ArticleGenes & development2000
Antiapoptotic activity of Stat5 required during terminal stages of myeloid differentiation.
Article in Genes & development, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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Who cites it
72 citing papers in PubMed, 185 citations in OpenAlex.
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- Discovery of key regulators in classical monocyte phenotypes linked to COVID-19 severity using single-cell multi-omics sequencing.iScience · 2026Article
- Molecular Basis of Simalikalactone D Sensitivity in Triple-Negative Breast Cancer Cells.Biomolecules · 2025Article
- Maintenance of hematopoietic stem cells by tyrosine-unphosphorylated STAT5 and JAK inhibition.Blood advances · 2025Article
- Age-associated myeloid malignancies - the role of STAT3 and STAT5 in myelodysplastic syndrome and acute myeloid leukemia.FEBS letters · 2024Review
- GM-CSF-activated STAT5A regulates macrophage functions and inflammation in atherosclerosis.Frontiers in immunology · 2023Article
- Suppression of tumor-associated neutrophils by lorlatinib attenuates pancreatic cancer growth and improves treatment with immune checkpoint blockade.Nature communications · 2021Article
- CD123 Is Consistently Expressed onCancers · 2021Article
- MKL-1 is a coactivator for STAT5b, the regulator of Treg cell development and function.Cell communication and signaling : CCS · 2020Article
- Balancing STAT Activity as a Therapeutic Strategy.Cancers · 2019Review
- The Signal Transducer and Activator of Transcription 5B (STAT5B) Gene Promotes Proliferation and Drug Resistance of Human Mantle Cell Lymphoma Cells by Activating the Akt Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- STAT5 is essential for IL-7-mediated viability, growth, and proliferation of T-cell acute lymphoblastic leukemia cells.Blood advances · 2018Article
- Transcriptional Regulation of Emergency Granulopoiesis in Leukemia.Frontiers in immunology · 2018Review
- The combination effect of homoharringtonine and ibrutinib on FLT3-ITD mutant acute myeloid leukemia.Oncotarget · 2017Article
- Production of interleukin‑4 in CD133+ cervical cancer stem cells promotes resistance to apoptosis and initiates tumor growth.Molecular medicine reports · 2016Article
- Article
- Src family kinases interfere with dimerization of STAT5A through a phosphotyrosine-SH2 domain interaction.Cell communication and signaling : CCS · 2015Article
- Accumulation of FLT3(+) CD11c (+) dendritic cells in psoriatic lesions and the anti-psoriatic effect of a selective FLT3 inhibitor.Immunologic research · 2014Article
- Gain-of-function of Stat5 leads to excessive granulopoiesis and lethal extravasation of granulocytes to the lung.PloS one · 2013Article
- Biology and significance of the JAK/STAT signalling pathways.Growth factors (Chur, Switzerland) · 2012Review
12 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
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stat5 is activated by multiple receptors of hematopoietic cytokines. To study its role during hematopoiesis, we have generated primary chicken myeloblasts expressing different dominant-negative (dn) alleles of Stat5. This caused a striking inability to generate mature cells, due to massive apoptosis during differentiation. Bcl-2 was able to rescue differentiating cells expressing dnStat5 from apoptosis, suggesting that during cytokine-dependent differentiation the main function of the protein is to ensure cell survival. Our findings with dnStat5-expressing chicken myeloblasts were confirmed with primary hematopoietic cells from Stat5a/Stat5b-deficient mice. Bone marrow cells from these animals displayed a strong increase in apoptotic cell death during GM-CSF-dependent functional maturation in vitro. The antiapoptotic protein Bcl-x was induced by GM-CSF and IL-3 in a Stat5-dependent fashion. Ectopic expression of Bcl-x rescued Stat5-deficient bone marrow cells from apoptosis, indicating that Stat5 promotes the survival of myeloid progenitor cells through its ability to induce transcription of the bcl-x gene. Finally, the recruitment of myeloid cells to inflammatory sites was found strongly impeded in Stat5-deficient mice. Taken together, our findings suggest that Stat5 may promote cytokine-dependent survival and proliferation of differentiating myeloid progenitor cells in stress or pathological situations, such as inflammation.
Indexed as
Identifiers
10652277PMC316353W1837973866What 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.