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Protein / target

Protein S100-A12

Encoded byS100A12P80511Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
High-Quality Pocket
1
Research papers

Protein at a glance

Biological role

Calcium-dependent protein binding

Strongest disease association

Periodontitis

Via encoding gene S100A12 · Genetic evidence · score 0.15

Research activity

Emerging research

1 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

S100A12 is a calcium-, zinc- and copper-binding protein which plays a prominent role in the regulation of inflammatory processes and immune response.

View complete UniProt function annotation

S100A12 is a calcium-, zinc- and copper-binding protein which plays a prominent role in the regulation of inflammatory processes and immune response. Its pro-inflammatory activity involves recruitment of leukocytes, promotion of cytokine and chemokine production, and regulation of leukocyte adhesion and migration. Acts as an alarmin or a danger associated molecular pattern (DAMP) molecule and stimulates innate immune cells via binding to receptor for advanced glycation endproducts (AGER). Binding to AGER activates the MAP-kinase and NF-kappa-B signaling pathways leading to production of pro-inflammatory cytokines and up-regulation of cell adhesion molecules ICAM1 and VCAM1. Acts as a monocyte and mast cell chemoattractant. Can stimulate mast cell degranulation and activation which generates chemokines, histamine and cytokines inducing further leukocyte recruitment to the sites of inflammation. Can inhibit the activity of matrix metalloproteinases; MMP2, MMP3 and MMP9 by chelating Zn(2+) from their active sites. Possesses filariacidal and filariastatic activity. Calcitermin possesses antifungal activity against C.albicans and is also active against E.coli and P.aeruginosa but not L.monocytogenes and S.aureus

Subcellular location

SecretedCytoplasmCytoplasm, cytoskeletonCell membrane
Domains and Gene Ontology detail (29)

Domains & features

EF-hand 1EF-hand 2

Gene Ontology

  • Ccytoplasm
  • Ccytoskeleton
  • Ccytosol
  • Cextracellular region
  • Cnucleus
  • Cplasma membrane
  • Csecretory granule lumen
  • Fcalcium ion binding
  • Fcalcium-dependent protein binding
  • Fcopper ion binding
  • Fidentical protein binding
  • FRAGE receptor binding

92 aa · 11 kDa

Biological roles

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

Cell migrationGOImmune signallingUniProt · GO
View supporting evidence

Cell migration

  • ·endothelial cell migration
  • ·monocyte chemotaxis
  • ·neutrophil chemotaxis

Immune signalling

  • ·S100A12 is a calcium-, zinc- and copper-binding protein which plays a prominent role in…
  • ·antimicrobial humoral immune response mediated by antimicrobial peptide
  • ·inflammatory response
  • ·innate immune response

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 S100A12

Gene-level evidence surfaced through the gene S100A12 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.

Periodontitis
0.24Preliminary

Genetic evidence dominant · Open Targets 0.11

Alzheimer's Disease
0.20Preliminary

Pathway evidence dominant · Open Targets 0.19 · no direct causal or clinical evidence

COVID-19
0.16Preliminary

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

Inflammatory Bowel Diseases
0.14Preliminary

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

Parkinson's Disease
0.13Preliminary

Pathway evidence dominant · Open Targets 0.18 · no direct causal or clinical evidence

View evidence synthesis (5)
PeriodontitisPreliminary
0.24
agreement 0.100.38
Genetic60%Literature40%

Open Targets aggregate 0.11 · 2 independent evidence families

Alzheimer's DiseasePreliminary
0.20
agreement 0.030.38
Pathway53%Literature48%

Open Targets aggregate 0.19 · 2 independent evidence families · no direct causal or clinical evidence

COVID-19Preliminary
0.16
agreement 0.000.35
Literature82%RNA expression18%

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

Inflammatory Bowel DiseasesPreliminary
0.14
agreement 0.000.33
Literature96%RNA expression4%

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

Parkinson's DiseasePreliminary
0.13
agreement 0.000.31
Pathway86%Literature14%

Open Targets aggregate 0.18 · 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
Alzheimer's Disease0.19
Parkinson's Disease0.18
Multiple Sclerosis0.17
Neurodegenerative Diseases0.17
Lysosomal Storage Diseases0.17
Periodontitis0.11
COVID-190.11
Inflammatory Bowel Diseases0.11
Arthritis, Rheumatoid0.10

Tractability

Small moleculesEmerging

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

AntibodiesEmerging

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

Protein degradersEmerging

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

View underlying tractability evidence (4)
SM · High-Quality PocketAB · UniProt loc high confAB · GO CC high confPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 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

Recent

Europe PMC papers linked directly to this protein.