ArticleCell death and differentiation2007
The N-terminal conformation of Bax regulates cell commitment to apoptosis.
Article in Cell death and differentiation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
30 citing papers in PubMed.
- Volumetric localization microscopy with deep learning.Nature communications · 2025Article
- Identification and Analysis of Anticancer Therapeutic Targets from the Polysaccharide Krestin (PSK) and Polysaccharopeptide (PSP) Using Inverse Docking.Molecules (Basel, Switzerland) · 2024Article
- Unconventional Source of Neurotoxic Protein Aggregation from Organelle Off-Target Bax∆2 in Alzheimer's Disease.Biomolecules · 2023Article
- A connection in life and death: The BCL-2 family coordinates mitochondrial network dynamics and stem cell fate.International review of cell and molecular biology · 2020Review
- Review
- Topology of active, membrane-embedded Bax in the context of a toroidal pore.Cell death and differentiation · 2018Article
- A neuroprotective agent that inactivates prodegenerative TrkA and preserves mitochondria.The Journal of cell biology · 2017Article
- Photo-activation of the delocalized lipophilic cation D112 potentiates cancer selective ROS production and apoptosis.Cell death & disease · 2017Article
- Direct Activation of Bax Protein for Cancer Therapy.Medicinal research reviews · 2016Review
- Sensitization of Melanoma Cells for Death Ligand TRAIL Is Based on Cell Cycle Arrest, ROS Production, and Activation of Proapoptotic Bcl-2 Proteins.The Journal of investigative dermatology · 2015Article
- ROS-dependent phosphorylation of Bax by wortmannin sensitizes melanoma cells for TRAIL-induced apoptosis.Cell death & disease · 2013Article
- Non-canonical function of Bax in stress-induced nuclear protein redistribution.Cellular and molecular life sciences : CMLS · 2013Article
- A highly-conserved single-stranded DNA-binding protein in Xanthomonas functions as a harpin-like protein to trigger plant immunity.PloS one · 2013Article
- The dynamics of Bax channel formation: influence of ionic strength.Biophysical journal · 2012Article
- NLRP5 mediates mitochondrial function in mouse oocytes and embryos.Biology of reproduction · 2012Article
- RASSF1A and the BH3-only mimetic ABT-737 promote apoptosis in pediatric medulloblastoma cell lines.Neuro-oncology · 2011Article
- BAX unleashed: the biochemical transformation of an inactive cytosolic monomer into a toxic mitochondrial pore.Trends in biochemical sciences · 2011Review
- Identification of Bax-voltage-dependent anion channel 1 complexes in digitonin-solubilized cerebellar granule neurons.Journal of neurochemistry · 2011Article
- The sphingolipid degradation product trans-2-hexadecenal induces cytoskeletal reorganization and apoptosis in a JNK-dependent manner.Cellular signalling · 2011Article
- Utilizing mitochondrial events as biomarkers for imaging apoptosis.Cell death & disease · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The Bcl-2 protein Bax normally resides in the cytosol, but during apoptosis it translocates to mitochondria where it is responsible for releasing apoptogenic factors. Using anoikis as a model, we have shown that Bax translocation does not commit cells to apoptosis, and they can be rescued by reattachment to extracellular matrix within a specific time. Bax undergoes an N-terminal conformational change during apoptosis that has been suggested to regulate conversion from its benign, cytosolic form to the active, membrane bound pore. We now show that the Bax N-terminus regulates commitment and mitochondrial permeabilisation, but not the translocation to mitochondria. We identify Proline 13 within the N-terminus of Bax as critical for this regulation. The subcellular distribution of Proline 13 mutant Bax was identical to wild-type Bax in both healthy and apoptotic cells. However, Proline 13 mutant Bax induced rapid progression to commitment, mitochondrial permeabilisation and death. Our data identify changes in Bax controlling commitment to apoptosis that are mechanistically distinct from those controlling its subcellular localisation. Together, they indicate that multiple regulatory steps are required to activate the proapoptotic function of Bax.
Indexed as
Identifiers
What OpenQuestion holds
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.