Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
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
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Inhibition of Bid-induced apoptosis by Bcl-2. tBid insertion, Bax translocation, and Bax/Bak oligomerization suppressed.
Three novel Bid proteins generated by alternative splicing of the human Bid gene.
Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis.
Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function.
Inhibition of mitochondrial neural cell death pathways by protein transduction of Bcl-2 family proteins.
Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.
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.
Functional and structural studies of the vaccinia virus virulence factor N1 reveal a Bcl-2-like anti-apoptotic protein.
No death without life: vital functions of apoptotic effectors.
Mechanism of apoptosis induction by inhibition of the anti-apoptotic BCL-2 proteins.
Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements.
Autophagy protein microtubule-associated protein 1 light chain-3B (LC3B) activates extrinsic apoptosis during cigarette smoke-induced emphysema.
Heterodimerization of BAK and MCL-1 activated by detergent micelles.
BH3 domains other than Bim and Bid can directly activate Bax/Bak.
MK-STYX, a catalytically inactive phosphatase regulating mitochondrially dependent apoptosis.
Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.
Bortezomib primes neuroblastoma cells for TRAIL-induced apoptosis by linking the death receptor to the mitochondrial pathway.
Bortezomib primes glioblastoma, including glioblastoma stem cells, for TRAIL by increasing tBid stability and mitochondrial apoptosis.
Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis.
BID-induced structural changes in BAK promote apoptosis.
BAK multimerization for apoptosis, but not bid binding, is inhibited by negatively charged residue in the BAK hydrophobic groove.
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.
A proteome-scale map of the human interactome network.
PLEKHN1 promotes apoptosis by enhancing Bax-Bak hetro-oligomerization through interaction with Bid in human colon cancer.
An AMPK-caspase-6 axis controls liver damage in nonalcoholic steatohepatitis.
A reference map of the human binary protein interactome.
Humanin selectively prevents the activation of pro-apoptotic protein BID by sequestering it into fibers.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
BID: a novel BH3 domain-only death agonist.
The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4.
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors.
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis.
Sequestration of tBID by BCL-2
Granzyme-B activates BID by cleavage
tBID activates BAK protein
BAD displaces tBID from BCL-2 sequestration
Caspase-8 activates BID by cleavage
tBID activates BAX protein
Translocation of tBID to mitochondria
Myristoylation of tBID by NMT1
tBID binds to inactive BAK protein
tBID binds to inactive BAX protein
BH3 only proteins associate with and inactivate anti-apoptotic BCL-XL
TP53 stimulates BID gene expression
BID UniProtKB record P55957
Manual BID curation notes