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Protein / target

Early growth response protein 1

Encoded byEGR1P18146Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
1
Clinical candidates
Degrader-tractable
Druggability
UniProt Ubiquitination
2
Research papers

Protein at a glance

Biological role

Sequence-specific double-stranded DNA binding

Strongest disease association

Atrial Fibrillation

Via encoding gene EGR1 · Genetic evidence · score 0.38

Therapeutic position

Clinically advancing target

Research activity

Emerging research

2 papers · latest 2001

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

Transcriptional regulator.

View complete UniProt function annotation

Transcriptional regulator (PubMed:20121949). Recognizes and binds to the DNA sequence 5'-GCG(T/G)GGGCG-3'(EGR-site) in the promoter region of target genes (By similarity). Binds double-stranded target DNA, irrespective of the cytosine methylation status (PubMed:25258363, PubMed:25999311). Regulates the transcription of numerous target genes, and thereby plays an important role in regulating the response to growth factors, DNA damage, and ischemia. Plays a role in the regulation of cell survival, proliferation and cell death. Activates expression of p53/TP53 and TGFB1, and thereby helps prevent tumor formation. Required for normal progress through mitosis and normal proliferation of hepatocytes after partial hepatectomy. Mediates responses to ischemia and hypoxia; regulates the expression of proteins such as IL1B and CXCL2 that are involved in inflammatory processes and development of tissue damage after ischemia. Regulates biosynthesis of luteinizing hormone (LHB) in the pituitary (By similarity). Regulates the amplitude of the expression rhythms of clock genes: BMAL1, PER2 and NR1D1 in the liver via the activation of PER1 (clock repressor) transcription. Regulates the rhythmic expression of core-clock gene BMAL1 in the suprachiasmatic nucleus (SCN) (By similarity)

Subcellular location

NucleusCytoplasm
Domains and Gene Ontology detail (48)

Gene Ontology

  • Cchromatin
  • Ccytoplasm
  • Cnucleoplasm
  • Cnucleus
  • FDNA binding
  • FDNA-binding transcription activator activity, RNA polymerase II-specific
  • FDNA-binding transcription factor activity
  • FDNA-binding transcription factor activity, RNA polymerase II-specific
  • Fdouble-stranded methylated DNA binding
  • Fhemi-methylated DNA-binding
  • Fhistone acetyltransferase binding
  • Fpromoter-specific chromatin binding

543 aa · 58 kDa

Biological roles

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

Cell proliferation & survivalUniProtTranscriptional regulationUniProt · GOImmune signallingGO
View supporting evidence

Cell proliferation & survival

  • ·Transcriptional regulator (PubMed:20121949). Recognizes and binds to the DNA sequence 5'…

Transcriptional regulation

  • ·Transcriptional regulator (PubMed:20121949). Recognizes and binds to the DNA sequence 5'…
  • ·DNA-binding transcription activator activity, RNA polymerase II-specific
  • ·DNA-binding transcription factor activity
  • ·DNA-binding transcription factor activity, RNA polymerase II-specific

Immune signalling

  • ·cellular response to interleukin-8
  • ·interleukin-1-mediated signaling pathway
  • ·positive regulation of interleukin-1 beta production

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 EGR1

Gene-level evidence surfaced through the gene EGR1that 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.

Atrial Fibrillation
0.43Limited support

Genetic evidence dominant · Open Targets 0.25

Diabetes Mellitus, Type 2
0.28Limited support

Genetic evidence dominant · Open Targets 0.16

Neurodegenerative Diseases
0.25Preliminary

Pathway evidence dominant · Open Targets 0.37 · no direct causal or clinical evidence

Breast Neoplasms
0.22Preliminary

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

Carcinoma, Hepatocellular
0.20Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

View evidence synthesis (5)
Atrial FibrillationLimited support
0.43
agreement 0.290.57
Genetic80%Literature20%

Open Targets aggregate 0.25 · 2 independent evidence families

Diabetes Mellitus, Type 2Limited support
0.28
agreement 0.140.42
Genetic86%Literature14%

Open Targets aggregate 0.16 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary
0.25
agreement 0.070.43
Pathway97%Literature3%

Open Targets aggregate 0.37 · 2 independent evidence families · no direct causal or clinical evidence

Breast NeoplasmsPreliminary
0.22
agreement 0.030.41
Literature58%RNA expression42%

Open Targets aggregate 0.11 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, HepatocellularPreliminary
0.20
agreement 0.010.39
Literature68%RNA expression32%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. 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 Diseases0.37
Atrial Fibrillation0.25
Diabetes Mellitus, Type 20.16
Carcinoma, Hepatocellular0.12
Carcinoma, Squamous Cell0.12
Neoplasms0.12
Breast Neoplasms0.11
Infections0.11
Lung carcinoma0.11

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (1)
BRIVOLIGIDEPhase 2

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Protein degradersEmerging

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

Other modalitiesStrong

Advanced Clinical support this modality.

View underlying tractability evidence (2)
PR · UniProt UbiquitinationOC · Advanced Clinical

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

2 papers · to 2001

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

Most cited

Guzowski JF · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001

Recent

Europe PMC papers linked directly to this protein.