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Protein / target

Tumor necrosis factor ligand superfamily member 9

Encoded byTNFSF9P41273Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
High-Quality Pocket
2
Research papers

Protein at a glance

Biological role

Tumor necrosis factor receptor superfamily binding

Strongest disease association

Amyotrophic Lateral Sclerosis

Via encoding gene TNFSF9 · Genetic evidence · score 0.29

Research activity

Emerging research

2 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

Cytokine that binds to TNFRSF9.

View complete UniProt function annotation

Cytokine that binds to TNFRSF9. Induces the proliferation of activated peripheral blood T-cells. May have a role in activation-induced cell death (AICD). May play a role in cognate interactions between T-cells and B-cells/macrophages

Subcellular location

Membrane
Domains and Gene Ontology detail (13)

Domains & features

THD

Gene Ontology

  • Cextracellular space
  • Cplasma membrane
  • Fcytokine activity
  • Fsignaling receptor binding
  • Ftumor necrosis factor receptor binding
  • Ftumor necrosis factor receptor superfamily binding
  • Pcell-cell signaling
  • Pimmune response
  • Ppositive regulation of activated T cell proliferation
  • Ppositive regulation of cytotoxic T cell differentiation
  • Pregulation of apoptotic process
  • Pregulation of T cell proliferation

254 aa · 27 kDa

Biological roles

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

Immune signallingUniProt · GO
View supporting evidence

Immune signalling

  • ·Cytokine that binds to TNFRSF9. Induces the proliferation of activated peripheral blood…
  • ·cytokine activity
  • ·immune response
  • ·positive regulation of activated T cell proliferation

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 TNFSF9

Gene-level evidence surfaced through the gene TNFSF9that 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.

Amyotrophic Lateral Sclerosis
0.29Limited support

Genetic evidence dominant · Open Targets 0.17

Depressive Disorder
0.28Limited support

Genetic evidence dominant · Open Targets 0.17

Neoplasms
0.14Preliminary

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

Pancreatic Neoplasms
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Melanoma
0.10Preliminary

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

View evidence synthesis (5)
Amyotrophic Lateral SclerosisLimited support
0.29
agreement 0.170.41
Genetic100%

Open Targets aggregate 0.17 · 1 independent evidence family

Depressive DisorderLimited support
0.28
agreement 0.160.40
Genetic100%

Open Targets aggregate 0.17 · 1 independent evidence family

NeoplasmsPreliminary
0.14
agreement 0.000.41
Literature100%

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

Pancreatic NeoplasmsPreliminary
0.11
agreement 0.000.38
Literature100%

Open Targets aggregate 0.09 · 1 independent evidence family · no direct causal or clinical evidence

MelanomaPreliminary
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
Amyotrophic Lateral Sclerosis0.17
Depressive Disorder0.17
Neoplasms0.11
Neurodegenerative Diseases0.11
Pancreatic Neoplasms0.09
Melanoma0.08
Colonic Neoplasms0.08

Tractability

Small moleculesEmerging

Feasibility evidence (high-quality pocket) — no clinical-stage drug of this modality recorded.

AntibodiesEmerging

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

Protein degradersEmerging

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

View underlying tractability evidence (4)
SM · High-Quality PocketAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 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

Segal NH · Clinical cancer research : an official journal of the American Association for Cancer Research · 2017

Recent

Results from an Integrated Safety Analysis of Urelumab, an Agonist Anti-CD137 Monoclonal Antibody.

Segal NH · Clinical cancer research : an official journal of the American Association for Cancer Research · 2017

Europe PMC papers linked directly to this protein.