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Protein / target

Metalloproteinase inhibitor 1

Encoded byTIMP1P01033Homo sapiensSwiss-Prot
UniProt: P01033Ensembl: ENSG00000102265HGNC: HGNC:11820NCBI Gene: 7076
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Metalloendopeptidase inhibitor

Strongest disease association

Neoplasms

Via encoding gene TIMP1 · Literature evidence · score 0.12

Research activity

Emerging research

1 papers · latest 2020

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

Metalloproteinase inhibitor that functions by forming one to one complexes with target metalloproteinases, such as collagenases, and irreversibly inactivates them by binding to their catalytic zinc cofactor.

View complete UniProt function annotation

Metalloproteinase inhibitor that functions by forming one to one complexes with target metalloproteinases, such as collagenases, and irreversibly inactivates them by binding to their catalytic zinc cofactor. Acts on MMP1, MMP2, MMP3, MMP7, MMP8, MMP9, MMP10, MMP11, MMP12, MMP13 and MMP16. Does not act on MMP14. Also functions as a growth factor that regulates cell differentiation, migration and cell death and activates cellular signaling cascades via CD63 and ITGB1. Plays a role in integrin signaling. Mediates erythropoiesis in vitro; but, unlike IL3, it is species-specific, stimulating the growth and differentiation of only human and murine erythroid progenitors

Subcellular location

Secreted
Domains and Gene Ontology detail (29)

Domains & features

NTR

Gene Ontology

  • Cbasement membrane
  • Cendoplasmic reticulum lumen
  • Cextracellular exosome
  • Cextracellular matrix
  • Cextracellular region
  • Cextracellular space
  • Cplatelet alpha granule lumen
  • Fcytokine activity
  • Fgrowth factor activity
  • Fmetalloendopeptidase inhibitor activity
  • Fpeptidase inhibitor activity
  • Fprotease binding

207 aa · 23 kDa

Biological roles

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

Cell proliferation & survivalGOCell migrationGOProteolysisGOImmune signallingGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Cell migration

  • ·negative regulation of trophoblast cell migration

Proteolysis

  • ·protease binding
  • ·negative regulation of endopeptidase activity
  • ·negative regulation of membrane protein ectodomain proteolysis
  • ·negative regulation of metallopeptidase activity

Immune signalling

  • ·cytokine activity
  • ·negative regulation of trophoblast cell migration
  • ·response to cytokine

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 TIMP1

Gene-level evidence surfaced through the gene TIMP1 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.

Glioblastoma
0.18Preliminary

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

Neoplasms
0.15Preliminary

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

Pulmonary Disease, Chronic Obstructive
0.14Preliminary

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

Atrial Fibrillation
0.13Preliminary

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

Neurodegenerative Diseases
0.08Preliminary

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

View evidence synthesis (5)
GlioblastomaPreliminary
0.18
agreement 0.00–0.37
Literature74%RNA expression26%

Open Targets aggregate 0.12 · 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

Pulmonary Disease, Chronic ObstructivePreliminary
0.14
agreement 0.00–0.42
Literature100%

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

Atrial FibrillationPreliminary
0.13
agreement 0.00–0.41
Literature100%

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

Neurodegenerative DiseasesPreliminary
0.08
agreement 0.00–0.26
Pathway91%Literature9%

Open Targets aggregate 0.12 · 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
Neoplasms0.12
Glioblastoma0.12
Neurodegenerative Diseases0.12
Pulmonary Disease, Chronic Obstructive0.12
Atrial Fibrillation0.11

Tractability

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.

View underlying tractability evidence (4)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of transcription factor activityToxCastregulation of gene expressionToxCast

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 2020

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

Most cited

The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases.1,154 cites

Cabral-Pacheco GA · International journal of molecular sciences · 2020

Recent

The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases.

Cabral-Pacheco GA · International journal of molecular sciences · 2020

Europe PMC papers linked directly to this protein.