ArticleThe EMBO journal2015
Differential retrotranslocation of mitochondrial Bax and Bak.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 167 citations in OpenAlex.
- Spatiotemporal dynamics of Mcl-1 abundance and its influence on apoptosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Allosteric regulation of BH3-in-groove interactions by tail anchors of BCL-xL complexes limits BH3 mimetic antagonism.Nature communications · 2025Article
- Tumor nutrient stress gives rise to a drug tolerant cell state in pancreatic cancer.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial Dysfunction is a Crucial Immune Checkpoint for Neuroinflammation and Neurodegeneration: mtDAMPs in Focus.Molecular neurobiology · 2025Review
- Senolysis by ABT-263 is associated with inherent apoptotic dependence of cancer cells derived from the non-senescent state.Cell death and differentiation · 2025Article
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Rhodiola crenulata induces apoptosis in bone metastatic breast cancer cells via activation of caspase-9 and downregulation of MtMP activity.Scientific reports · 2025Article
- Apoptosis signaling is activated as a transient pulse in neurons.Cell death and differentiation · 2025Article
- Promoting the transition from pyroptosis to apoptosis in endothelial cells: a novel approach to alleviate methylglyoxal-induced vascular damage.Journal of translational medicine · 2025Article
- Inhibition of BAK-mediated apoptosis by the BH3-only protein BNIP5.Cell death and differentiation · 2025Article
- Mitochondrial priming in therapy-induced senescence: implications for CAR-T/NK immunosenolytic therapy.Frontiers in immunology · 2025Review
- Apoptosis-induced translocation of nesprin-2 from the nuclear envelope to mitochondria is associated with mitochondrial dysfunction.Nucleus (Austin, Tex.) · 2024Article
- The C-terminal sequences of Bcl-2 family proteins mediate interactions that regulate cell death.The Biochemical journal · 2024Review
- Disarib, a Specific BCL2 Inhibitor, Induces Apoptosis in Triple-Negative Breast Cancer Cells and Impedes Tumour Progression in Xenografts by Altering Mitochondria-Associated Processes.International journal of molecular sciences · 2024Article
- Lipid unsaturation promotes BAX and BAK pore activity during apoptosis.Nature communications · 2024Article
- Decreased apoptotic priming and loss of BCL-2 dependence are functional hallmarks of Richter's syndrome.Cell death & disease · 2024Article
- Phenotyping of cancer-associated somatic mutations in the BCL2 transmembrane domain.Oncogenesis · 2024Article
- Endogenous BAX and BAK form mosaic rings of variable size and composition on apoptotic mitochondria.Cell death and differentiation · 2024Article
- LINC complex protein nesprin-2 has pro-apoptotic activity via Bcl-2 family proteins.Cell death discovery · 2024Article
41 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
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Bcl-2 proteins Bax and Bak can permeabilize the outer mitochondrial membrane and commit cells to apoptosis. Pro-survival Bcl-2 proteins control Bax by constant retrotranslocation into the cytosol of healthy cells. The stabilization of cytosolic Bax raises the question whether the functionally redundant but largely mitochondrial Bak shares this level of regulation. Here we report that Bak is retrotranslocated from the mitochondria by pro-survival Bcl-2 proteins. Bak is present in the cytosol of human cells and tissues, but low shuttling rates cause predominant mitochondrial Bak localization. Interchanging the membrane anchors of Bax and Bak reverses their subcellular localization compared to the wild-type proteins. Strikingly, the reduction of Bax shuttling to the level of Bak retrotranslocation results in full Bax toxicity even in absence of apoptosis induction. Thus, fast Bax retrotranslocation is required to protect cells from commitment to programmed 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.