Affinage

BAX

Apoptosis regulator BAX · UniProt Q07812

Round 2 corrected
Length
192 aa
Mass
21.2 kDa
Annotated
2026-04-28
130 papers in source corpus 54 papers cited in narrative 54 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BAX is a central pro-apoptotic effector of the BCL-2 family that converts from an autoinhibited cytosolic monomer—whose α9 helix occupies the BH3-binding groove—into an oligomeric pore-forming complex in the outer mitochondrial membrane, thereby releasing cytochrome c and enabling inner membrane herniation with mtDNA efflux to activate cGAS/STING innate immunity (PMID:11106734, PMID:29472455). Activation is initiated when BH3-only proteins (tBID, BIM, PUMA) or cytosolic p53 engage a distinct N-terminal trigger site, displacing α9 and exposing the C-terminal transmembrane domain for VDAC2-dependent mitochondrial targeting, cardiolipin-promoted membrane insertion, and assembly into symmetric BH3:groove dimer-based macropores (PMID:18948948, PMID:10629050, PMID:30478310, PMID:12419244, PMID:25458844). Anti-apoptotic BCL-2 family members oppose BAX by retrotranslocating it from mitochondria to the cytosol and by sequestering membrane-inserted monomers, while phosphorylation at S184 by Akt or PKCζ and cytosolic sequestration by deacetylated Ku70 maintain BAX in an inactive state (PMID:21458670, PMID:16642033, PMID:29987135, PMID:17525161, PMID:15205477). BAX also functions in healthy cells to promote MFN2-dependent mitochondrial fusion and acts as a tumor suppressor whose inactivation—by frameshift mutation in microsatellite-unstable cancers—accelerates tumorigenesis (PMID:17035996, PMID:9020077, PMID:9024662).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1993 High

    Identification of BAX as a BCL-2-interacting protein that homodimerizes and accelerates apoptosis established the concept that the BCL-2/BAX ratio governs cell survival, answering the question of whether BCL-2 has pro-apoptotic counterparts.

    Evidence Co-immunoprecipitation and yeast two-hybrid in IL-3-dependent cells

    PMID:8358790

    Open questions at the time
    • Mechanism by which BAX promotes death was unknown
    • Whether BAX acts at mitochondria was not addressed
    • No structural information on BAX
  2. 1995 High

    Demonstration that p53 directly transactivates the bax promoter linked the tumor suppressor pathway to BAX-mediated apoptosis, answering how DNA damage signals converge on the BCL-2 family.

    Evidence Reporter gene assays, EMSA, and site-directed mutagenesis of p53-binding sites

    PMID:7834749

    Open questions at the time
    • Whether p53 also acts on BAX post-translationally was unknown
    • In vivo relevance of p53-BAX axis not yet demonstrated
  3. 1997 High

    Three concurrent advances—BAX channel formation in lipid bilayers, stimulus-dependent translocation from cytosol to mitochondrial puncta requiring the C-terminal domain, and BAX tumor suppressor function in vivo—established BAX as a mitochondria-targeting pore-forming protein with physiological anti-tumor activity.

    Evidence Planar lipid bilayer electrophysiology; GFP-BAX live imaging with C-terminal deletion mutagenesis; Bax-knockout mouse tumor model

    PMID:9020077 PMID:9024662 PMID:9219694 PMID:9382873

    Open questions at the time
    • How the cytosolic-to-mitochondrial transition is regulated was unknown
    • Identity of the mitochondrial receptor unclear
    • Whether BAX forms channels alone or with partners was debated
  4. 1998 High

    Discovery that the N-terminal domain autoinhibits the C-terminal transmembrane signal-anchor, and that BAX cooperates with mitochondrial channel proteins ANT and VDAC to form cytochrome c–releasing pores, resolved how BAX is kept inactive in the cytosol and how it permeabilizes mitochondria.

    Evidence Domain chimera mutagenesis and subcellular fractionation; reconstituted BAX-ANT and BAX-VDAC channels in lipid bilayers; ANT-null and VDAC-null yeast

    PMID:9748162 PMID:9763432 PMID:9843949

    Open questions at the time
    • Whether BAX oligomers alone suffice for MOMP was unclear
    • The role of lipids was not dissected
    • BH3-only activator identity unknown
  5. 2000 High

    The NMR structure of monomeric BAX revealed that α9 occupies the BH3-binding groove (dual autoinhibition), while parallel work showed tBID directly converts BAX from soluble monomer to membrane-inserted oligomer, solving the structural basis of autoinhibition and identifying the first direct activator.

    Evidence NMR solution structure of full-length BAX; in vitro tBID-induced BAX oligomerization and membrane insertion with isolated mitochondria

    PMID:10629050 PMID:11106734 PMID:11139284

    Open questions at the time
    • Where on BAX tBID binds was unknown
    • Role of specific lipids not yet addressed
    • Whether other BH3-only proteins act identically was untested
  6. 2002 High

    Reconstitution of BAX/BID-dependent supramolecular pores in defined liposomes requiring cardiolipin, plus discovery that BAX foci colocalize with DRP1 at mitochondrial fission sites, established that BAX forms lipid-assisted macropores and coordinates with the fission machinery.

    Evidence Cell-free reconstitution with purified BAX, tBID, and cardiolipin-containing liposomes passing 2-MDa dextran; live-cell colocalization with DRP1 and dominant-negative DRP1

    PMID:12419244 PMID:12499352

    Open questions at the time
    • Whether BAX directly binds DRP1 was not established
    • Structure of the BAX pore was unknown
    • Cholesterol and other lipid effects unexplored
  7. 2004 High

    Cytosolic p53 was shown to directly activate BAX in vitro with kinetics comparable to tBID, and SIRT1-mediated Ku70 deacetylation was found to sequester BAX from mitochondria, revealing both a transcription-independent p53 mechanism and a metabolic regulatory axis for BAX.

    Evidence Purified p53-BAX MOMP reconstitution; SIRT1/Ku70 deacetylation biochemistry with BAX sequestration assay

    PMID:14963330 PMID:15205477

    Open questions at the time
    • p53 binding site on BAX not mapped
    • Relative contributions of transcriptional vs. direct p53 activation unclear
    • In vivo relevance of Ku70-BAX sequestration under physiological conditions unknown
  8. 2006 High

    Two unexpected BAX functions were uncovered: BCL-2 undergoes conformational change to sequester membrane-inserted BAX monomers (a new anti-apoptotic mechanism), and BAX/BAK promote MFN2-dependent mitochondrial fusion in healthy cells, revealing a non-apoptotic homeostatic role.

    Evidence Disulfide-tethered BCL-2 mutagenesis with oligomerization assay; Bax/Bak double-KO MEFs with MFN2 assembly and FLIP assays

    PMID:16642033 PMID:17035996

    Open questions at the time
    • How BAX switches between fusion-promoting and pore-forming modes was unknown
    • BCL-2 conformational change mechanism not fully resolved structurally
  9. 2008 High

    NMR mapping of BIM SAHB binding to a novel N-terminal trigger site on BAX (distinct from the BH3 groove), plus discovery that cholesterol inhibits BAX membrane integration and that PKCζ phosphorylation of S184 prevents BAX activation, defined the activation switch and two major inhibitory mechanisms.

    Evidence NMR chemical shift mapping with trigger-site mutagenesis and MOMP assay; purified BAX in cholesterol-defined liposomes; in vitro PKCζ kinase assay with S184 mutants

    PMID:17525161 PMID:18590739 PMID:18948948

    Open questions at the time
    • How trigger-site engagement propagates to α9 displacement structurally was incomplete
    • Whether the cholesterol effect is relevant in vivo was untested
    • Interplay between S184 phosphorylation and BH3 activation unknown
  10. 2009 High

    Systematic mutagenesis defined the stepwise allosteric cascade: activator BH3 proteins engage α1, displace α9, expose the transmembrane domain, and remain associated via BH1 to drive oligomerization, while PUMA was shown to act both as a direct activator and as a sensitizer that liberates BAX from BCL-XL.

    Evidence Domain-specific mutagenesis with conformational change and epistasis assays; real-time FRET for PUMA-BAX interaction in living cells

    PMID:19439449 PMID:19917256

    Open questions at the time
    • Structure of the active BAX oligomer remained unknown
    • How many BH3 activators bind per BAX monomer unclear
  11. 2011 High

    Discovery that BCL-XL continuously retrotranslocates BAX from mitochondria back to the cytosol in healthy cells revealed that BAX localization is a dynamic equilibrium rather than a static on/off switch, fundamentally revising the model of apoptotic priming.

    Evidence FLIP analysis of BAX shuttling; intramolecular disulfide tethering blocking retrotranslocation; cell-free MOMP validation

    PMID:21458670

    Open questions at the time
    • Mitochondrial receptor for retrotranslocation not identified in this study
    • Whether retrotranslocation requires ATP or specific cofactors was unknown
  12. 2014 High

    DEER spectroscopy in liposomes resolved the active BAX pore architecture: symmetric BH3:groove dimers assemble via flexible α5-α6 'piercing' domains into higher-order structures, while separate work showed BAX requires a minimum mitochondrial membrane size (MFN1-dependent) to stabilize α9 insertion.

    Evidence DEER EPR in liposomes and isolated mitochondria; MFN1-KO/overexpression with BAX-membrane association assay

    PMID:25458844 PMID:25482509

    Open questions at the time
    • Complete atomic-resolution structure of BAX pore in a membrane still lacking
    • Stoichiometry of the functional pore not determined
  13. 2016 High

    Crystal structure of an inactive BAX dimer revealed a previously unknown autoinhibited state requiring dissociation before activation, and VDAC2 was identified as the mitochondria-specific platform for BAX targeting and retrotranslocation, answering two long-standing questions about BAX regulation.

    Evidence Full-length BAX crystal structure with cellular validation of dimer-to-monomer transition; VDAC2 knockdown with FLIP and subcellular fractionation

    PMID:27425408 PMID:27620692

    Open questions at the time
    • What controls dimer-to-monomer conversion in cells was unknown
    • Whether VDAC2 channel activity is mechanistically linked to BAX retrotranslocation was not resolved
  14. 2018 High

    Multiple regulatory dimensions converged: Akt-mediated S184 phosphorylation converts BAX into an anti-apoptotic BH3 sequestrant; BAK/BAX macropores enable inner membrane herniation and cGAS/STING activation via mtDNA efflux; and genome-wide CRISPR screening confirmed VDAC2 as specifically required for BAX (not BAK) apoptotic function.

    Evidence Akt kinase assay with S184 mutants and BH3-binding assay; lattice light-sheet microscopy with BAK/BAX-DKO MEFs and cGAS/STING readout; genome-wide CRISPR screen with VDAC2-KO and in vivo tumor suppression

    PMID:29472455 PMID:29987135 PMID:30478310

    Open questions at the time
    • Whether phospho-BAX BH3 sequestration operates in vivo at physiological stoichiometries was unknown
    • Structural basis of inner membrane herniation through BAX pores not resolved
    • Why VDAC2 is specific for BAX and not BAK structurally unclear
  15. 2022 High

    DRP1 was established as a noncanonical direct BAX activator through physical interaction requiring the BAX N-terminal region; forced BAX-DRP1 dimerization triggers co-activation and mitochondrial permeabilization without apoptotic stimuli, linking fission machinery directly to MOMP commitment.

    Evidence Co-immunoprecipitation, proximity ligation, forced dimerization construct, super-resolution microscopy

    PMID:35023587

    Open questions at the time
    • Binding interface on BAX for DRP1 not mapped at residue resolution
    • Physiological contexts where DRP1-driven BAX activation predominates over BH3-only activation unknown
  16. 2024 High

    Lipidomic profiling of the BAX pore microenvironment revealed enrichment of unsaturated lipids that promote pore activity, with FADS2-dependent desaturation enhancing both apoptosis sensitivity and cGAS/STING signaling, establishing lipid composition as a tunable determinant of BAX pore function.

    Evidence Comparative lipidomics of lipid nanodiscs, reconstituted BAX pore assays, FADS2 genetic manipulation, molecular dynamics simulations

    PMID:38830851

    Open questions at the time
    • Whether tumors modulate FADS2/lipid desaturation to evade BAX-dependent death in vivo is untested
    • How cholesterol and unsaturated lipids jointly regulate BAX pore dynamics at atomic resolution is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • A complete atomic-resolution structure of the functional BAX macropore in a native membrane, the precise stoichiometry of the pore, and the mechanism by which BAX switches between its homeostatic fusion-promoting and apoptotic pore-forming activities remain unresolved.
  • No high-resolution cryo-EM structure of the assembled BAX pore in a lipid bilayer
  • Mechanism of BAX dimer-to-monomer conversion in cells not defined
  • How BAX non-apoptotic mitochondrial fusion function is molecularly separated from pore formation is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 6 GO:0005829 cytosol 4
Pathway
R-HSA-5357801 Programmed Cell Death 7 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-168256 Immune System 2
Partners
BCL2BCL2L1BCL2L11BIDDRP1MFN2VDAC2XRCC6
Complex memberships
BAX homo-oligomeric poreBAX-VDAC2 platform complex

Evidence

Reading pass · 54 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 BAX was identified as a BCL-2-interacting protein that heterodimerizes with BCL-2 in vivo; BAX also homodimerizes, and overexpressed BAX accelerates apoptotic death and counters BCL-2's death-repressor activity, establishing that the BCL-2:BAX ratio determines cell survival or death. Co-immunoprecipitation, yeast two-hybrid, overexpression in IL-3-dependent cell line Cell High 8358790
1995 The bax gene promoter contains p53-binding sites; wild-type p53 directly transactivates bax transcription, establishing bax as a p53 primary-response gene in the apoptotic pathway. Reporter gene cotransfection, gel retardation/EMSA, site-directed mutagenesis of p53-binding sites Cell High 7834749
1997 BAX forms pH- and voltage-dependent ion-conducting channels in planar lipid bilayers, and this channel-forming activity is inhibited by BCL-2, providing a biochemical mechanism for BAX's pro-apoptotic function. Planar lipid bilayer electrophysiology, liposome dye-release assay Science High 9219694
1997 Upon apoptosis induction, GFP-BAX moves from a diffuse cytosolic distribution to punctate mitochondria-associated foci within 30 min, before nuclear condensation; removal of the C-terminal hydrophobic domain inhibits this redistribution and abolishes death-promoting activity. GFP fusion live-cell confocal microscopy, FRAP/photobleaching, C-terminal deletion mutagenesis The Journal of cell biology High 9382873
1997 BAX acts as a tumor suppressor in vivo; p53-dependent bax expression is induced in apoptotic brain tumors, and Bax-deficient mice show accelerated tumor growth with ~50% reduction in apoptosis, placing BAX as a required component of the p53-mediated apoptotic response. Transgenic mouse brain tumor model, Bax knockout mice, histological apoptosis quantification Nature High 9024662
1997 BAX-induced cell death in fission yeast S. pombe is suppressed by BCL-XL and partially by BCL-2 (but not by BCL-2-G145A, which cannot heterodimerize with BAX), confirming an evolutionarily conserved functional interaction; however, unlike mammalian apoptosis, yeast BAX death is caspase-independent and lacks internucleosomal DNA fragmentation. Heterologous expression in S. pombe, genetic co-expression, electron microscopy, ICE/CED-3 protease assays Molecular biology of the cell Medium 9190211
1997 BAX frameshift mutations in a poly-G tract occur in >50% of microsatellite-unstable colon adenocarcinomas, inactivating BAX and providing a p53-independent tumor suppressor pathway. PCR sequencing of primary tumors and cell lines, allele-specific mutation analysis Science High 9020077
1998 BAX is cytosolic in healthy cells because its N-terminal domain represses the transmembrane signal-anchor function of the C-terminal domain; a death signal relieves this autoinhibition to drive mitochondrial membrane insertion, and caspase activity (partially via caspase-8) contributes to this regulated targeting. Deletion and chimeric domain mutagenesis, subcellular fractionation, in vitro mitochondrial targeting with caspase inhibitor zVAD-fmk The Journal of cell biology High 9763432
1998 BAX interacts with the adenine nucleotide translocator (ANT) of the mitochondrial permeability transition pore complex (PTPC); BAX and ANT together form atractyloside-responsive channels in artificial membranes, and BAX induces cell death in ANT-proficient but not ANT-deficient yeast, establishing cooperative action within the PTPC. Co-immunoprecipitation, yeast two-hybrid, reconstituted lipid bilayer with purified proteins, ANT-deficient yeast Science High 9748162
1998 BAX interacts with the voltage-dependent anion channel (VDAC) component of the permeability transition pore; BAX/BAK-BH3 peptides (but not mutant BH3) are sufficient to induce PT pore opening, Ca2+-dependent mitochondrial swelling, and cytochrome c release from isolated mitochondria; BCL-XL and BCL-2 oppose these effects. Recombinant protein addition to isolated mitochondria, co-immunoprecipitation, BH3 peptide mutagenesis, cyclosporin A/bongkrekic acid pharmacology Proceedings of the National Academy of Sciences High 9843949
1999 BCL-2 family proteins regulate cytochrome c release through the mitochondrial porin VDAC: pro-apoptotic BAX and BAK accelerate VDAC opening to allow cytochrome c passage, whereas anti-apoptotic BCL-XL closes VDAC by binding it directly; VDAC1-deficient yeast mitochondria are resistant to BAX/BAK-induced membrane potential loss. VDAC-containing liposome reconstitution, cytochrome c release assay, VDAC1-null yeast mitochondria, direct binding assay Nature High 10365962
2000 The NMR solution structure of BAX shows 9 α-helices; the C-terminal α9 helix occupies the hydrophobic BH3-binding groove that normally mediates heterodimer formation, providing simultaneous autoinhibition of mitochondrial targeting and dimer formation. NMR structure determination of full-length BAX Cell High 11106734
2000 Truncated BID (tBID) induces oligomerization and insertion of BAX into the outer mitochondrial membrane, triggering cytochrome c release; this establishes that a BH3-only protein directly converts BAX from a soluble monomer to an integral membrane oligomer. In vitro oligomerization assay, isolated mitochondria membrane-insertion assay, cytochrome c release assay Molecular and cellular biology High 10629050
2000 tBID-induced BAX membrane insertion relieves N-terminal autoinhibition of the transmembrane signal-anchor; this can occur through a BID-dependent pathway (caspase-8-cleaved tBID) and a parallel BID-independent pathway (in Bid-null MEFs in response to TNFα or E1A), though cytochrome c release is uncoupled from BAX insertion in the BID-independent case. In vivo and in vitro BAX membrane insertion assays, Bid-null MEFs, dominant-negative caspase-8 Cell death and differentiation High 11139284
2000 Mitochondria-dependent apoptotic stimuli (including BAX overexpression) induce rapid BCL-2-inhibitable mitochondrial alkalinization followed by cytosol acidification; cytosol acidification in turn enhances caspase activation by cytochrome c in vitro, revealing a pH-based amplification mechanism downstream of BAX. pH-sensitive GFP in living cells, in vitro caspase activation at defined pH, protonophore experiments, FoF1-ATPase-deficient yeast Nature cell biology High 10854321
2001 After apoptosis induction, BAX associated with mitochondria forms high-molecular-weight oligomeric complexes (96 kDa and 260 kDa) that are integrated into the mitochondrial membrane; BCL-2 prevents this oligomerization and membrane integration; VDAC and ANT do not co-elute with these complexes by gel filtration, suggesting BAX oligomers may themselves form the cytochrome c-conducting channel. Gel filtration, sucrose gradient fractionation, immunoprecipitation, apoptosis induction in HeLa cells The Journal of biological chemistry High 11136736
2002 During apoptosis, BAX translocates to discrete foci at mitochondrial fission sites; these foci colocalize with DRP1 and MFN2 but not other morphology regulators; dominant-negative DRP1-K38A blocks mitochondrial scission but not BAX translocation, establishing that BAX and DRP1 cooperate at fission sites. Fluorescence microscopy, dominant-negative DRP1 expression, colocalization with fission markers The Journal of cell biology High 12499352
2002 BAX undergoes biphasic translocation to mitochondria: in phase 1, small amounts of BAX target mitochondrial intermembrane contact sites and cytochrome c is released; in phase 2, BAX is packaged into large aggregates on mitochondria; co-immunoprecipitation revealed association with VDAC (outer membrane) and ANT (inner membrane). GFP-BAX live imaging, RFP-cytochrome c co-imaging, immunoprecipitation from fractionated cells The Biochemical journal Medium 12097139
2002 In adenovirus-infected cells, E1B-19K anti-apoptotic protein binds BAK, preventing BAK-BAX interaction and BAX conformational change; cells deficient for both BAX and BAK are completely resistant to apoptosis and show dramatically increased viral replication, establishing BAX and BAK as redundant antiviral effectors. Co-immunoprecipitation, BAX/BAK single and double knockout MEFs, conformational change assays, viral replication quantification Journal of virology High 11932420
2002 BAX and BID cooperate with lipids (cardiolipin required) to form supramolecular openings in the outer mitochondrial membrane large enough to pass 2-MDa dextran molecules; BCL-XL directly inhibits this process; reconstitution from defined molecules shows no requirement for matrix, inner membrane, or other proteins. Cell-free reconstitution with purified proteins in liposomes, electron microscopy, cardiolipin requirement assay Cell High 12419244
2003 Humanin (HN), a 24-amino-acid peptide, directly binds BAX and prevents its translocation from cytosol to mitochondria; reducing HN expression by siRNA sensitizes cells to BAX and increases BAX membrane translocation; HN also blocks BAX association with isolated mitochondria and suppresses cytochrome c release in vitro. Co-immunoprecipitation, siRNA knockdown, in vitro mitochondrial association assay, cytochrome c release Nature High 12732850
2004 Cytosolic p53 protein directly activates BAX in vitro in the absence of any other proteins to permeabilize mitochondria and release cytochrome c; the transcription-independent p53-BAX interaction occurs with similar kinetics and concentrations to activated BID, establishing p53 as a direct BH3-like BAX activator. In vitro MOMP assay with purified proteins and isolated mitochondria, cell-free system with defined components Science High 14963330
2004 SIRT1 deacetylates Ku70, causing Ku70 to sequester BAX away from mitochondria and thereby inhibit stress-induced apoptosis; this mechanism links caloric restriction-induced SIRT1 expression to enhanced cell survival. Co-immunoprecipitation, deacetylation assay, Ku70 overexpression/siRNA, caloric restriction in rats Science High 15205477
2004 Mitochondrial p53 interacts with pro-apoptotic BAK, inducing BAK oligomerization and cytochrome c release, coincident with disruption of the Bak-Mcl1 complex; p53-BAX interactions are implicated by the broader context of direct cytosolic p53 action. Co-immunoprecipitation in isolated mitochondria, cytochrome c release assay, Mcl1 complex disruption Nature cell biology High 15077116
2006 BCL-2 undergoes a conformational change in the mitochondrial membrane in response to apoptotic agonists (tBID, BAX) and in this changed state binds and sequesters membrane-integral BAX monomers and small oligomers to prevent productive oligomerization; a disulfide tether that restricts α5-α6 mobility abolishes this activity. Transfected cells, isolated mitochondria, disulfide-tethered BCL-2 mutant, tBID-induced oligomerization assay The EMBO journal High 16642033
2006 In healthy cells, BAX and BAK are required for normal mitochondrial fusion; BAX promotes mitochondrial fusion by activating assembly of the large GTPase MFN2 and altering its submitochondrial distribution and membrane mobility, correlating with different GTP-bound states. Bax/Bak double-knockout MEFs, MFN2 assembly and FLIP experiments, GTP-binding assay Nature High 17035996
2006 RASSF1A directly interacts with the BAX-binding protein MOAP-1; this interaction (enhanced by activated K-RAS) enables RASSF1A to activate BAX via MOAP-1; a tumor-derived RASSF1A point mutant defective for MOAP-1 binding fails to activate BAX. Co-immunoprecipitation, shRNA knockdown of RASSF1A, BAX conformational change assay, tumor-derived point mutant analysis The Journal of biological chemistry Medium 16344548
2007 Protein kinase Cζ (PKCζ) directly phosphorylates BAX at serine 184 in vitro and in cells; phospho-S184-BAX accumulates in the cytoplasm, is prevented from conformational change, and purified PKCζ can directly dissociate BAX from mitochondria, thus abrogating its pro-apoptotic function. In vitro kinase assay with purified PKCζ and BAX, S184 mutagenesis, subcellular fractionation, RNA interference The Journal of biological chemistry High 17525161
2008 BIM SAHB binds BAX at a novel N-terminal interaction site (distinct from the canonical BH3-binding groove) identified by NMR; point mutagenesis at this site disrupts BAX activation, establishing it as the trigger site for direct BAX activation. NMR chemical shift analysis, point mutagenesis of BAX trigger site, functional MOMP assay Nature High 18948948
2008 HDAC6 binds KU70 and BAX in the cytoplasm of neuroblastoma cells; HDAC6-specific inhibition or knockdown triggers KU70 acetylation and BAX-dependent cell death, establishing HDAC6 as the deacetylase that maintains KU70 in a deacetylated (BAX-sequestering) state. Co-immunoprecipitation, HDAC6-specific inhibitor/siRNA knockdown, apoptosis assays Neoplasia Medium 21847364
2008 TCTP (translationally controlled tumor protein) contains H2-H3 helices structurally similar to BAX H5-H6 helices; TCTP inserts into the mitochondrial membrane and inhibits BAX dimerization; site-directed mutagenesis of H2-H3 abolishes anti-apoptotic function. Crystal structure of TCTP at 2.0 Å, structural comparison with BAX, site-directed mutagenesis, mitochondrial membrane insertion assay, BAX dimerization assay Cell death and differentiation High 18274553
2008 Cholesterol in lipid bilayers or mitochondrial membranes increases BAX membrane binding but markedly inhibits BAX membrane integration and subsequent pore activation; activation (but not oligomerization) is required for membrane binding, and oligomerization/pore formation occur only after integration. Purified monomeric BAX, defined liposomes with controlled cholesterol content, isolated mitochondria, pore-formation assay Journal of molecular biology High 18590739
2009 BAX undergoes stepwise structural reorganization: the α1 helix keeps the α9 helix in the dimerization pocket maintaining BAX as a cytosolic monomer; activator BH3 proteins (tBID/BIM/PUMA) engage and expose α1, causing α9 disengagement and mitochondrial insertion; activator BH3s remain associated with the exposed BAX N-terminus via the BH1 domain to drive homo-oligomerization. Domain-specific mutagenesis, conformational change assays, epistasis with activator-deficient BH3 mutants, BAK comparison Molecular cell High 19917256
2009 PUMA promotes BAX translocation by two mechanisms: direct interaction with BAX (FRET-confirmed), and competitive binding to BCL-XL that liberates BAX from BCL-XL sequestration; both mechanisms operate during UV-induced apoptosis. Real-time FRET in living cells, co-immunoprecipitation, p53 inhibitor and cycloheximide controls Molecular biology of the cell Medium 19439449
2009 Akt/PI3K-mediated phosphorylation of BAX suppresses its translocation to mitochondria and prevents cytochrome c release; inhibition of PI3K with LY294002 blocks BAX phosphorylation and restores BAX mitochondrial translocation and apoptosis. PI3K inhibitor LY294002, subcellular fractionation, cytochrome c release assay, phospho-BAX detection Biochimie Medium 19278624
2009 Bax activates endophilin B1 (Endo B1) oligomerization from tetramers to much larger complexes, requiring the Endo B1 SH3 domain; together, Bax and Endo B1 induce massive vesiculation of giant unilamellar liposomes, suggesting a role for this interaction in membrane remodeling during apoptosis. Purified recombinant protein interaction, dynamic light scattering, giant unilamellar vesicle assay The Journal of biological chemistry Medium 19805544
2010 Mitochondrial fragmentation facilitates BAX insertion and activation in mitochondrial membranes; overexpression of mitofusins or dominant-negative DRP1 prevents fragmentation and blocks BAX membrane insertion and oligomerization (but not translocation/accumulation), and reduces cytochrome c/AIF release and apoptosis. Mitofusin overexpression, dominant-negative DRP1, DRP1 siRNA, Bax conformational change and membrane insertion assays, MFN-null MEFs American journal of physiology. Cell physiology High 21160028
2011 BCL-XL retrotranslocates BAX from mitochondria back into the cytoplasm in healthy cells; FLIP analysis shows constant retrotranslocation of wild-type BAX but not disulfide-tethered BAX; Bax retrotranslocation depends on pro-survival BCL-2 family proteins, and its inhibition causes BAX accumulation on mitochondria. FLIP (fluorescence loss in photobleaching), intramolecular disulfide tethering, cell-free MOMP assay Cell High 21458670
2012 Computational screening identified a small molecule that directly engages the BAX N-terminal trigger site (confirmed by NMR and biochemical assays), promotes functional BAX oligomerization and BAX-dependent cell death without interacting with anti-apoptotic proteins or BAK. NMR chemical shift mapping, BAX oligomerization assay, BAX-specific cell death assay, computational docking Nature chemical biology High 22634637
2012 The cytomegalovirus protein vMIA contacts BAX at a novel regulatory site (NMR structure of BAX-vMIA peptide complex); vMIA stabilizes key structural elements needed for BAX membrane insertion and oligomerization, preventing these steps; interface mutations disrupt vMIA-mediated BAX mitochondrial recruitment and increase cytochrome c release. NMR structure of BAX-vMIA peptide complex, BAX localization assay in human cells, cytochrome c release assay, charge-reversal interface rescue mutagenesis Proceedings of the National Academy of Sciences High 23213219
2014 Active BAX at the membrane forms assemblies of dimers: each monomer contains a stable dimerization domain and a flexible 'piercing domain' (helices 5-6 open into a clamp-like conformation) involved in interdimer interactions and pore formation, as determined by DEER spectroscopy in liposomes and isolated mitochondria. Double electron-electron resonance (DEER) spectroscopy in liposomes and isolated mitochondria, 3D structural modeling Molecular cell High 25458844
2014 BAX requires a minimum mitochondrial size (established by MFN1-mediated fusion) to stably interact with the outer membrane via its α9 helix and induce MOMP; cells with hyperfragmented mitochondria fail to support BAX membrane association and permeabilization due to inability to stabilize BAX-α9-membrane interactions. MFN1 knockout/overexpression, size-restricted OMM model systems, BAX-membrane association assay, in vivo and ex vivo complementary studies Molecular cell High 25482509
2015 The BCL-2 BH4 domain binds to a non-canonical groove on BAX formed by α1, α1-α2 loop, and α2-α3/α5-α6 hairpins, independently inhibiting the N-terminal conformational changes in BAX induced by BIM BH3; this reveals a second BAX inhibitory mechanism distinct from canonical BH3-groove sequestration. Hydrogen-deuterium exchange mass spectrometry, NMR, synthetic α-helical BH4 peptide binding assay Molecular cell High 25684204
2016 Cytosolic BAX exists in an inactive dimer conformation (in addition to the well-known monomer); the crystal structure of the full-length inactive BAX dimer reveals an asymmetric interface that inhibits N-terminal conformational change of one protomer and displaces α9 of the second; the dimer must dissociate to monomers before BAX can be activated. Full-length BAX crystal structure, cellular and biochemical characterization of BAX dimer vs. monomer Molecular cell High 27425408
2016 VDAC2 serves as the mitochondrial platform for BAX retrotranslocation; VDAC2 ensures mitochondria-specific membrane association of BAX, and in VDAC2-deficient cells BAX localizes to other compartments; retrotranslocation is also regulated by nucleotides and calcium, suggesting VDAC2 ion transport influences this process. VDAC2 knockdown, subcellular fractionation, FLIP analysis with isolated mitochondria Scientific reports Medium 27620692
2017 An NMR fragment screen identified a compound binding to a pocket at the junction of BAX α3-α4 and α5-α6 hairpins that allosterically mobilizes the α1-α2 loop and BAX BH3 helix, sensitizing BAX activation; this reveals a new allosteric sensitization site distinct from the trigger site. NMR-based fragment screen, biochemical BAX activation assay, HDX-MS structural analysis Nature chemical biology High 28692068
2018 VDAC2 is specifically required for BAX (but not BAK) apoptotic function; VDAC2 deletion abrogates BAX association with mitochondrial VDAC-containing complexes and phenocopies BAX loss in tumor suppression; identified by genome-wide CRISPR/Cas9 screen. Genome-wide CRISPR/Cas9 screen, VDAC2 genetic deletion, BAX-VDAC complex co-immunoprecipitation, tumor cell killing assays, in vivo tumor suppression Nature communications High 30478310
2018 After BAK/BAX activation and cytochrome c loss, large BAK/BAX macropores form in the outer mitochondrial membrane; these macropores allow the inner mitochondrial membrane to herniate into the cytosol carrying mtDNA, enabling cGAS/STING innate immune activation; apoptotic caspases suppress but do not prevent herniation. Lattice light-sheet live-cell microscopy, BAK/BAX double-KO MEFs, cGAS/STING pathway readout Science High 29472455
2018 Akt phosphorylates BAX at S184, converting it from a pro-apoptotic to an anti-apoptotic protein: phospho-S184-BAX binds pro-apoptotic activator BH3 proteins in solution and is prevented from inserting into mitochondria, thus sequestering activator BH3 proteins and conferring resistance to BH3 mimetics. Akt kinase assay with BAX S184 mutants, BH3-protein binding in solution, mitochondrial insertion assay, primary ovarian cancer cells EMBO reports High 29987135
2018 Parkin suppresses BAX-mediated apoptosis during mitophagy through an indirect mechanism (without ubiquitinating BAX), while directly ubiquitinating BAK; PINK1-dependent Parkin activation is promoted by BAK-dependent MOMP during apoptosis, creating a regulatory feedback. Parkin overexpression, ubiquitination assays, BAK/BAX co-immunoprecipitation, mitophagy induction The EMBO journal Medium 30573668
2019 Small-molecule BAX inhibitors (BAIs) bind to a novel pocket around hydrophobic helix α5 through hydrophobic and hydrogen bonding interactions, allosterically stabilizing the BAX hydrophobic core and inhibiting conformational activation, mitochondrial translocation, and oligomerization. NMR binding validation, BAX conformational change assay, mitochondrial translocation assay, BAX oligomerization assay Nature chemical biology High 30718816
2021 Eltrombopag, an FDA-approved drug, directly binds the BAX trigger site (N-terminal activation site) in a manner distinct from BH3 activators, preventing activator BH3 proteins from triggering BAX conformational transformation and simultaneously stabilizing the inactive BAX structure. NMR binding mapping, BAX conformational change assay, cell death assays with BAX-dependent apoptosis induction Nature communications High 33602934
2022 BAX and DRP1 physically interact in the membrane environment, requiring the BAX N-terminal region; DRP1 enhances the membrane activity of BAX, and forced dimerization of BAX and DRP1 triggers their co-activation and translocation to mitochondria, inducing remodeling and permeabilization even without apoptotic triggers, establishing DRP1 as a noncanonical direct BAX activator. Co-immunoprecipitation, proximity ligation assay, forced dimerization construct, super-resolution microscopy, mitochondrial permeabilization assay The EMBO journal High 35023587
2024 Unsaturated lipids are enriched in the proximal membrane environment of BAK and BAX during apoptosis (by lipidomics of lipid nanodiscs); unsaturated lipids promote BAX pore activity in model membranes, isolated mitochondria, and cells (supported by molecular dynamics simulations); the fatty acid desaturase FADS2 enhances both apoptosis sensitivity and cGAS/STING pathway activation downstream of mtDNA release. Comparative lipidomics of lipid nanodiscs, BAX pore activity in liposomes and isolated mitochondria, FADS2 genetic manipulation, molecular dynamics simulations, cGAS/STING readout Nature communications High 38830851

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 5634 8358790
1995 Tumor suppressor p53 is a direct transcriptional activator of the human bax gene. Cell 3821 7834749
1999 Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC. Nature 1811 10365962
2004 Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis. Science (New York, N.Y.) 1679 14963330
2004 Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase. Science (New York, N.Y.) 1596 15205477
1997 Movement of Bax from the cytosol to mitochondria during apoptosis. The Journal of cell biology 1530 9382873
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2002 Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane. Cell 1198 12419244
1997 Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype. Science (New York, N.Y.) 1179 9020077
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2005 Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. Genes & development 1059 15901672
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
1998 Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis. Science (New York, N.Y.) 1007 9748162
2000 Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane. Molecular and cellular biology 968 10629050
2000 Structure of Bax: coregulation of dimer formation and intracellular localization. Cell 908 11106734
1997 Inhibition of Bax channel-forming activity by Bcl-2. Science (New York, N.Y.) 905 9219694
2007 Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science (New York, N.Y.) 903 17289999
2006 Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia. Cancer cell 885 17097560
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2018 BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis. Science (New York, N.Y.) 830 29472455
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
1998 Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proceedings of the National Academy of Sciences of the United States of America 823 9843949
2017 Bax, Bak and beyond - mitochondrial performance in apoptosis. The FEBS journal 714 28755482
2002 Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis. The Journal of cell biology 708 12499352
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2004 Mitochondrial p53 activates Bak and causes disruption of a Bak-Mcl1 complex. Nature cell biology 661 15077116
1995 Initial assessment of human gene diversity and expression patterns based upon 83 million nucleotides of cDNA sequence. Nature 660 7566098
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2000 Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis. Nature cell biology 620 10854321
2004 Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3. Cell 587 14980220
1997 Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature 577 9024662
2008 BAX activation is initiated at a novel interaction site. Nature 574 18948948
2001 Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells. The Journal of biological chemistry 566 11136736
1998 Regulated targeting of BAX to mitochondria. The Journal of cell biology 535 9763432
2006 Role of Bax and Bak in mitochondrial morphogenesis. Nature 519 17035996
2003 Humanin peptide suppresses apoptosis by interfering with Bax activation. Nature 509 12732850
2011 Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosol. Cell 503 21458670
2009 Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis. Molecular cell 499 19917256
2003 JNK-mediated BIM phosphorylation potentiates BAX-dependent apoptosis. Neuron 433 12818176
2010 Molecular biology of Bax and Bak activation and action. Biochimica et biophysica acta 411 21195116
2003 p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation. The Journal of biological chemistry 307 14634023
2001 Prion protein protects human neurons against Bax-mediated apoptosis. The Journal of biological chemistry 289 11522774
1998 Bax involvement in p53-mediated neuronal cell death. The Journal of neuroscience : the official journal of the Society for Neuroscience 281 9454845
2002 Deficiency in Bak and Bax perturbs thymic selection and lymphoid homeostasis. Nature immunology 246 12244308
2006 How do Bax and Bak lead to permeabilization of the outer mitochondrial membrane? Current opinion in cell biology 234 17046225
2008 Bid: a Bax-like BH3 protein. Oncogene 233 19641510
2021 Physiological and pharmacological modulation of BAX. Trends in pharmacological sciences 225 34848097
2006 Bcl-2 changes conformation to inhibit Bax oligomerization. The EMBO journal 219 16642033
2007 The pathological role of Bax in cisplatin nephrotoxicity. Kidney international 196 17410096
2014 Structural model of active Bax at the membrane. Molecular cell 185 25458844
2015 Direct Activation of Bax Protein for Cancer Therapy. Medicinal research reviews 183 26395559
2001 Mammalian Bax-induced plant cell death can be down-regulated by overexpression of Arabidopsis Bax Inhibitor-1 (AtBI-1). Proceedings of the National Academy of Sciences of the United States of America 175 11593047
2014 Mitochondrial shape governs BAX-induced membrane permeabilization and apoptosis. Molecular cell 172 25482509
2008 TCTP protects from apoptotic cell death by antagonizing bax function. Cell death and differentiation 167 18274553
1998 Bax. The pro-apoptotic Bcl-2 family member, Bax. The international journal of biochemistry & cell biology 159 9695020
2016 Bax and Bak Pores: Are We Closing the Circle? Trends in cell biology 152 27932064
2018 VDAC2 enables BAX to mediate apoptosis and limit tumor development. Nature communications 148 30478310
2003 Mitochondrial membrane permeabilisation by Bax/Bak. Biochemical and biophysical research communications 146 12729579
2005 HSP60, Bax, apoptosis and the heart. Journal of cellular and molecular medicine 145 15784164
1997 Bax- and Bak-induced cell death in the fission yeast Schizosaccharomyces pombe. Molecular biology of the cell 137 9190211
2012 Direct and selective small-molecule activation of proapoptotic BAX. Nature chemical biology 135 22634637
2010 Fragmented mitochondria are sensitized to Bax insertion and activation during apoptosis. American journal of physiology. Cell physiology 134 21160028
1998 Nuclear targeting of Bax during apoptosis in human colorectal cancer cells. Oncogene 126 9747879
2005 The RASSF1A tumor suppressor activates Bax via MOAP-1. The Journal of biological chemistry 118 16344548
2022 DRP1 interacts directly with BAX to induce its activation and apoptosis. The EMBO journal 117 35023587
2015 Inhibition of Pro-apoptotic BAX by a noncanonical interaction mechanism. Molecular cell 117 25684204
2016 Physiological and Pharmacological Control of BAK, BAX, and Beyond. Trends in cell biology 114 27498846
2000 BID-dependent and BID-independent pathways for BAX insertion into mitochondria. Cell death and differentiation 102 11139284
2005 MAP-1 is a mitochondrial effector of Bax. Proceedings of the National Academy of Sciences of the United States of America 100 16199525
2018 Parkin inhibits BAK and BAX apoptotic function by distinct mechanisms during mitophagy. The EMBO journal 91 30573668
2012 Inhibition of Bax protects neuronal cells from oligomeric Aβ neurotoxicity. Cell death & disease 89 22592316
2011 HDAC6 deacetylates Ku70 and regulates Ku70-Bax binding in neuroblastoma. Neoplasia (New York, N.Y.) 88 21847364
2010 BAX-dependent and BAX-independent regulation of Kiss1 neuron development in mice. Endocrinology 87 20926580
2019 Small-molecule allosteric inhibitors of BAX. Nature chemical biology 83 30718816
2015 DRAM1 regulates apoptosis through increasing protein levels and lysosomal localization of BAX. Cell death & disease 83 25633293
2018 Phosphorylation switches Bax from promoting to inhibiting apoptosis thereby increasing drug resistance. EMBO reports 81 29987135
2007 Bax-inhibiting peptides derived from Ku70 and cell-penetrating pentapeptides. Biochemical Society transactions 80 17635151
2019 Targeting BAX to drug death directly. Nature chemical biology 77 31209350
2007 Cathepsin D-Bax death pathway in oxidative stressed neuroblastoma cells. Free radical biology & medicine 76 17395004
2004 Bax-inhibiting peptide derived from mouse and rat Ku70. Biochemical and biophysical research communications 75 15358121
2002 Biphasic translocation of Bax to mitochondria. The Biochemical journal 75 12097139
2002 Bak and Bax function to limit adenovirus replication through apoptosis induction. Journal of virology 73 11932420
2016 An Autoinhibited Dimeric Form of BAX Regulates the BAX Activation Pathway. Molecular cell 71 27425408
2006 Nucleophosmin is a novel Bax chaperone that regulates apoptotic cell death. Oncogene 71 17072349
2016 The porin VDAC2 is the mitochondrial platform for Bax retrotranslocation. Scientific reports 70 27620692
2010 Multistep and multitask Bax activation. Mitochondrion 68 20709625
2006 Androgen and its receptor promote Bax-mediated apoptosis. Molecular and cellular biology 68 16479009
2009 Hydrogen peroxide-induced Akt phosphorylation regulates Bax activation. Biochimie 66 19278624
2011 Bax inhibitor 1 in apoptosis and disease. Oncogene 65 21297665
2009 PUMA promotes Bax translocation by both directly interacting with Bax and by competitive binding to Bcl-X L during UV-induced apoptosis. Molecular biology of the cell 65 19439449
2014 BCL2 and related prosurvival proteins require BAK1 and BAX to affect autophagy. Autophagy 64 24991825
2002 Bax, Bcl-2, and p53 expression in endometrial cancer. Gynecologic oncology 63 12217750
2007 Protein kinase Czeta abrogates the proapoptotic function of Bax through phosphorylation. The Journal of biological chemistry 60 17525161
2017 Pore formation by dimeric Bak and Bax: an unusual pore? Philosophical transactions of the Royal Society of London. Series B, Biological sciences 59 28630157
2000 Bcl-xS and Bax induce different apoptotic pathways in PC12 cells. Oncogene 59 10777212
2009 Apoptosis commitment and activation of mitochondrial Bax during anoikis is regulated by p38MAPK. Cell death and differentiation 58 19662026
2010 Relationship between apoptotic markers (Bax and Bcl-2) and biochemical markers in type 2 diabetes mellitus. Singapore medical journal 57 20200776
2012 Structural mechanism of Bax inhibition by cytomegalovirus protein vMIA. Proceedings of the National Academy of Sciences of the United States of America 55 23213219
2014 Activation of Bax in three models of retinitis pigmentosa. Investigative ophthalmology & visual science 54 24825107
2024 Lipid unsaturation promotes BAX and BAK pore activity during apoptosis. Nature communications 52 38830851
2022 BAX and BAK dynamics control mitochondrial DNA release during apoptosis. Cell death and differentiation 49 35347233
2008 Apoptosis: Stabbed in the BAX. Nature 49 18948940
2021 Eltrombopag directly inhibits BAX and prevents cell death. Nature communications 48 33602934
2016 Natural pyrethrins induces apoptosis in human hepatocyte cells via Bax- and Bcl-2-mediated mitochondrial pathway. Chemico-biological interactions 48 27939866
2017 Apoptotic foci at mitochondria: in and around Bax pores. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 47 28630156
2010 The p53-, Bax- and p21-dependent inhibition of colon cancer cell growth by 5-hydroxy polymethoxyflavones. Molecular nutrition & food research 47 21462329
2019 Completion of BAX recruitment correlates with mitochondrial fission during apoptosis. Scientific reports 46 31719602
2013 Hsp90 inhibitors promote p53-dependent apoptosis through PUMA and Bax. Molecular cancer therapeutics 46 23966620
2015 Regulation of Bax/mitochondria interaction by AKT. FEBS letters 45 26763134
1996 Bax homodimerization is not required for Bax to accelerate chemotherapy-induced cell death. The Journal of biological chemistry 45 8943258
2008 Higher expression of Bax in regulatory T cells increases vascular inflammation. Frontiers in bioscience : a journal and virtual library 43 18508723
2007 Mcl-1 determines the Bax dependency of Nbk/Bik-induced apoptosis. The Journal of cell biology 43 18025305
2002 Cell death, Bcl-2, Bax, and the cerebellum. Cerebellum (London, England) 43 12879966
2010 Prostaglandins antagonistically control Bax activation during apoptosis. Cell death and differentiation 42 20966963
2018 Ensemble Properties of Bax Determine Its Function. Structure (London, England : 1993) 41 30122452
2014 P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism. Human molecular genetics 41 24876160
2009 Bax activates endophilin B1 oligomerization and lipid membrane vesiculation. The Journal of biological chemistry 41 19805544
2000 Characterization of Bax-sigma, a cell death-inducing isoform of Bax. Biochemical and biophysical research communications 40 10772918
2020 BAX inhibitor-1: between stress and survival. The FEBS journal 39 31841271
2012 Zerumbone causes Bax- and Bak-mediated apoptosis in human breast cancer cells and inhibits orthotopic xenograft growth in vivo. Breast cancer research and treatment 39 23053663
2017 Allosteric sensitization of proapoptotic BAX. Nature chemical biology 38 28692068
2008 Cholesterol effects on BAX pore activation. Journal of molecular biology 38 18590739
1999 p53 and Bax: putative death factors in taste cell turnover. The Journal of comparative neurology 38 10464378
2023 Mitophagy restricts BAX/BAK-independent, Parkin-mediated apoptosis. Science advances 37 37224250
2011 Bid and Bax are involved in granulosa cell apoptosis during follicular atresia in porcine ovaries. The Journal of reproduction and development 37 21441714
2008 Mitochondria potential, bax "activation," and programmed cell death. Methods in molecular biology (Clifton, N.J.) 37 18175815
2012 A BAX/BAK and cyclophilin D-independent intrinsic apoptosis pathway. PloS one 35 22719850
2006 Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma. Cancer 34 16353209
2004 Bim, Bad, and Bax: a deadly combination in epileptic seizures. The Journal of clinical investigation 34 15057301