Gene Ontology annotation through association of InterPro records with GO terms

Annotation inferences using phylogenetic trees

Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping

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

Automatic assignment of GO terms using logical inference, based on on inter-ontology links

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods

Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC.

Interaction of Alzheimer's presenilin-1 and presenilin-2 with Bcl-X(L). A potential role in modulating the threshold of cell death.

MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain.

Bcl-G, a novel pro-apoptotic member of the Bcl-2 family.

MAP-1, a novel proapoptotic protein containing a BH3-like motif that associates with Bax through its Bcl-2 homology domains.

A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl-2 on endoplasmic reticulum and reduces their anti-apoptotic activity.

Bcl-B, a novel Bcl-2 family member that differentially binds and regulates Bax and Bak.

PUMA induces the rapid apoptosis of colorectal cancer cells.

BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis.

The association of Aiolos transcription factor and Bcl-xL is involved in the control of apoptosis.

c-Abl tyrosine kinase regulates the human Rad9 checkpoint protein in response to DNA damage.

Siva-1 binds to and inhibits BCL-X(L)-mediated protection against UV radiation-induced apoptosis.

p53 has a direct apoptogenic role at the mitochondria.

HSpin1, a transmembrane protein interacting with Bcl-2/Bcl-xL, induces a caspase-independent autophagic cell death.

The Siva-1 putative amphipathic helical region (SAH) is sufficient to bind to BCL-XL and sensitize cells to UV radiation induced apoptosis.

Human alphaA- and alphaB-crystallins bind to Bax and Bcl-X(S) to sequester their translocation during staurosporine-induced apoptosis.

FAST is a BCL-X(L)-associated mitochondrial protein.

Towards a proteome-scale map of the human protein-protein interaction network.

PUMA Dissociates Bax and Bcl-X(L) to induce apoptosis in colon cancer cells.

Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.

Bcl-2 and Bcl-XL regulate proinflammatory caspase-1 activation by interaction with NALP1.

Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.

ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.

An empirical framework for binary interactome mapping.

DAP-kinase-mediated phosphorylation on the BH3 domain of beclin 1 promotes dissociation of beclin 1 from Bcl-XL and induction of autophagy.

Transcriptomic and proteomic approach to studying SNX-2112-induced K562 cells apoptosis and anti-leukemia activity in K562-NOD/SCID mice.

Antagonism of Beclin 1-dependent autophagy by BCL-2 at the endoplasmic reticulum requires NAF-1.

RACK1 promotes Bax oligomerization and dissociates the interaction of Bax and Bcl-XL.

Regulation of cell death in human fetal and adult ovaries--role of Bok and Bcl-X(L).

BH3 domains other than Bim and Bid can directly activate Bax/Bak.

Pore-forming activity of BAD is regulated by specific phosphorylation and structural transitions of the C-terminal part.

Mutation to Bax beyond the BH3 domain disrupts interactions with pro-survival proteins and promotes apoptosis.

Structural changes in the BH3 domain of SOUL protein upon interaction with the anti-apoptotic protein Bcl-xL.

Bcl-xL phosphorylation at Ser49 by polo kinase 3 during cell cycle progression and checkpoints.

Protein oligomerization mediated by the transmembrane carboxyl terminal domain of Bcl-XL.

Toward an understanding of the protein interaction network of the human liver.

The anti-apoptotic Bcl-B protein inhibits BECN1-dependent autophagic cell death.

Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.

Plasminogen kringle 5 induces endothelial cell apoptosis by triggering a voltage-dependent anion channel 1 (VDAC1) positive feedback loop.

A proteome-scale map of the human interactome network.

Lifeguard Inhibits Fas Ligand-mediated Endoplasmic Reticulum-Calcium Release Mandatory for Apoptosis in Type II Apoptotic Cells.

Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing.

The deubiquitinase Usp27x stabilizes the BH3-only protein Bim and enhances apoptosis.

Pooled-matrix protein interaction screens using Barcode Fusion Genetics.

Transmembrane E3 ligase RNF183 mediates ER stress-induced apoptosis by degrading Bcl-xL.

LuTHy: a double-readout bioluminescence-based two-hybrid technology for quantitative mapping of protein-protein interactions in mammalian cells.

Maximizing binary interactome mapping with a minimal number of assays.

Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.

Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).

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.

Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.

AI-guided pipeline for protein-protein interaction drug discovery identifies a SARS-CoV-2 inhibitor.

Multimodal cell maps as a foundation for structural and functional genomics.

Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal.

bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death.

The apoptosis and proliferation of SAC-activated B cells by IL-10 are associated with changes in Bcl-2, Bcl-xL, and Mcl-1 expression.

BH3 domain of BAD is required for heterodimerization with BCL-XL and pro-apoptotic activity.

Dimerization properties of human BAD. Identification of a BH-3 domain and analysis of its binding to mutant BCL-2 and BCL-XL proteins.

Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria.

Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria.

BH3 only proteins associate with and inactivate anti-apoptotic BCL-XL

Expression of BCL2, BCL2L1

Bcl-2 and Bcl-XL bind NLRP1

pS181-S-Farn-Me KRAS4B binds BCL2L1

FLT3 ITD- and STAT5-dependent BCL2L1 gene expression

SARS-CoV-1 E binds BCL2L1

SARS-CoV-1 7a binds BCL2L1

NFE2L2 dependent BCL2L1 expression

Deep research report on BCL2L1

Deep research report on BCL2L1 (falcon provider)

BCL-X(L) inhibitors enhance the apoptotic efficacy of BRAF inhibitors in BRAF(V600E) colorectal cancer.

Modification of BCLX pre-mRNA splicing has antitumor efficacy alone or in combination with radiotherapy in human glioblastoma cells.

CBFA2T3::GLIS2 pediatric acute megakaryoblastic leukemia is sensitive to BCL-XL inhibition by navitoclax and DT2216.