · Cited by 284
Self-citationBatandier, C., Leverve, X., & Fontaine, E. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m310329200 · Cited by 264
Chen, M., Gan, H., & Remold, H. G. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.176.6.3707 · Cited by 255
Apoptosis of Retinal Ganglion Cells in Glaucoma
Nickells, R. W. (1999) · Survey of Ophthalmology · doi:10.1016/s0039-6257(99)00029-6 · Cited by 232
Bonora, M., & Pinton, P. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00302 · Cited by 208
A Possible Site of Superoxide Generation in the Complex I Segment of Rat Heart Mitochondria
Ohnishi, S. T., Ohnishi, T., Muranaka, S., Fujita, H., Kimura, H., Uemura, K., Yoshida, K.-I., & Utsumi, K. (2005) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-005-4117-y · Cited by 123
Ido, Y., Muto, N., Inada, A., Kohroki, J., Mano, M., Odani, T., Itoh, N., Yamamoto, K., & Tanaka, K. (1999) · Cell Proliferation · doi:10.1046/j.1365-2184.1999.3210063.x · Cited by 52
Rey, C., Mauduit, C., Naureils, O., Benahmed, M., Louisot, P., & Gasnier, F. (2000) · Biochemical Pharmacology · doi:10.1016/s0006-2952(00)00500-1 · Cited by 36
Mouse thymocyte apoptosis and cell loss in response to exercise and antioxidant administration
Quadrilatero, J., & Hoffman-Goetz, L. (2005) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2004.12.004 · Cited by 25
Metadata
- Authors
- Marchetti, P., Castedo, M., Susin, S. A., Zamzami, N., Hirsch, T., Macho, A., Haeffner, A., Hirsch, F., Geuskens, M., & Kroemer, G.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1996-09-01
- Volume
- 184
- Issue
- 3
- Pages
- 1155-1160
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2150476216
- Cited by
- 847
- References
- 3
- FWCI
- 23.63
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
