The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Regulation of the mitochondrial apoptosis-induced channel, MAC, by BCL-2 family proteins
Open accessAbstract
Programmed cell death or apoptosis is central to many physiological processes and pathological conditions such as organogenesis, tissue homeostasis, cancer, and neurodegenerative diseases. Bcl-2 family proteins tightly control this cell death program by regulating the permeabilization of the mitochondrial outer membrane and, hence, the release of cytochrome c and other pro-apoptotic factors. Control of the formation of the mitochondrial apoptosis-induced channel, or MAC, is central to the regulation of apoptosis by Bcl-2 family proteins. MAC is detected early in apoptosis by patch clamping the mitochondrial outer membrane. The focus of this review is on the regulation of MAC activity by Bcl-2 family proteins. The role of MAC as the putative cytochrome c release channel during early apoptosis and insights concerning its molecular composition are also discussed.
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
Danial, N. N., & Korsmeyer, S. J. (2004) · Cell · doi:10.1016/s0092-8674(04)00046-7 · Cited by 4,651
Baines, C. P., Kaiser, R. A., Purcell, N. H., Blair, N. S., Osinska, H., Hambleton, M. A., Brunskill, E. W., Sayen, M. R., Gottlieb, R. A., Dorn, G. W., et al. (2005) · Nature · doi:10.1038/nature03434 · Cited by 2,280
Shimizu, S., Narita, M., Tsujimoto, Y., & Tsujimoto, Y. (1999) · Nature · doi:10.1038/20959 · Cited by 2,178
Nakagawa, T., Shimizu, S., Watanabe, T., Yamaguchi, O., Otsu, K., Yamagata, H., Inohara, H., Kubo, T., & Tsujimoto, Y. (2005) · Nature · doi:10.1038/nature03317 · Cited by 1,635 · cited 1×
“Remarkably, cyclophilin-D deficient cells died normally in response to apoptotic stimuli known to activate both the extrinsic and intrinsic pathways, but showed resistance to necrotic cell death induced by reactive oxygen species and Ca overload [12].”
BackgroundVDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis
Cheng, E. H.-Y., Sheiko, T. V., Fisher, J. K., Craigen, W. J., & Korsmeyer, S. J. (2003) · Science · doi:10.1126/science.1083995 · Cited by 852
Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D
Basso, E., Fante, L., Fowlkes, J., Petronilli, V., Forte, M. A., & Bernardi, P. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.c500089200 · Cited by 808 · cited 1×
“However, it was recently shown that sustained PTP opening is primarily involved in necrosis and ischemia–reperfusion [12–14].”
Background
Cited by
Mechanisms of Acetaminophen-Induced Liver Necrosis
Hinson, J. A., Roberts, D. W., & James, L. P. (2010) · Handbook of Experimental Pharmacology · doi:10.1007/978-3-642-00663-0_12 · Cited by 1,006
VDAC, a multi-functional mitochondrial protein regulating cell life and death
Shoshan-Barmatz, V., De Pinto, V., Zweckstetter, M., Raviv, Z., Keinan, N., & Arbel, N. (2010) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2010.03.002 · Cited by 782
Oxidative stress and disuse muscle atrophy
Powers, S. K., Kavazis, A. N., & McClung, J. M. (2007) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01202.2006 · Cited by 472
Maier, P., Hartmann, L., Wenz, F., & Herskind, C. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17010102 · Cited by 414
O’Rourke, B. (2007) · Annual Review of Physiology · doi:10.1146/annurev.physiol.69.031905.163804 · Cited by 310
Metadata
- Authors
- Dejean, L. M., Martinez-Caballero, S., Manon, S., & Kinnally, K. W.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2006-02
- Volume
- 1762
- Issue
- 2
- Pages
- 191-201
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2097088463
- Cited by
- 200
- References
- 6
- FWCI
- 2.77
- 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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Regulation of the mitochondrial apoptosis-induced channel, MAC, by BCL-2 family proteins. https://app.cochat.ai/papers/10.1016/j.bbadis.2005.07.002
- The paper
- Dejean, L. M., Martinez-Caballero, S., Manon, S., & Kinnally, K. W. (2006). Regulation of the mitochondrial apoptosis-induced channel, MAC, by BCL-2 family proteins. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. https://doi.org/10.1016/j.bbadis.2005.07.002
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.