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Protein / target

DNA repair protein RAD51 homolog 1

Encoded byRAD51Q06609Homo sapiensSwiss-Prot
UniProt: Q06609Ensembl: ENSG00000051180HGNC: HGNC:9817NCBI Gene: 5888
Small-molecule tractable
Druggability
Structure with Ligand
2
Research papers

Protein at a glance

Biological role

ATP-dependent DNA damage sensor

Strongest disease association

Fanconi Anemia

Via encoding gene RAD51 · Genetic literature evidence · score 0.87

Research activity

Emerging research

2 papers · latest 2021

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

Homologous DNA recombinase that catalyzes strand exchange, a key step in DNA repair through homologous recombination (HR).

View complete UniProt function annotation

Homologous DNA recombinase that catalyzes strand exchange, a key step in DNA repair through homologous recombination (HR) (PubMed:12205100, PubMed:12442171, PubMed:15937124, PubMed:17515904, PubMed:17515903, PubMed:18417535, PubMed:19303847, PubMed:20231364, PubMed:20348101, PubMed:22325354, PubMed:23509288, PubMed:23754376, PubMed:24141787, PubMed:26681308, PubMed:27941124, PubMed:28575658, PubMed:32640219, PubMed:37499663, PubMed:38509361, PubMed:7988572). Binds to single-stranded DNA (ssDNA) in an ATP-dependent manner to form nucleoprotein filaments which are essential for the homology search and strand exchange (PubMed:12205100, PubMed:15937124, PubMed:17515904, PubMed:17515903, PubMed:18417535, PubMed:19303847, PubMed:15226506, PubMed:20231364, PubMed:20348101, PubMed:23509288, PubMed:23754376, PubMed:26681308, PubMed:28575658, PubMed:37499663, PubMed:39636933, PubMed:41166468, PubMed:38509361, PubMed:7988572). Catalyzes the recognition of homology and strand exchange between homologous DNA partners to form a joint molecule between a processed DNA break and the repair template (PubMed:12205100, PubMed:18417535, PubMed:19303847, PubMed:20231364, PubMed:20348101, PubMed:23509288, PubMed:23754376, PubMed:26681308, PubMed:28575658, PubMed:38459011). RAD51 targeting to ssDNA promotes removal of replication protein-A (RPA) from ssDNA and stabilization of RAD51-ssDNA filaments by blocking ATP hydrolysis (PubMed:20729859). Nucleosomal DNA is peeled from the histone surface by the RAD51 filament (PubMed:38509361). Recruited to resolve stalled replication forks during replication stress (PubMed:27797818, PubMed:31844045). Also required for homologous recombination during meiosis by acting as an non-catalytic accessory factor for DMC1 recombinase, enabling proper chromosome pairing and crossing over (By similarity). Plays a role in regulating mitochondrial DNA copy number under conditions of oxidative stress in the presence of RAD51C and XRCC3 (PubMed:20413593). Also involved in interstrand cross-link repair (PubMed:26253028)

Subcellular location

ChromosomeNucleusCytoplasmCytoplasm, perinuclear regionMitochondrion matrixCytoplasm, cytoskeleton, microtubule organizing center, centrosome
Domains and Gene Ontology detail (59)

Domains & features

HhH

Gene Ontology

  • Ccentrosome
  • Cchromatin
  • Cchromosome, telomeric region
  • Ccondensed chromosome
  • Ccondensed nuclear chromosome
  • Ccytoplasm
  • Ccytosol
  • Clateral element
  • Cmitochondrial matrix
  • Cmitochondrion
  • Cnuclear chromosome
  • Cnucleolus

339 aa · 37 kDa · 4 isoforms

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 RAD51

Gene-level evidence surfaced through the gene RAD51 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.

Fanconi Anemia
0.71Moderately supported

Genetic literature evidence dominant · Open Targets 0.63

Genetic Diseases, Inborn
0.69Moderately supported

Genetic evidence dominant · Open Targets 0.42

Neoplasms
0.44Preliminary

Pathway evidence dominant · Open Targets 0.56 · no direct causal or clinical evidence

Alcohol drinking
0.38Limited support

Genetic evidence dominant · Open Targets 0.23

View evidence synthesis (4)
Fanconi AnemiaModerately supported
0.71
agreement 0.55–0.86
Genetic literature97%Literature4%Geneticdup

Open Targets aggregate 0.63 · 2 independent evidence families · 1 not counted as duplicate

Genetic Diseases, InbornModerately supported
0.69
agreement 0.55–0.82
Genetic99%Literature1%

Open Targets aggregate 0.42 · 2 independent evidence families

NeoplasmsPreliminary
0.44
agreement 0.26–0.62
Pathway71%Literature29%

Open Targets aggregate 0.56 · 2 independent evidence families · no direct causal or clinical evidence

Alcohol drinkingLimited support
0.38
agreement 0.26–0.50
Genetic100%

Open Targets aggregate 0.23 · 1 independent evidence family

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
Fanconi Anemia0.63
Neoplasms0.56
Genetic Diseases, Inborn0.42
Alcohol drinking0.23

Tractability

Small molecules — Emerging

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

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (6)
SM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2021

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

Most cited

Genetic mechanisms of critical illness in COVID-19.1,129 cites

Pairo-Castineira E · Nature · 2021

Combining PARP with ATR inhibition overcomes PARP inhibitor and platinum resistance in ovarian cancer models.282 cites

Kim H · Nature communications · 2020

Recent

Genetic mechanisms of critical illness in COVID-19.

Pairo-Castineira E · Nature · 2021

Combining PARP with ATR inhibition overcomes PARP inhibitor and platinum resistance in ovarian cancer models.

Kim H · Nature communications · 2020

Europe PMC papers linked directly to this protein.