ArticleCell death and differentiation2013
The C-terminal helix of Bcl-x(L) mediates Bax retrotranslocation from the mitochondria.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- BAX-dependent mitochondrial outer membrane rupture in cochlear hair cells facilitates cisplatin ototoxicity.Communications biology · 2026Article
- A gated hydrophobic funnel within BAX binds bioactive lipids to potentiate pro-apoptotic function.Nature communications · 2026Article
- Article
- Allosteric regulation of BH3-in-groove interactions by tail anchors of BCL-xL complexes limits BH3 mimetic antagonism.Nature communications · 2025Article
- BAX-mediated ammonia-driven cell death: a novel prognostic and therapeutic target in clear cell renal cell carcinoma.Human genomics · 2025Article
- BCL-2 and BOK regulate apoptosis by interaction of their C-terminal transmembrane domains.EMBO reports · 2024Article
- Lipid unsaturation promotes BAX and BAK pore activity during apoptosis.Nature communications · 2024Article
- Development of novel cytoprotective small compounds inhibiting mitochondria-dependent cell death.iScience · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- Apoptosis Regulation in Osteoarthritis and the Influence of Lipid Interactions.International journal of molecular sciences · 2023Review
- Bcl-xL Is Spontaneously Inserted into Preassembled Nanodiscs and Stimulates Bax Insertion in a Cell-Free Protein Synthesis System.Biomolecules · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Visualization of BOK pores independent of BAX and BAK reveals a similar mechanism with differing regulation.Cell death and differentiation · 2023Article
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- Acetic acid triggers cytochrome c release in yeast heterologously expressing human Bax.Apoptosis : an international journal on programmed cell death · 2022Article
- How Do Hexokinases Inhibit Receptor-Mediated Apoptosis?Biology · 2022Review
- Yeast as a tool to decipher the molecular mechanisms underlying the functions of Bcl-2 family.Exploration of targeted anti-tumor therapy · 2022Review
- Hexokinases inhibit death receptor-dependent apoptosis on the mitochondria.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
- Intrinsically Connected: Therapeutically Targeting the Cathepsin Proteases and the Bcl-2 Family of Protein Substrates as Co-regulators of Apoptosis.International journal of molecular sciences · 2021Review
11 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
Abstract
The proapoptotic Bcl-2 protein Bax can commit a cell to apoptosis by translocation from the cytosol to the mitochondria and permeabilization of the outer mitochondrial membrane. Prosurvival Bcl-2 family members, such as Bcl-x(L), control Bax activity. Bcl-x(L) recognizes Bax after a conformational change in the N-terminal segment of Bax on the mitochondria and retrotranslocates it back into the cytoplasm, stabilizing the inactive form of Bax. Here we show that Bax retrotranslocation depends on the C-terminal helix of Bcl-x(L). Deletion or substitution of this segment reduces Bax retrotranslocation and correlates with the accumulation of GFP-tagged or endogenous Bax on the mitochondria of non-apoptotic cells. Unexpectedly, the substitution of the Bcl-x(L) membrane anchor by the corresponding Bax segment reverses the Bax retrotranslocation activity of Bcl-x(L), but not that of Bcl-x(L) shuttling. Bax retrotranslocation depends on interaction to the Bcl-x(L) membrane anchor and interaction between the Bax BH3 domain and the Bcl-x(L) hydrophobic cleft. Interference with either interaction increases mitochondrial levels of endogenous Bax. In healthy cells, mitochondrial Bax does not permeabilize the outer mitochondrial membrane, but increases cell death after apoptosis induction.
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