ArticleMolecular and cellular biology2006
Essential role for cyclin D3 in granulocyte colony-stimulating factor-driven expansion of neutrophil granulocytes.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 44 citations in OpenAlex.
- Stage-Specific Degradation of Cyclin D3 Orchestrates Myelopoiesis and Restrains Myeloproliferative Neoplasm Development.Cancer research · 2026Article
- D-Type Cyclins in Development and Disease.Genes · 2023Review
- A curious case of cyclin-dependent kinases in neutrophils.Journal of leukocyte biology · 2022Review
- Continuous treatment with abemaciclib leads to sustained and efficient inhibition of breast cancer cell proliferation.Oncotarget · 2022Article
- Immunomodulation by anticancer cell cycle inhibitors.Nature reviews. Immunology · 2020Review
- Immunomodulatory Roles of Cell Cycle Regulators.Frontiers in cell and developmental biology · 2019Review
- The potent and selective cyclin-dependent kinases 4 and 6 inhibitor ribociclib (LEE011) is a versatile combination partner in preclinical cancer models.Oncotarget · 2018Article
- Lack of cyclin D3 induces skeletal muscle fiber-type shifting, increased endurance performance and hypermetabolism.Scientific reports · 2018Article
- Cell cycle proteins as promising targets in cancer therapy.Nature reviews. Cancer · 2017Review
- Stromal derived factor-1 and granulocyte-colony stimulating factor treatment improves regeneration of Pax7-/- mice skeletal muscles.Journal of cachexia, sarcopenia and muscle · 2016Article
- Targeting CDK4 and CDK6: From Discovery to Therapy.Cancer discovery · 2016Review
- Article
- Loss of mTOR complex 1 induces developmental blockage in early T-lymphopoiesis and eradicates T-cell acute lymphoblastic leukemia cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- New Approaches to Target T-ALL.Frontiers in oncology · 2014Review
- Cyclin D3 critically regulates the balance between self-renewal and differentiation in skeletal muscle stem cells.Stem cells (Dayton, Ohio) · 2013Article
- Article
- The requirement for cyclin D function in tumor maintenance.Cancer cell · 2012Article
- Cyclin D3 coordinates the cell cycle during differentiation to regulate erythrocyte size and number.Genes & development · 2012Article
- Translational repression of cyclin D3 by a stable G-quadruplex in its 5' UTR: implications for cell cycle regulation.RNA biology · 2012Article
- Bcl3 prevents acute inflammatory lung injury in mice by restraining emergency granulopoiesis.The Journal of clinical investigation · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
The proliferation of neutrophil granulocyte lineage is driven largely by granulocyte colony-stimulating factor (G-CSF) acting via the G-CSF receptors. In this study, we show that mice lacking cyclin D3, a component of the core cell cycle machinery, are refractory to stimulation by the G-CSF. Consequently, cyclin D3-null mice display deficient maturation of granulocytes in the bone marrow and have reduced levels of neutrophil granulocytes in their peripheral blood. The mutant mice are unable to mount a normal response to bacterial challenge and succumb to microbial infections. In contrast, the expansion of hematopoietic stem cells and lineage-committed myeloid progenitors proceeds relatively normally in mice lacking cyclin D3, revealing that the requirement for cyclin D3 function operates at later stages of neutrophil development. Importantly, we verified that this requirement is specific to cyclin D3, as mice lacking other G(1) cyclins (D1, D2, E1, or E2) display normal granulocyte counts. Our analyses revealed that in the bone marrow cells of wild-type mice, activation of the G-CSF receptor leads to upregulation of cyclin D3. Collectively, these results demonstrate that cyclin D3 is an essential cell cycle recipient of G-CSF signaling, and they provide a molecular link of how G-CSF-dependent signaling triggers cell proliferation.
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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.