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Protein / target

Tumor necrosis factor ligand superfamily member 6

Encoded byFASLGP48023Homo sapiensSwiss-Prot
UniProt: P48023Ensembl: ENSG00000117560HGNC: HGNC:11936NCBI Gene: 356
Clinical-stage
Therapeutic maturity
1
Clinical candidates
Antibody-tractable
Druggability
UniProt loc high conf
2
Research papers

Protein at a glance

Biological role

Tumor necrosis factor receptor binding

Strongest disease association

Glaucoma, Open-Angle

Via encoding gene FASLG · Genetic evidence · score 0.66

Therapeutic position

Clinically advancing target

Research activity

Emerging research

2 papers · latest 2019

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

Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells.

View complete UniProt function annotation

Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells (PubMed:26334989, PubMed:9228058). Involved in cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development (PubMed:7528780, PubMed:9228058, PubMed:9427603). Initiates fratricidal/suicidal activation-induced cell death (AICD) in antigen-activated T-cells contributing to the termination of immune responses (By similarity). TNFRSF6/FAS-mediated apoptosis also has a role in the induction of peripheral tolerance (By similarity). Binds to TNFRSF6B/DcR3, a decoy receptor that blocks apoptosis (PubMed:27806260)

Subcellular location

Cell membraneCytoplasmic vesicle lumenLysosome lumenSecretedNucleus
Domains and Gene Ontology detail (42)

Domains & features

THD

Gene Ontology

  • Ccaveola
  • Ccell surface
  • Ccytoplasmic vesicle lumen
  • Cextracellular exosome
  • Cextracellular region
  • Cextracellular space
  • Clysosomal lumen
  • Cnucleus
  • Cperinuclear region of cytoplasm
  • Cplasma membrane
  • Fcytokine activity
  • Fdeath receptor binding

281 aa · 31 kDa · 2 isoforms

Biological roles

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

Chloride transportGOGrowth-factor signallingGOCell proliferation & survivalGOImmune signallingUniProt · GOApoptosis & cell deathGOTranscriptional regulationGO
View supporting evidence

Chloride transport

  • ·intracellular chloride ion homeostasis

Growth-factor signalling

  • ·positive regulation of epidermal growth factor receptor signaling pathway

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Immune signalling

  • ·Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into…
  • ·cytokine activity
  • ·T cell apoptotic process

Apoptosis & cell death

  • ·apoptotic process
  • ·inflammatory cell apoptotic process
  • ·positive regulation of apoptotic process
  • ·positive regulation of endothelial cell apoptotic process

Transcriptional regulation

  • ·DNA-templated transcription
  • ·negative regulation of transcription by RNA polymerase II

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 FASLG

Gene-level evidence surfaced through the gene FASLGthat 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.

Glaucoma, Open-Angle
0.74Moderately supported

Genetic evidence dominant · Open Targets 0.42

Lupus Erythematosus, Systemic
0.62Moderately supported

Genetic literature evidence dominant · Open Targets 0.44

Lung Neoplasms
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

Dermatitis, Atopic
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

Celiac Disease
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

View evidence synthesis (5)
Glaucoma, Open-AngleModerately supported
0.74
agreement 0.62–0.86
Genetic74%Animal model23%Literature3%

Open Targets aggregate 0.42 · 3 independent evidence families

Lupus Erythematosus, SystemicModerately supported
0.62
agreement 0.50–0.75
Genetic literature63%Literature19%Animal model18%Geneticdup

Open Targets aggregate 0.44 · 3 independent evidence families · 1 not counted as duplicate

Lung NeoplasmsModerately supported
0.55
agreement 0.41–0.69
Genetic85%Literature15%

Open Targets aggregate 0.33 · 2 independent evidence families

Dermatitis, AtopicLimited support
0.48
agreement 0.34–0.62
Genetic97%Literature4%

Open Targets aggregate 0.29 · 2 independent evidence families

Celiac DiseaseLimited support
0.48
agreement 0.34–0.62
Genetic98%Literature2%

Open Targets aggregate 0.29 · 2 independent evidence families

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
Lupus Erythematosus, Systemic0.44
Glaucoma, Open-Angle0.42
Lung Neoplasms0.33
Dermatitis, Atopic0.29
Celiac Disease0.29
Rhinitis, Allergic0.28
Psoriasis0.27

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)
ASUNERCEPTPhase 3

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

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

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

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (5)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · UniProt UbiquitinationOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2019

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

Most cited

Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.943 cites

Brochard V · The Journal of clinical investigation · 2009

Killing Mechanisms of Chimeric Antigen Receptor (CAR) T Cells.381 cites

Benmebarek MR · International journal of molecular sciences · 2019

Recent

Killing Mechanisms of Chimeric Antigen Receptor (CAR) T Cells.

Benmebarek MR · International journal of molecular sciences · 2019

Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease.

Brochard V · The Journal of clinical investigation · 2009

Europe PMC papers linked directly to this protein.