Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria.
Structural basis of BFL-1 for its interaction with BAX and its anti-apoptotic action in mammalian and yeast cells.
SH3GLB, a new endophilin-related protein family featuring an SH3 domain.
Bcl-B, a novel Bcl-2 family member that differentially binds and regulates Bax and Bak.
Deficiency of caspase-3 in MCF7 cells blocks Bax-mediated nuclear fragmentation but not cell death.
Tumor necrosis factor-alpha induces Bax-Bak interaction and apoptosis, which is inhibited by adenovirus E1B 19K.
The G2/M regulator 14-3-3sigma prevents apoptosis through sequestration of Bax.
The expression of a new variant of the pro-apoptotic molecule Bax, Baxpsi, is correlated with an increased survival of glioblastoma multiforme patients.
Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis.
Humanin peptide suppresses apoptosis by interfering with Bax activation.
Hepatitis C virus NS5A as a potential viral Bcl-2 homologue interacts with Bax and inhibits apoptosis in hepatocellular carcinoma.
Interaction with a membrane surface triggers a reversible conformational change in Bax normally associated with induction of apoptosis.
ASC is a Bax adaptor and regulates the p53-Bax mitochondrial apoptosis pathway.
Human alphaA- and alphaB-crystallins bind to Bax and Bcl-X(S) to sequester their translocation during staurosporine-induced apoptosis.
Quantitation of mitochondrial dynamics by photolabeling of individual organelles shows that mitochondrial fusion is blocked during the Bax activation phase of apoptosis.
Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis.
BOK and NOXA are essential mediators of p53-dependent apoptosis.
Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase.
Apoptosis via the B cell antigen receptor requires Bax translocation and involves mitochondrial depolarization, cytochrome C release, and caspase-9 activation.
The permeability transition pore triggers Bax translocation to mitochondria during neuronal apoptosis.
Involvement of Noxa in cellular apoptotic responses to interferon, double-stranded RNA, and virus infection.
Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins.
Clusterin inhibits apoptosis by interacting with activated Bax.
PUMA couples the nuclear and cytoplasmic proapoptotic function of p53.
MAP-1 is a mitochondrial effector of Bax.
Nuclear translocation of the pro-apoptotic Bcl-2 family member Bok induces apoptosis.
T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio.
The endoplasmic reticulum is a key component of the plasma cell death pathway.
Interaction of F1L with the BH3 domain of Bak is responsible for inhibiting vaccinia-induced apoptosis.
Inhibition of Bax activity is crucial for the antiapoptotic function of the human papillomavirus E6 oncoprotein.
IAN family critically regulates survival and development of T lymphocytes.
PUMA Dissociates Bax and Bcl-X(L) to induce apoptosis in colon cancer cells.
Cell-based screening and validation of human novel genes associated with cell viability.
Differential contribution of Puma and Noxa in dual regulation of p53-mediated apoptotic pathways.
A stapled BID BH3 helix directly binds and activates BAX.
Vaccinia virus N1L protein resembles a B cell lymphoma-2 (Bcl-2) family protein.
Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak.
Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.
Identification of novel regulators of apoptosis using a high-throughput cell-based screen.
Functional and structural studies of the vaccinia virus virulence factor N1 reveal a Bcl-2-like anti-apoptotic protein.
ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
The mitochondrial TOM complex is required for tBid/Bax-induced cytochrome c release.
Protein kinase C-epsilon protects MCF-7 cells from TNF-mediated cell death by inhibiting Bax translocation.
Cytosolic accumulation of HSP60 during apoptosis with or without apparent mitochondrial release: evidence that its pro-apoptotic or pro-survival functions involve differential interactions with caspase-3.
No death without life: vital functions of apoptotic effectors.
Bcl-XL inhibits membrane permeabilization by competing with Bax.
Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes.
A short Nur77-derived peptide converts Bcl-2 from a protector to a killer.
BAX activation is initiated at a novel interaction site.
Apoptosis is triggered when prosurvival Bcl-2 proteins cannot restrain Bax.
Membrane binding by tBid initiates an ordered series of events culminating in membrane permeabilization by Bax.
Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements.
BimL directly neutralizes Bcl-xL to promote Bax activation during UV-induced apoptosis.
A novel pro-apoptotic function of RACK1: suppression of Src activity in the intrinsic and Akt pathways.
Bax activates endophilin B1 oligomerization and lipid membrane vesiculation.
Defining the membrane proteome of NK cells.
Mcl-1(128-350) fragment induces apoptosis through direct interaction with Bax.
IBRDC2, an IBR-type E3 ubiquitin ligase, is a regulatory factor for Bax and apoptosis activation.
Viral apoptosis is induced by IRF-3-mediated activation of Bax.
MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis.
RACK1 promotes Bax oligomerization and dissociates the interaction of Bax and Bcl-XL.
Membrane remodeling induced by the dynamin-related protein Drp1 stimulates Bax oligomerization.
Autophagy protein microtubule-associated protein 1 light chain-3B (LC3B) activates extrinsic apoptosis during cigarette smoke-induced emphysema.
Mutation to Bax beyond the BH3 domain disrupts interactions with pro-survival proteins and promotes apoptosis.
MK-STYX, a catalytically inactive phosphatase regulating mitochondrially dependent apoptosis.
Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosol.
Human nuclear clusterin mediates apoptosis by interacting with Bcl-XL through C-terminal coiled coil domain.
UV irradiation resistance-associated gene suppresses apoptosis by interfering with BAX activation.
Role of Bim in apoptosis induced in H460 lung tumor cells by the spindle poison Combretastatin-A4.
The APP intracellular domain (AICD) potentiates ER stress-induced apoptosis.
The unfolded protein response: integrating stress signals through the stress sensor IRE1α.
The cytosolic domain of human Tom22 modulates human Bax mitochondrial translocation and conformation in yeast.
The endoplasmic reticulum stress response in aging and age-related diseases.
Human Bop is a novel BH3-only member of the Bcl-2 protein family.
Structural mechanism of Bax inhibition by cytomegalovirus protein vMIA.
The restricted binding repertoire of Bcl-B leaves Bim as the universal BH3-only prosurvival Bcl-2 protein antagonist.
Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis.
The DNA-binding domain mediates both nuclear and cytosolic functions of p53.
Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.
Tom70 mediates Sendai virus-induced apoptosis on mitochondria.
Small-Molecule Bcl2 BH4 Antagonist for Lung Cancer Therapy.
An interconnected hierarchical model of cell death regulation by the BCL-2 family.
Enterovirus 71 2B Induces Cell Apoptosis by Directly Inducing the Conformational Activation of the Proapoptotic Protein Bax.
PLEKHN1 promotes apoptosis by enhancing Bax-Bak hetro-oligomerization through interaction with Bid in human colon cancer.
GSK3β‑mediated Ser156 phosphorylation modulates a BH3‑like domain in BCL2L12 during TMZ‑induced apoptosis and autophagy in glioma cells.
Humanin induces conformational changes in the apoptosis regulator BAX and sequesters it into fibers, preventing mitochondrial outer-membrane permeabilization.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
Deubiquitinating Enzyme USP12 Regulates the Pro-Apoptosis Protein Bax.
Multimodal cell maps as a foundation for structural and functional genomics.
Interaction of CED-4 with CED-3 and CED-9: a molecular framework for cell death.
A common binding site mediates heterodimerization and homodimerization of Bcl-2 family members.
Inhibition of Bax channel-forming activity by Bcl-2.
Dimerization properties of human BAD. Identification of a BH-3 domain and analysis of its binding to mutant BCL-2 and BCL-XL proteins.
The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4.
Hematopoietic malignancies demonstrate loss-of-function mutations of BAX.
Bax inhibitor-1, a mammalian apoptosis suppressor identified by functional screening in yeast.
Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria.
Identification and characterization of baxepsilon, a novel bax variant missing the BH2 and the transmembrane domains.
Translocation of activated BAX to the mitochondria
Oligomerization of BAX at the mitochondrial membrane
tBID activates BAX protein
tBID binds to inactive BAX protein
TP53 family members stimulate BAX transcription
BAX gene expression is stimulated by RUNX2