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Protein / target

Bcl2-associated agonist of cell death

Encoded byBADQ92934Homo sapiensSwiss-Prot
UniProt: Q92934Ensembl: ENSG00000002330HGNC: HGNC:936NCBI Gene: 572
Small-molecule tractable
Druggability
High-Quality Ligand
1
Research papers

Protein at a glance

Biological role

Cysteine-type endopeptidase activator

Strongest disease association

Alzheimer's Disease

Via encoding gene BAD · Genetic evidence · score 0.13

Research activity

Emerging research

1 papers · latest 1999

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Promotes cell death.

View complete UniProt function annotation

Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways

Subcellular location

Mitochondrion outer membraneCytoplasm
Domains and Gene Ontology detail (33)

Gene Ontology

  • CBAD-BCL-2 complex
  • Ccytosol
  • Cmitochondrial outer membrane
  • Cmitochondrion
  • Fcysteine-type endopeptidase activator activity
  • Flipid binding
  • Fphospholipid binding
  • Fprotein kinase binding
  • Fprotein phosphatase binding
  • PADP metabolic process
  • Papoptotic process
  • PATP metabolic process

168 aa · 18 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Growth-factor signallingUniProtApoptosis & cell deathGOMetabolic enzyme activityGO
View supporting evidence

Growth-factor signalling

  • ·Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W,…

Apoptosis & cell death

  • ·apoptotic process
  • ·negative regulation of apoptotic process
  • ·positive regulation of apoptotic process

Metabolic enzyme activity

  • ·ADP metabolic process
  • ·ATP metabolic process

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene BAD

Gene-level evidence surfaced through the gene BAD that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Neurodegenerative Diseases
0.33Preliminary

Pathway evidence dominant · Open Targets 0.49 · no direct causal or clinical evidence

Alzheimer's Disease
0.23Preliminary

Genetic evidence dominant · Open Targets 0.11

Arthritis, Rheumatoid
0.21Preliminary

Genetic evidence dominant · Open Targets 0.10

Infections
0.12Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Neoplasms
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

View evidence synthesis (5)
Neurodegenerative DiseasesPreliminary
0.33
agreement 0.15–0.50
Pathway97%Literature3%

Open Targets aggregate 0.49 · 2 independent evidence families · no direct causal or clinical evidence

Alzheimer's DiseasePreliminary
0.23
agreement 0.09–0.36
Genetic55%Literature45%

Open Targets aggregate 0.11 · 2 independent evidence families

Arthritis, RheumatoidPreliminary
0.21
agreement 0.07–0.35
Genetic56%Literature44%

Open Targets aggregate 0.10 · 2 independent evidence families

InfectionsPreliminary
0.12
agreement 0.00–0.39
Literature100%

Open Targets aggregate 0.09 · 1 independent evidence family · no direct causal or clinical evidence

NeoplasmsPreliminary
0.11
agreement 0.00–0.38
Literature100%

Open Targets aggregate 0.09 · 1 independent evidence family · no direct causal or clinical evidence

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Neurodegenerative Diseases0.49
Alzheimer's Disease0.11
Arthritis, Rheumatoid0.10
Infections0.09
Neoplasms0.09
Carcinoma, Hepatocellular0.09
Carcinoma, Non-Small-Cell Lung0.08
Prostate carcinoma0.08

Tractability

Small molecules — Emerging

Feasibility evidence (high-quality ligand and druggable family) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (half-life data and small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (4)
SM · High-Quality LigandSM · Druggable FamilyPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of transcription factor activityToxCast

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 1999

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Cellular survival: a play in three Akts.3,130 cites

Datta SR · Genes & development · 1999

Recent

Cellular survival: a play in three Akts.

Datta SR · Genes & development · 1999

Europe PMC papers linked directly to this protein.