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Protein / target

Keratin, type I cytoskeletal 16

Encoded byKRT16P08779Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
GO CC med conf
1
Research papers

Protein at a glance

Biological role

Structural constituent of skin epidermis

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene KRT16 · Genetic evidence · score 0.32

Research activity

Emerging research

1 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

Epidermis-specific type I keratin that plays a key role in skin.

View complete UniProt function annotation

Epidermis-specific type I keratin that plays a key role in skin. Acts as a regulator of innate immunity in response to skin barrier breach: required for some inflammatory checkpoint for the skin barrier maintenance

Domains and Gene Ontology detail (21)

Domains & features

IF rod

Gene Ontology

  • Ccornified envelope
  • Ccytoskeleton
  • Ccytosol
  • Cextracellular exosome
  • Cintermediate filament
  • Ckeratin filament
  • Cnucleus
  • Fstructural constituent of cytoskeleton
  • Fstructural constituent of skin epidermis
  • Pcytoskeleton organization
  • Pestablishment of skin barrier
  • Phair cycle

473 aa · 51 kDa

Biological roles

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

Cell migrationGOImmune signallingGO
View supporting evidence

Cell migration

  • ·negative regulation of cell migration

Immune signalling

  • ·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 KRT16

Gene-level evidence surfaced through the gene KRT16 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
0.32Limited support

Genetic evidence dominant · Open Targets 0.19

Psoriasis
0.20Preliminary

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

Neoplasms
0.13Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

View evidence synthesis (3)
Genetic Diseases, InbornLimited support
0.32
agreement 0.180.46
Genetic99%Literature1%

Open Targets aggregate 0.19 · 2 independent evidence families

PsoriasisPreliminary
0.20
agreement 0.010.39
Literature57%RNA expression43%

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

NeoplasmsPreliminary
0.13
agreement 0.000.40
Literature100%

Open Targets aggregate 0.10 · 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
Genetic Diseases, Inborn0.19
Psoriasis0.11
Neoplasms0.10

Tractability

AntibodiesEmerging

Feasibility evidence (go cc med conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

View underlying tractability evidence (3)
AB · GO CC med confPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 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

Recent

Europe PMC papers linked directly to this protein.