ReviewOncogene2010
Still embedded together binding to membranes regulates Bcl-2 protein interactions.
Review in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed.
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026Review
- Dynamical analysis of a model of BCL-2-dependent cellular decision making.NPJ systems biology and applications · 2025Article
- Multiple entanglements of different cell death pathways, in which caspase-8 and BID interact with cardiolipin*, have been identified.Frontiers in cell and developmental biology · 2025Review
- Targeting Bcl-2 with Indole Scaffolds: Emerging Drug Design Strategies for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Review
- A novel inhibitory BAK antibody enables assessment of non-activated BAK in cancer cells.Cell death and differentiation · 2024Article
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- Computational modeling of DLBCL predicts response to BH3-mimetics.NPJ systems biology and applications · 2023Article
- Structure-destabilizing mutations unleash an intrinsic perforation activity of antiapoptotic Bcl-2 in the mitochondrial membrane enabling apoptotic cell death.Mitochondrial communications · 2023Article
- Membrane interactions of apoptotic inhibitor Bcl-xL: What can be learned using fluorescence spectroscopy.BBA advances · 2023Article
- Efficacy and specificity of inhibitors of BCL-2 family protein interactions assessed by affinity measurements in live cells.Science advances · 2022Article
- Lipids modulate the BH3-independent membrane targeting and activation of BAX and Bcl-xL.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Direct Measurement of the Affinity between tBid and Bax in a Mitochondria-Like Membrane.International journal of molecular sciences · 2021Article
- Mitochondrial outer membrane permeabilization at the single molecule level.Cellular and molecular life sciences : CMLS · 2021Review
- Methods for Studying Myofibroblast Apoptotic Pathways.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Crosstalk between Noxa, Bcl-2, and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.Molecular and cellular biochemistry · 2020Article
- A redox switch regulates the structure and function of anti-apoptotic BFL-1.Nature structural & molecular biology · 2020Article
- BCL-xL, a Mitochondrial Protein Involved in Successful Aging: FromInternational journal of molecular sciences · 2020Review
- The third model of Bax/Bak activation: a Bcl-2 family feud finally resolved?F1000Research · 2020Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The dysregulation of apoptosis is a key step in developing tumours, and mediates resistance to cancer therapy. Many different signals for cell death converge on permeabilization of the outer mitochondrial membrane, which is controlled by the Bcl-2 family of proteins. The importance of this step is becoming increasingly relevant as the first generation of small molecules that inhibit the interaction of Bcl-2 family proteins enters clinical trials as anticancer agents. The Bcl-2 family can be divided into three classes: BH3-only proteins that are activated by various forms of cellular stress, Bax and Bak proteins that mediate mitochondrial membrane permeabilization, and inhibitory proteins such as Bcl-2 and Bcl-XL. The recently proposed embedded together model emphasizes the fact that many of the regulatory interactions between different classes of Bcl-2 family members occur at intracellular membranes, and binding to membranes causes conformational changes in the proteins that dictate functions in a dynamic manner. Within this context, recent results indicate that Bcl-XL functions as a dominant-negative Bax, a concept that resolves the paradox of similar structures but opposite functions of Bcl-XL and Bax. We have also shown that the conformational change that allows Bax to insert into the outer mitochondrial membrane is the rate-limiting step in the multistep process of Bax activation. Nevertheless, investigating the structure of activated Bax or Bak as monomers and as components of the oligomeric structures that mediate membrane permeabilization is the focus of ongoing research (and controversy) at many laboratories worldwide.
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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.