ArticleThe American journal of pathology2011
Mitochondrial apoptosis-induced channel (MAC) function triggers a Bax/Bak-dependent bystander effect.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Unlocking the potential of tumor-targeting peptides in precision oncology.Oncology research · 2025Review
- Quantitative systems pharmacology modeling of tumor heterogeneity in response to BH3-mimetics using virtual tumors calibrated with cell viability assays.CPT: pharmacometrics & systems pharmacology · 2024Article
- The Diversity of the Mitochondrial Outer Membrane Protein Import Channels: Emerging Targets for Modulation.Molecules (Basel, Switzerland) · 2021Review
- Fetal liver mesenchymal stem cells restore ovarian function in premature ovarian insufficiency by targeting MT1.Stem cell research & therapy · 2019Article
- 14,15-EET Suppresses Neuronal Apoptosis in Ischemia-Reperfusion Through the Mitochondrial Pathway.Neurochemical research · 2017Article
- MAC inhibitors antagonize the pro-apoptotic effects of tBid and disassemble Bax / Bak oligomers.Journal of bioenergetics and biomembranes · 2017Article
- Voltage-Dependent Anion Channel 1 As an Emerging Drug Target for Novel Anti-Cancer Therapeutics.Frontiers in oncology · 2017Review
- The effect of aging on mitochondrial and cytosolic hepatic intrinsic death pathway and apoptosis associated proteins in Fischer 344 rats.Experimental gerontology · 2015Article
- Temporal effect of in vivo tendon fatigue loading on the apoptotic response explained in the context of number of fatigue loading cycles and initial damage parameters.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2014Article
- Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs).Cells · 2013Article
- Transfer of IP₃ through gap junctions is critical, but not sufficient, for the spread of apoptosis.Cell death and differentiation · 2012Article
- The therapeutic potential of mitochondrial channels in cancer, ischemia-reperfusion injury, and neurodegeneration.Mitochondrion · 2012Review
- The 65th Symposium of the Society for General Physiologists: energizing research in mitochondrial physiology and medicine.The Journal of general physiology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Collateral spread of apoptosis to nearby cells is referred to as the bystander effect, a process that is integral to tissue homeostasis and a challenge to anticancer therapies. In many systems, apoptosis relies on permeabilization of the mitochondrial outer membrane to factors such as cytochrome c and Smac/DIABLO. This permeabilization occurs via formation of a mitochondrial apoptosis-induced channel (MAC) and was mimicked here by single-cell microinjection of cytochrome c into Xenopus laevis embryos. Waves of apoptosis were observed in vivo from the injected to the neighboring cells. This finding indicates that a death signal generated downstream of cytochrome c release diffused to neighboring cells and ultimately killed the animals. The role of MAC in bystander effects was then assessed in mouse embryonic fibroblasts that did or did not express its main components, Bax and/or Bak. Exogenous expression of green fluorescent protein-Bax triggered permeabilization of the outer membrane and apoptosis in these cells. Time-lapse videos showed that neighboring cells also underwent apoptosis, but expression of Bax and/or Bak was essential to this effect, because no bystanders were observed in cells lacking both of these MAC components. These results may guide development of novel therapeutic strategies to selectively eliminate tumors or minimize the size of tissue injury in degenerative or traumatic cell death.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.