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Protein / target

Serum response factor

Encoded bySRFP11831Homo sapiensSwiss-Prot
1
Research papers

Protein at a glance

Biological role

Sequence-specific double-stranded DNA binding

Strongest disease association

Neurodegenerative Diseases

Via encoding gene SRF · Pathway evidence · score 0.55

Research activity

Emerging research

1 papers · latest 1996

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

SRF is a transcription factor that binds to the serum response element (SRE), a short sequence of dyad symmetry located 300 bp to the 5' of the site of transcription initiation of some genes (such as FOS).

View complete UniProt function annotation

SRF is a transcription factor that binds to the serum response element (SRE), a short sequence of dyad symmetry located 300 bp to the 5' of the site of transcription initiation of some genes (such as FOS). Together with MRTFA transcription coactivator, controls expression of genes regulating the cytoskeleton during development, morphogenesis and cell migration. The SRF-MRTFA complex activity responds to Rho GTPase-induced changes in cellular globular actin (G-actin) concentration, thereby coupling cytoskeletal gene expression to cytoskeletal dynamics. Required for cardiac differentiation and maturation

Subcellular location

Nucleus
Domains and Gene Ontology detail (45)

Domains & features

MADS-box

Gene Ontology

  • Cchromatin
  • Ccytoplasm
  • Cnucleoplasm
  • Cnucleus
  • Fchromatin DNA binding
  • 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 factor binding
  • Fhistone deacetylase binding
  • Fprimary miRNA binding
  • Fprotein homodimerization activity

508 aa · 52 kDa

Biological roles

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

Cell migrationUniProt · GOCell proliferation & survivalGOTranscriptional regulationUniProt · GO
View supporting evidence

Cell migration

  • ·SRF is a transcription factor that binds to the serum response element (SRE), a short se…
  • ·cell migration involved in sprouting angiogenesis
  • ·negative regulation of cell migration

Cell proliferation & survival

  • ·negative regulation of cell population proliferation

Transcriptional regulation

  • ·SRF is a transcription factor that binds to the serum response element (SRE), a short se…
  • ·DNA-binding transcription activator activity, RNA polymerase II-specific
  • ·DNA-binding transcription factor activity
  • ·DNA-binding transcription factor 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 SRF

Gene-level evidence surfaced through the gene SRF 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
0.37Preliminary

Pathway evidence dominant · Open Targets 0.55 · no direct causal or clinical evidence

Carcinoma, Hepatocellular
0.13Preliminary

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

Neoplasms
0.13Preliminary

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

Infections
0.10Preliminary

Literature evidence dominant · Open Targets 0.08 · no direct causal or clinical evidence

Prostate carcinoma
0.10Preliminary

Literature evidence dominant · Open Targets 0.08 · no direct causal or clinical evidence

View evidence synthesis (5)
Neurodegenerative DiseasesPreliminary
0.37
agreement 0.190.55
Pathway97%Literature3%

Open Targets aggregate 0.55 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, HepatocellularPreliminary
0.13
agreement 0.000.40
Literature100%

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

NeoplasmsPreliminary
0.13
agreement 0.000.40
Literature100%

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

InfectionsPreliminary
0.10
agreement 0.000.38
Literature100%

Open Targets aggregate 0.08 · 1 independent evidence family · no direct causal or clinical evidence

Prostate carcinomaPreliminary
0.10
agreement 0.000.37
Literature100%

Open Targets aggregate 0.08 · 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 Diseases0.55
Carcinoma, Hepatocellular0.11
Neoplasms0.11
Infections0.08
Prostate carcinoma0.08
Prostatic Neoplasms0.08

Research activity

1 papers · to 1996

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

Most cited

Xia Z · The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996

Recent

Calcium influx via the NMDA receptor induces immediate early gene transcription by a MAP kinase/ERK-dependent mechanism.

Xia Z · The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996

Europe PMC papers linked directly to this protein.