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Protein / target

Tyrosine-protein kinase Mer

Encoded byMERTKQ12866Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
1
Clinical candidates
Small-molecule tractable
Druggability
Advanced Clinical
2
Research papers

Protein at a glance

Biological role

Transmembrane receptor protein tyrosine kinase

Strongest disease association

Retinitis Pigmentosa

Via encoding gene MERTK · Genetic evidence · score 0.89

Therapeutic position

Clinically advancing target

Small molecules

Research activity

Emerging research

2 papers · latest 2021

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

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including LGALS3, TUB, TULP1 or GAS6.

View complete UniProt function annotation

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including LGALS3, TUB, TULP1 or GAS6. Regulates many physiological processes including cell survival, migration, differentiation, and phagocytosis of apoptotic cells (efferocytosis). Ligand binding at the cell surface induces autophosphorylation of MERTK on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with GRB2 or PLCG2 and induces phosphorylation of MAPK1, MAPK2, FAK/PTK2 or RAC1. MERTK signaling plays a role in various processes such as macrophage clearance of apoptotic cells, platelet aggregation, cytoskeleton reorganization and engulfment (PubMed:32640697). Functions in the retinal pigment epithelium (RPE) as a regulator of rod outer segments fragments phagocytosis. Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces production of suppressors of cytokine signaling SOCS1 and SOCS3

Subcellular location

Cell membrane
Domains and Gene Ontology detail (21)

Domains & features

Ig-like C2-type 1Ig-like C2-type 2Fibronectin type-III 1Fibronectin type-III 2Protein kinase

Gene Ontology

  • Ccytoplasm
  • Cextracellular space
  • Cphotoreceptor outer segment
  • Cplasma membrane
  • Creceptor complex
  • FATP binding
  • Ftransmembrane receptor protein tyrosine kinase activity
  • Pcell migration
  • Pcell surface receptor protein tyrosine kinase signaling pathway
  • Pcell surface receptor signaling pathway
  • Pcell-cell signaling
  • Pnegative regulation of leukocyte apoptotic process

999 aa · 110 kDa

Biological roles

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

Receptor tyrosine kinase signallingUniProt · GOCell proliferation & survivalUniProtCell migrationGO
View supporting evidence

Receptor tyrosine kinase signalling

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…
  • ·transmembrane receptor protein tyrosine kinase activity
  • ·cell surface receptor protein tyrosine kinase signaling pathway

Cell proliferation & survival

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…

Cell migration

  • ·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 MERTK

Gene-level evidence surfaced through the gene MERTKthat 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.

Retinitis Pigmentosa
0.94Well supported

Genetic evidence dominant · Open Targets 0.80

Genetic Diseases, Inborn
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.42

Leber Congenital Amaurosis
0.64Moderately supported

Genetic literature evidence dominant · Open Targets 0.39

Atrial Fibrillation
0.59Moderately supported

Genetic evidence dominant · Open Targets 0.36

Retinal Diseases
0.52Moderately supported

Genetic evidence dominant · Open Targets 0.38

View evidence synthesis (5)
Retinitis PigmentosaWell supported
0.94
agreement 0.811.00
Genetic69%Animal model30%Literature2%Genetic literaturedup

Open Targets aggregate 0.80 · 3 independent evidence families · 1 not counted as duplicate

Genetic Diseases, InbornModerately supported
0.68
agreement 0.540.82
Genetic100%Literature0%

Open Targets aggregate 0.42 · 2 independent evidence families

Leber Congenital AmaurosisModerately supported
0.64
agreement 0.520.77
Genetic literature61%Animal model36%Literature3%

Open Targets aggregate 0.39 · 3 independent evidence families

Atrial FibrillationModerately supported
0.59
agreement 0.460.73
Genetic98%Literature2%

Open Targets aggregate 0.36 · 2 independent evidence families

Retinal DiseasesModerately supported
0.52
agreement 0.380.65
Genetic92%Literature8%

Open Targets aggregate 0.38 · 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
Retinitis Pigmentosa0.80
Dengue0.50
Genetic Diseases, Inborn0.42
Leber Congenital Amaurosis0.39
Retinal Diseases0.38
Eye Diseases0.37
Atrial Fibrillation0.36

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)
NINGETINIBPhase 2

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

Small moleculesStrong

Advanced Clinical and Structure with Ligand support this modality.

AntibodiesEmerging

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

Protein degradersEmerging

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

View underlying tractability evidence (13)
SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · LiteraturePR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2021

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

Most cited

Diaz-Aparicio I · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020

Recent

Microglia Actively Remodel Adult Hippocampal Neurogenesis through the Phagocytosis Secretome.

Diaz-Aparicio I · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020

Europe PMC papers linked directly to this protein.