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Protein / target

Steroid hormone receptor ERR1

Encoded byESRRAP11474Homo sapiensSwiss-Prot
UniProt: P11474Ensembl: ENSG00000173153HGNC: HGNC:3471NCBI Gene: 2101
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Sequence-specific double-stranded DNA binding

Strongest disease association

Heart Septal Defects, Ventricular

Via encoding gene ESRRA · Genetic evidence · score 0.22

Research activity

Emerging research

1 papers · latest 2024

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

Binds to an ERR-alpha response element (ERRE) containing a single consensus half-site, 5'-TNAAGGTCA-3'.

View complete UniProt function annotation

Binds to an ERR-alpha response element (ERRE) containing a single consensus half-site, 5'-TNAAGGTCA-3'. Can bind to the medium-chain acyl coenzyme A dehydrogenase (MCAD) response element NRRE-1 and may act as an important regulator of MCAD promoter. Binds to the C1 region of the lactoferrin gene promoter. Requires dimerization and the coactivator, PGC-1A, for full activity. The ERRalpha/PGC1alpha complex is a regulator of energy metabolism. Induces the expression of PERM1 in the skeletal muscle

Subcellular location

NucleusCytoplasm
Domains and Gene Ontology detail (22)

Domains & features

NR LBD

Gene Ontology

  • Cchromatin
  • Ccytoplasm
  • Cfibrillar center
  • Cnucleoplasm
  • Cnucleus
  • FDNA-binding transcription activator activity, RNA polymerase II-specific
  • FDNA-binding transcription factor activity
  • FDNA-binding transcription factor activity, RNA polymerase II-specific
  • FDNA-binding transcription repressor activity, RNA polymerase II-specific
  • Festrogen response element binding
  • Fnuclear receptor activity
  • Fnuclear steroid receptor activity

423 aa · 46 kDa · 2 isoforms

Biological roles

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

Nuclear receptor signallingGOTranscriptional regulationGO
View supporting evidence

Nuclear receptor signalling

  • ·nuclear receptor activity

Transcriptional regulation

  • ·DNA-binding transcription activator activity, RNA polymerase II-specific
  • ·DNA-binding transcription factor activity
  • ·DNA-binding transcription factor activity, RNA polymerase II-specific
  • ·DNA-binding transcription repressor activity, RNA polymerase II-specific

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 ESRRA

Gene-level evidence surfaced through the gene ESRRA 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.

Heart Septal Defects, Ventricular
0.22Preliminary

Genetic evidence dominant · Open Targets 0.13

Neoplasms
0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Prostate carcinoma
0.13Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Familial prostate cancer
0.13Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Prostatic Neoplasms
0.13Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

View evidence synthesis (5)
Heart Septal Defects, VentricularPreliminary
0.22
agreement 0.10–0.34
Genetic100%

Open Targets aggregate 0.13 · 1 independent evidence family

NeoplasmsPreliminary
0.14
agreement 0.00–0.41
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Prostate carcinomaPreliminary
0.13
agreement 0.00–0.40
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Familial prostate cancerPreliminary
0.13
agreement 0.00–0.40
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Prostatic NeoplasmsPreliminary
0.13
agreement 0.00–0.40
Literature100%

Open Targets aggregate 0.11 · 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
Heart Septal Defects, Ventricular0.13
Neoplasms0.11
Prostate carcinoma0.11
Familial prostate cancer0.11
Prostatic Neoplasms0.11

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

View underlying tractability evidence (8)
SM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketSM · Druggable FamilyPR · LiteraturePR · UniProt UbiquitinationPR · Database UbiquitinationPR · 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 2024

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

Most cited

APOE2 protects against Aβ pathology by improving neuronal mitochondrial function through ERRα signaling.9 cites

Ning Z · Cellular & molecular biology letters · 2024

Recent

APOE2 protects against Aβ pathology by improving neuronal mitochondrial function through ERRα signaling.

Ning Z · Cellular & molecular biology letters · 2024

Europe PMC papers linked directly to this protein.