Protein / target

Triggering receptor expressed on myeloid cells 1

Encoded byTREM1Q9NP99Homo sapiensSwiss-Prot

UniProt: Q9NP99 Ensembl: ENSG00000124731 HGNC: HGNC:17760 NCBI Gene: 54210

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Transmembrane signaling receptor

Strongest disease association

Neurodegenerative Diseases

Via encoding gene TREM1 · Pathway evidence · score 0.24

Therapeutic position

Clinically advancing target

Research activity

Emerging research

3 papers · latest 2023

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

Cell surface receptor that plays important roles in innate and adaptive immunity by amplifying inflammatory responses.

View complete UniProt function annotation

Cell surface receptor that plays important roles in innate and adaptive immunity by amplifying inflammatory responses (PubMed:10799849, PubMed:21393102). Upon activation by various ligands such as PGLYRP1, HMGB1 or HSP70, multimerizes and forms a complex with transmembrane adapter TYROBP/DAP12 (PubMed:17568691, PubMed:25595774, PubMed:29568119). In turn, initiates a SYK-mediated cascade of tyrosine phosphorylation, activating multiple downstream mediators such as BTK, MAPK1, MAPK3 or phospholipase C-gamma (PubMed:14656437, PubMed:21659545). This cascade promotes the neutrophil- and macrophage-mediated release of pro-inflammatory cytokines and/or chemokines, as well as their migration and thereby amplifies inflammatory responses that are triggered by bacterial and fungal infections (PubMed:17098818, PubMed:17568691). By also promoting the amplification of inflammatory signals that are initially triggered by Toll-like receptor (TLR) and NOD-like receptor engagement, plays a major role in the pathophysiology of acute and chronic inflammatory diseases of different etiologies including septic shock and atherosclerosis (PubMed:11323674, PubMed:21393102)

Subcellular location

Cell membraneSecreted

Domains and Gene Ontology detail (15)

Domains & features

Ig-like V-type

Gene Ontology

Ccell surface
Cextracellular region
Cextracellular space
Cplasma membrane
Freceptor decoy activity
Fscaffold protein binding
Fsignaling receptor activity
Ftransmembrane signaling receptor activity
Padaptive immune response
Phumoral immune response
Pinnate immune response
Pintracellular signal transduction

234 aa · 26 kDa · 3 isoforms

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

·neutrophil chemotaxis

Immune signalling

·Cell surface receptor that plays important roles in innate and adaptive immunity by ampl…
·adaptive immune response
·humoral immune 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 TREM1

Gene-level evidence surfaced through the gene TREM1that 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.

Central Nervous System Neoplasms

0.22Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

Neurodegenerative Diseases

0.17Preliminary

Pathway evidence dominant · Open Targets 0.24 · no direct causal or clinical evidence

Arthritis, Rheumatoid

0.15Preliminary

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

Neoplasms

0.15Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

Glioblastoma

0.14Preliminary

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

View evidence synthesis (5)

Central Nervous System NeoplasmsPreliminary

0.22

agreement 0.03–0.41

Literature58%RNA expression42%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

Neurodegenerative DiseasesPreliminary

0.17

agreement 0.00–0.34

Pathway96%Literature5%

Open Targets aggregate 0.24 · 2 independent evidence families · no direct causal or clinical evidence

Arthritis, RheumatoidPreliminary

0.15

agreement 0.00–0.34

Literature87%RNA expression13%

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

NeoplasmsPreliminary

0.15

agreement 0.00–0.42

Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · no direct causal or clinical evidence

GlioblastomaPreliminary

0.14

agreement 0.00–0.33

Literature94%RNA expression6%

Open Targets aggregate 0.11 · 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

Neurodegenerative Diseases0.24

Central Nervous System Neoplasms0.12

Neoplasms0.12

Glioblastoma0.11

Arthritis, Rheumatoid0.11

Carcinoma, Hepatocellular0.11

Glioma0.11

Colitis0.10

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)

NANGIBOTIDEPhase 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 molecules — Emerging

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

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

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (7)

SM · Structure with LigandSM · High-Quality PocketAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.