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
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
A novel adenovirus E1B19K-binding protein B5 inhibits apoptosis induced by Nip3 by forming a heterodimer through the C-terminal hydrophobic region.
Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis.
Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis.
High-throughput methods to detect dimerization of Bcl-2 family proteins.
Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function.
Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.
The vaccinia virus protein F1L interacts with Bim and inhibits activation of the pro-apoptotic protein Bax.
Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak.
ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
A novel BH3 ligand that selectively targets Mcl-1 reveals that apoptosis can proceed without Mcl-1 degradation.
RACK1 and CIS mediate the degradation of BimEL in cancer cells.
Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.
BAX activation is initiated at a novel interaction site.
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.
Mcl-1-Bim complexes accommodate surprising point mutations via minor structural changes.
Noxa is necessary for hydrogen peroxide-induced caspase-dependent cell death.
Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis.
The fast-mobility isoform of mouse Mcl-1 is a mitochondrial matrix-localized protein with attenuated anti-apoptotic activity.
BH3 domains other than Bim and Bid can directly activate Bax/Bak.
Mcl-1 is critical for survival in a subgroup of non-small-cell lung cancer cell lines.
Mutation to Bax beyond the BH3 domain disrupts interactions with pro-survival proteins and promotes apoptosis.
Role of bile salt in regulating Mcl-1 phosphorylation and chemoresistance in hepatocellular carcinoma cells.
Role of Bim in apoptosis induced in H460 lung tumor cells by the spindle poison Combretastatin-A4.
The unfolded protein response: integrating stress signals through the stress sensor IRE1α.
The anti-apoptotic Bcl-B protein inhibits BECN1-dependent autophagic cell death.
Chemical genomics identifies small-molecule MCL1 repressors and BCL-xL as a predictor of MCL1 dependency.
CHOP potentially co-operates with FOXO3a in neuronal cells to regulate PUMA and BIM expression in response to ER stress.
The restricted binding repertoire of Bcl-B leaves Bim as the universal BH3-only prosurvival Bcl-2 protein antagonist.
Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models.
Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis.
Polyubiquitination and proteasomal turnover controls the anti-apoptotic activity of Bcl-B.
Targeting BCL-2 with the BH3 mimetic ABT-199 in estrogen receptor-positive breast cancer.
Structure homology and interaction redundancy for discovering virus-host protein interactions.
A proteome-scale map of the human interactome network.
BAX-induced apoptosis can be initiated through a conformational selection mechanism.
Small-Molecule Bcl2 BH4 Antagonist for Lung Cancer Therapy.
Exploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy Combination.
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.
Multimodal cell maps as a foundation for structural and functional genomics.
BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with diverse antiapoptotic Bcl-2 members.
Phosphorylation of BIM by JNK
Translocation of BIM to mitochondria
JNK phosphorylates BIM, BAD and other targets
BH3 only proteins associate with and inactivate anti-apoptotic BCL-XL
BH3-only proteins associate with and inactivate anti-apoptotic BCL-2
BCL2L11 (BIM) gene expression
BCL2L11 (BIM) gene transcription is stimulated by RUNX3
FOXO3-dependent BCL2L11 gene expression
BCL2L11 UniProtKB record O43521
Manual BCL2L11 curation notes
The NF-kappaB regulator Bcl-3 and the BH3-only proteins Bim and Puma control the death of activated T cells.