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Protein / target

Glial fibrillary acidic protein

Encoded byGFAPP14136Homo sapiensSwiss-Prot
Degrader-tractable
Druggability
Half-life Data
19
Research papers

Protein at a glance

Biological role

Structural constituent of cytoskeleton

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene GFAP · Genetic evidence · score 0.74

Research activity

Emerging research

19 papers · latest 2025

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

GFAP, a class-III intermediate filament, is a cell-specific marker that, during the development of the central nervous system, distinguishes astrocytes from other glial cells

Subcellular location

Cytoplasm
Domains and Gene Ontology detail (20)

Domains & features

IF rod

Gene Ontology

  • Castrocyte end-foot
  • Ccell body
  • Ccell projection
  • Ccytoplasm
  • Ccytoplasmic side of lysosomal membrane
  • Ccytosol
  • Cintermediate filament
  • Cintermediate filament cytoskeleton
  • Fidentical protein binding
  • Fintegrin binding
  • Fkinase binding
  • Fstructural constituent of cytoskeleton

432 aa · 50 kDa · 3 isoforms

Biological roles

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

Cell migrationGO
View supporting evidence

Cell migration

  • ·neural crest cell migration

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 GFAP

Gene-level evidence surfaced through the gene GFAP 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.

Genetic Diseases, Inborn
0.74Moderately supported

Genetic evidence dominant · Open Targets 0.45

Leukodystrophy, Metachromatic
0.52Moderately supported

Genetic evidence dominant · Open Targets 0.28

Scoliosis
0.44Limited support

Genetic evidence dominant · Open Targets 0.26

View evidence synthesis (3)
Genetic Diseases, InbornModerately supported
0.74
agreement 0.600.88
Genetic99%Literature1%

Open Targets aggregate 0.45 · 2 independent evidence families

Leukodystrophy, MetachromaticModerately supported
0.52
agreement 0.400.64
Genetic76%Animal model19%Literature5%

Open Targets aggregate 0.28 · 3 independent evidence families

ScoliosisLimited support
0.44
agreement 0.300.58
Genetic95%Literature5%

Open Targets aggregate 0.26 · 2 independent evidence families

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
Genetic Diseases, Inborn0.45
Leukodystrophy, Metachromatic0.28
Scoliosis0.26

Tractability

Protein degradersEmerging

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

View underlying tractability evidence (1)
PR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

19 papers · to 2025

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

Most cited

Faulkner JR · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004

Bushong EA · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002

Lim GP · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001

McKeon RJ · The Journal of neuroscience : the official journal of the Society for Neuroscience · 1991

Halassa MM · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007

Recent

Neuroinflammation and neurodegeneration following traumatic brain injuries.

Boulton M · Anatomical science international · 2025

Serum NfL and GFAP as biomarkers of progressive neurodegeneration in TBI.

Shahim P · Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024

Associations of Neurological Biomarkers in Serum With Gait Measures: The Cardiovascular Health Study.

Nadkarni AN · The journals of gerontology. Series A, Biological sciences and medical sciences · 2024

Europe PMC papers linked directly to this protein.