Protein / target

Granulocyte colony-stimulating factor

Encoded byCSF3P09919Homo sapiensSwiss-Prot

UniProt: P09919 Ensembl: ENSG00000108342 HGNC: HGNC:2438 NCBI Gene: 1440

Small-molecule tractable

Druggability

High-Quality Pocket

Research papers

Protein at a glance

Biological role

Granulocyte colony-stimulating factor receptor binding

Strongest disease association

Asthma

Via encoding gene CSF3 · Genetic evidence · score 0.68

Research activity

Emerging research

2 papers · latest 2005

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

Granulocyte/macrophage colony-stimulating factors are cytokines that act in hematopoiesis by controlling the production, differentiation, and function of 2 related white cell populations of the blood, the granulocytes and the monocytes-macrophages.

View complete UniProt function annotation

Subcellular location

Secreted

Domains and Gene Ontology detail (22)

Gene Ontology

Cendocytic vesicle lumen
Cextracellular region
Cextracellular space
Clysosomal lumen
Fcytokine activity
Fenzyme binding
Fgranulocyte colony-stimulating factor receptor binding
Fgrowth factor activity
Pcellular response to cytokine stimulus
Pcellular response to lipopolysaccharide
Pcytokine-mediated signaling pathway
Pgranulocyte colony-stimulating factor signaling pathway

207 aa · 22 kDa · 3 isoforms

Biological roles

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

Cell proliferation & survivalGOImmune signallingUniProt · GO

View supporting evidence

Cell proliferation & survival

·positive regulation of cell population proliferation

Immune signalling

·Granulocyte/macrophage colony-stimulating factors are cytokines that act in hematopoiesi…
·cytokine activity
·cellular response to cytokine stimulus
·cytokine-mediated signaling pathway

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 CSF3

Gene-level evidence surfaced through the gene CSF3that 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.

Asthma

0.71Moderately supported

Genetic evidence dominant · Open Targets 0.43

Neutropenia

0.59Moderately supported

Genetic evidence dominant · Open Targets 0.35

COVID-19

0.35Limited support

Genetic evidence dominant · Open Targets 0.20

Pulmonary Disease, Chronic Obstructive

0.32Limited support

Genetic evidence dominant · Open Targets 0.18

Breast Neoplasms

0.27Preliminary

RNA expression evidence dominant · Open Targets 0.13 · no direct causal or clinical evidence

View evidence synthesis (5)

AsthmaModerately supported

0.71

agreement 0.57–0.84

Genetic90%Literature10%

Open Targets aggregate 0.43 · 2 independent evidence families

NeutropeniaModerately supported

0.59

agreement 0.46–0.73

Genetic79%Literature21%

Open Targets aggregate 0.35 · 2 independent evidence families

COVID-19Limited support

0.35

agreement 0.21–0.49

Genetic80%Literature20%

Open Targets aggregate 0.20 · 2 independent evidence families

Pulmonary Disease, Chronic ObstructiveLimited support

0.32

agreement 0.18–0.46

Genetic80%Literature20%

Open Targets aggregate 0.18 · 2 independent evidence families

Breast NeoplasmsPreliminary

0.27

agreement 0.08–0.46

RNA expression55%Literature45%

Open Targets aggregate 0.13 · 2 independent evidence families · 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

Asthma0.43

Neutropenia0.35

COVID-190.20

Pulmonary Disease, Chronic Obstructive0.18

Breast Neoplasms0.13

Lower respiratory tract disorder0.13

Neoplasms0.12

Tractability

Small molecules — Emerging

Feasibility evidence (high-quality pocket) — 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.

View underlying tractability evidence (4)

SM · High-Quality PocketAB · 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 2005

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

Most cited

T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines.1,089 cites

Fossiez F · The Journal of experimental medicine · 1996

Rapid mobilization of murine and human hematopoietic stem and progenitor cells with AMD3100, a CXCR4 antagonist.830 cites

Broxmeyer HE · The Journal of experimental medicine · 2005

Recent

Rapid mobilization of murine and human hematopoietic stem and progenitor cells with AMD3100, a CXCR4 antagonist.

Broxmeyer HE · The Journal of experimental medicine · 2005

T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines.

Fossiez F · The Journal of experimental medicine · 1996

Europe PMC papers linked directly to this protein.