Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

The Journal of clinical investigation - 1 Mar 2008

Liu Fulu, Kunter Ghada, Krem Maxwell M, Eades William C, Cain Jennifer A, Tomasson Michael H, Hennighausen Lothar, Link Daniel C

Abstract excerpt

A fundamental property of leukemic stem cells is clonal dominance of the bone marrow microenvironment. Truncation mutations of CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic progression in patients with severe congenital neutropenia. Here we show that expression of a truncated mutant Csf3r in mice confers a strong clonal advantage at the HSC level that is dependent upon exogenous...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Proliferation
Share to Granulocyte Colony-Stimulating Factor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hematopoietic Stem Cells

Share to Mice, Inbred C57BL

Share to Neutropenia

Share to STAT3 Transcription Factor

Share to STAT5 Transcription Factor

Source

Open in PubMed Open full text

Identifiers

PMID: 18292815
DOI: 10.1172/JCI32704
PMCID: PMC2248325

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.PMID 18292815Read ↗

Truncated CSF3 receptors induce pro-inflammatory responses in severe congenital neutropenia.Semantic proximity Read ↗

A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.Semantic proximity Read ↗

Signaling mechanisms coupled to tyrosines in the granulocyte colony-stimulating factor receptor orchestrate G-CSF-induced expansion of myeloid progenitor cells.Semantic proximity Read ↗

Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors.Semantic proximity Read ↗

Discovering early molecular determinants of leukemogenesis.Semantic proximity Read ↗

Granulocyte colony-stimulating factor receptor mutations in severe congenital neutropenia transforming to acute myelogenous leukemia confer resistance to apoptosis and enhance cell survival.Semantic proximity Read ↗

Selective activation of STAT5 unveils its role in stem cell self-renewal in normal and leukemic hematopoiesis.Semantic proximity Read ↗

Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPNSemantic proximity Read ↗

Sustained Receptor Activation and Hyperproliferation in Response to Granulocyte Colony-stimulating Factor (G-CSF) in Mice with a Severe Congenital Neutropenia/Acute Myeloid Leukemia–derived Mutation in the G-CSF Receptor GeneSemantic proximity Read ↗

Niche-mediated depletion of the normal hematopoietic stem cell reservoir by Flt3-ITD-induced myeloproliferation.Semantic proximity Read ↗

The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in mice that is responsive to therapeutic JAK inhibitionSemantic proximity Read ↗

Gain-of-function of Stat5 leads to excessive granulopoiesis and lethal extravasation of granulocytes to the lung.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.