ArticleBlood2010
STAT3 controls myeloid progenitor growth during emergency granulopoiesis.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
139 citing papers in PubMed, 225 citations in OpenAlex.
- Noncanonical NF-κB activation mediates STAT3-stimulated IDO upregulation in myeloid-derived suppressor cells in breast cancer.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Intraperitoneal G-CSF Stimulation Achieves Human-like Neutrophil Levels in NSG Mice Without Inducing Systemic Inflammation.International journal of molecular sciences · 2026Article
- BCR-ABL1 Drives Transcriptional Reprogramming of Chronic Myeloid Leukemia Cells for Immune Evasion Through C/EBPβ.MedComm · 2026Article
- Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer.Molecular oncology · 2026Review
- Single-cell RNA sequencing uncovers neutrophil clusters associated with autoimmune neuroinflammation.Journal of neuroinflammation · 2026Article
- ExploitingFrontiers in immunology · 2026Article
- Glucocorticoids and Neutrophil Biology: Impact on the Development of Resistance to Glucocorticoid Therapy.Neuroimmunomodulation · 2026Review
- The neutrophil collective.Cell · 2025Review
- A new STAT3-based potency assay for human G-CSF analog therapeutics.Journal of pharmaceutical and biomedical analysis · 2025Article
- Rewiring the bone marrow: Evolution and the transcriptional architecture of trained immunity.eLife · 2025Review
- TScience advances · 2025Article
- G-CSF-Induced Emergency Granulopoiesis Modulates Neutrophil Effector Function in Mice.Stem cell reviews and reports · 2025Article
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- Myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment and their targeting in cancer therapy.Molecular cancer · 2025Review
- From Defense to Dysfunction: Decoding the Paradox of Emergency Granulopoiesis in Sepsis Pathogenesis.Research (Washington, D.C.) · 2025Review
- The diverse roles of neutrophils from protection to pathogenesis.Nature immunology · 2024Review
- Made to order: emergency myelopoiesis and demand-adapted innate immune cell production.Nature reviews. Immunology · 2024Review
- STAT3 protects hematopoietic stem cells by preventing activation of a deleterious autocrine type-I interferon response.Leukemia · 2024Article
- Design, Synthesis, and Anti-Leukemic Evaluation of a Series of Dianilinopyrimidines by Regulating the Ras/Raf/MEK/ERK and STAT3/c-Myc Pathways.Molecules (Basel, Switzerland) · 2024Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Granulocyte colony-stimulating factor (G-CSF) mediates "emergency" granulopoiesis during infection, a process that is mimicked by clinical G-CSF use, yet we understand little about the intracellular signaling cascades that control demand-driven neutrophil production. Using a murine model with conditional deletion of signal transducer and activator of transcription 3 (STAT3) in bone marrow, we investigated the cellular and molecular mechanisms of STAT3 function in the emergency granulopoiesis response to G-CSF administration or infection with Listeria monocytogenes, a pathogen that is restrained by G-CSF signaling in vivo. Our results show that STAT3 deficiency renders hematopoietic progenitor cells and myeloid precursors refractory to the growth-promoting functions of G-CSF or L monocytogenes infection. STAT3 is necessary for accelerating granulocyte cell-cycle progression and maturation in response to G-CSF. STAT3 directly controls G-CSF-dependent expression of CCAAT-enhancer-binding protein β (C/EBPβ), a crucial factor in the emergency granulopoiesis response. Moreover, STAT3 and C/EBPβ coregulate c-Myc through interactions with the c-myc promoter that control the duration of C/EBPα occupancy during demand-driven granulopoiesis. These results place STAT3 as an essential mediator of emergency granulopoiesis by its regulation of transcription factors that direct G-CSF-responsive myeloid progenitor expansion.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.