ArticleCell death & disease2016
cBid, Bax and Bcl-xL exhibit opposite membrane remodeling activities.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
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- Bcl-2 and Bcl-xL in Diabetes: Contributions to Endocrine Pancreas Viability and Function.Biomedicines · 2025Review
- Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling.Chemical science · 2023Article
- Creation of distinctive Bax-lipid complexes at mitochondrial membrane surfaces drives pore formation to initiate apoptosis.Science advances · 2023Article
- Bcl-xL Is Spontaneously Inserted into Preassembled Nanodiscs and Stimulates Bax Insertion in a Cell-Free Protein Synthesis System.Biomolecules · 2023Article
- Visualization of BOK pores independent of BAX and BAK reveals a similar mechanism with differing regulation.Cell death and differentiation · 2023Article
- Domain-specific insight into the recognition of BH3-death motifs by the pro-survival Bcl-2 protein.Biophysical journal · 2022Article
- DRP1 interacts directly with BAX to induce its activation and apoptosis.The EMBO journal · 2022Article
- Artemether attenuates renal tubular injury by targeting mitochondria in adriamycin nephropathy mice.American journal of translational research · 2022Article
- Neutron reflectometry and NMR spectroscopy of full-length Bcl-2 protein reveal its membrane localization and conformation.Communications biology · 2021Article
- Mitochondrial outer membrane permeabilization at the single molecule level.Cellular and molecular life sciences : CMLS · 2021Review
- Action of Akt Pathway on La-Induced Hippocampal Neuron Apoptosis of Rats in the Growth Stage.Neurotoxicity research · 2020Article
- The Incomplete Puzzle of the BCL2 Proteins.Cells · 2019Review
- Apoptosis gene reprograming of human peripheral blood mononuclear cells induced by radioiodine-131 (The Indian journal of medical research · 2019Article
- Topology of active, membrane-embedded Bax in the context of a toroidal pore.Cell death and differentiation · 2018Article
- Bcl-2 proteins: Unraveling the details of a complex and dynamic network.Molecular & cellular oncology · 2018Article
- Role of Mitochondria in Methamphetamine-Induced Dopaminergic Neurotoxicity: Involvement in Oxidative Stress, Neuroinflammation, and Pro-apoptosis-A Review.Neurochemical research · 2018Review
- Pore formation by dimeric Bak and Bax: an unusual pore?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization.Biophysical reviews · 2017Review
- Quantitative interactome of a membrane Bcl-2 network identifies a hierarchy of complexes for apoptosis regulation.Nature communications · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The proteins of the Bcl-2 family have a crucial role in mitochondrial outer membrane permeabilization during apoptosis and in the regulation of mitochondrial dynamics. Current models consider that Bax forms toroidal pores at mitochondria that are responsible for the release of cytochrome c, whereas Bcl-xL inhibits pore formation. However, how Bcl-2 proteins regulate mitochondrial fission and fusion remains poorly understood. By using a systematic analysis at the single vesicle level, we found that cBid, Bax and Bcl-xL are able to remodel membranes in different ways. cBid and Bax induced a reduction in vesicle size likely related to membrane tethering, budding and fission, besides membrane permeabilization. Moreover, they are preferentially located at highly curved membranes. In contrast, Bcl-xL not only counterbalanced pore formation but also membrane budding and fission. Our findings support a mechanism of action by which cBid and Bax induce or stabilize highly curved membranes including non-lamellar structures. This molecular activity reduces the energy for membrane remodeling, which is a necessary step in toroidal pore formation, as well as membrane fission and fusion, and provides a common mechanism that links the two main functions of Bcl-2 proteins.
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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.