Protein / target

C-C motif chemokine 5

Encoded byCCL5P13501Homo sapiensSwiss-Prot

UniProt: P13501 Ensembl: ENSG00000271503 HGNC: HGNC:10632 NCBI Gene: 6352

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Phosphatidylinositol-4,5-bisphosphate phospholipase C

Strongest disease association

Poisoning

Via encoding gene CCL5 · Genetic evidence · score 0.26

Research activity

Emerging research

3 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

Chemoattractant for blood monocytes, memory T-helper cells and eosinophils.

View complete UniProt function annotation

Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the release of histamine from basophils and activates eosinophils. May activate several chemokine receptors including CCR1, CCR3, CCR4 and CCR5. One of the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant RANTES protein induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV). The processed form RANTES(3-68) acts as a natural chemotaxis inhibitor and is a more potent inhibitor of HIV-1-infection. The second processed form RANTES(4-68) exhibits reduced chemotactic and HIV-suppressive activity compared with RANTES(1-68) and RANTES(3-68) (PubMed:1380064, PubMed:15923218, PubMed:16791620, PubMed:8525373, PubMed:9516414). May also be an agonist of the G protein-coupled receptor GPR75, stimulating inositol trisphosphate production and calcium mobilization through its activation. Together with GPR75, may play a role in neuron survival through activation of a downstream signaling pathway involving the PI3, Akt and MAP kinases. By activating GPR75 may also play a role in insulin secretion by islet cells (PubMed:23979485)

Subcellular location

Secreted

Domains and Gene Ontology detail (73)

Gene Ontology

Ccytoplasm
Cextracellular region
Cextracellular space
Cmembrane
FCCR chemokine receptor binding
FCCR1 chemokine receptor binding
FCCR4 chemokine receptor binding
FCCR5 chemokine receptor binding
Fchemoattractant activity
Fchemokine activity
Fchemokine receptor antagonist activity
Fchemokine receptor binding

91 aa · 10 kDa

Biological roles

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

Cell migrationUniProt · GOGrowth-factor signallingGOG protein-coupled signallingUniProt · GOImmune signallingUniProt · GOCell adhesionGOApoptosis & cell deathGO

View supporting evidence

Cell migration

·Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the r…
·chemotaxis
·dendritic cell chemotaxis
·eosinophil chemotaxis

Growth-factor signalling

·cellular response to fibroblast growth factor stimulus

G protein-coupled signalling

·Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the r…
·G protein-coupled receptor signaling pathway
·negative regulation of G protein-coupled receptor signaling pathway
·phospholipase D-activating G protein-coupled receptor signaling pathway

Immune signalling

·Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the r…
·antimicrobial humoral immune response mediated by antimicrobial peptide
·cellular response to interleukin-1
·inflammatory response

Cell adhesion

·leukocyte cell-cell adhesion
·positive regulation of cell adhesion
·positive regulation of cell-cell adhesion mediated by integrin
·positive regulation of homotypic cell-cell adhesion

Apoptosis & cell death

·negative regulation of macrophage apoptotic process
·negative regulation of T cell apoptotic process
·positive regulation of T cell apoptotic process

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 CCL5

Gene-level evidence surfaced through the gene CCL5that 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.

Poisoning

0.26Limited support

Genetic evidence dominant · Open Targets 0.16

Asthma

0.17Preliminary

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

Arthritis, Rheumatoid

0.15Preliminary

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

Breast Neoplasms

0.15Preliminary

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

View evidence synthesis (5)

PoisoningLimited support

0.26

agreement 0.14–0.38

Genetic100%

Open Targets aggregate 0.16 · 1 independent evidence family

AsthmaPreliminary

0.17

agreement 0.00–0.36

Literature74%RNA expression26%

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

Arthritis, RheumatoidPreliminary

0.15

agreement 0.00–0.34

Literature90%RNA expression10%

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

Breast NeoplasmsPreliminary

0.15

agreement 0.00–0.42

Literature100%

Open Targets aggregate 0.12 · 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

Poisoning0.16

Neoplasms0.12

Breast Neoplasms0.12

Carcinoma, Hepatocellular0.11

Colorectal Neoplasms0.11

Arthritis, Rheumatoid0.11

Asthma0.11

Infections0.11

Tractability

Small molecules — Emerging

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

Antibodies — Emerging

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

Protein degraders — Emerging

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

View underlying tractability evidence (9)

SM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.