Back to discover

Protein / target

C-X-C motif chemokine 2

Encoded byCXCL2P19875Homo sapiensSwiss-Prot
UniProt: P19875Ensembl: ENSG00000081041HGNC: HGNC:4603NCBI Gene: 2920
Antibody-tractable
Druggability
GO CC high conf
2
Research papers

Protein at a glance

Biological role

Chemokine

Strongest disease association

Placental retention

Via encoding gene CXCL2 · Genetic evidence · score 0.34

Research activity

Emerging research

2 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

Produced by activated monocytes and neutrophils and expressed at sites of inflammation.

View complete UniProt function annotation

Produced by activated monocytes and neutrophils and expressed at sites of inflammation. Hematoregulatory chemokine, which, in vitro, suppresses hematopoietic progenitor cell proliferation. GRO-beta(5-73) shows a highly enhanced hematopoietic activity

Subcellular location

Secreted
Domains and Gene Ontology detail (7)

Gene Ontology

  • Cextracellular region
  • Cextracellular space
  • Fchemokine activity
  • Pchemotaxis
  • Pimmune response
  • Pinflammatory response
  • Presponse to molecule of bacterial origin

107 aa · 11 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

  • ·chemotaxis

Immune signalling

  • ·immune response
  • ·inflammatory 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 CXCL2

Gene-level evidence surfaced through the gene CXCL2that 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.

Placental retention
0.34Limited support

Genetic evidence dominant · Open Targets 0.20

Breast Neoplasms
0.25Preliminary

RNA expression evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Neurodegenerative Diseases
0.16Preliminary

Pathway evidence dominant · Open Targets 0.25 · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell Lung
0.15Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Carcinoma, Hepatocellular
0.15Preliminary

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

View evidence synthesis (5)
Placental retentionLimited support
0.34
agreement 0.22–0.46
Genetic100%

Open Targets aggregate 0.20 · 1 independent evidence family

Breast NeoplasmsPreliminary
0.25
agreement 0.06–0.44
RNA expression55%Literature45%

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

Neurodegenerative DiseasesPreliminary
0.16
agreement 0.00–0.34
Pathway98%Literature2%

Open Targets aggregate 0.25 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell LungPreliminary
0.15
agreement 0.00–0.34
Literature67%RNA expression33%

Open Targets aggregate 0.09 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, HepatocellularPreliminary
0.15
agreement 0.00–0.34
Literature94%RNA expression6%

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
Neurodegenerative Diseases0.25
Placental retention0.20
Neoplasms0.12
Carcinoma, Hepatocellular0.12
Breast Neoplasms0.11
Colorectal Neoplasms0.10
Carcinoma, Non-Small-Cell Lung0.09
Leukemia, Myeloid, Acute0.09

Tractability

Antibodies — Emerging

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

View underlying tractability evidence (3)
AB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 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

Targeting tumor-associated macrophages and granulocytic myeloid-derived suppressor cells augments PD-1 blockade in cholangiocarcinoma.263 cites

Loeuillard E · The Journal of clinical investigation · 2020

Single-cell immune profiling of mouse liver aging reveals Cxcl2+ macrophages recruit neutrophils to aggravate liver injury.53 cites

Liu Y · Hepatology (Baltimore, Md.) · 2024

Recent

Single-cell immune profiling of mouse liver aging reveals Cxcl2+ macrophages recruit neutrophils to aggravate liver injury.

Liu Y · Hepatology (Baltimore, Md.) · 2024

Targeting tumor-associated macrophages and granulocytic myeloid-derived suppressor cells augments PD-1 blockade in cholangiocarcinoma.

Loeuillard E · The Journal of clinical investigation · 2020

Europe PMC papers linked directly to this protein.