ArticleThe Journal of experimental medicine2000
Essential role of signal transducer and activator of transcription (Stat)5a but not Stat5b for Flt3-dependent signaling.
Article in The Journal of experimental medicine, 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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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
72 citing papers in PubMed, 202 citations in OpenAlex.
- TNK1 is a targetable JAK-independent driver of STAT signaling and inflammation.Genes & development · 2026Article
- Targeting FLT3 in Acute Myeloid Leukemia: Structural Insights and Key Challenges.ACS bio & med chem Au · 2026Review
- Special Issue "State-of-the-Art Cancer Immunotherapies-2nd Edition".International journal of molecular sciences · 2026Article
- Asymmetry and redundancy of STAT5 paralogs across CD8Communications biology · 2026Article
- Targeting of STAT5 using the small molecule topotecan hydrochloride suppresses acute myeloid leukemia progression.Oncology reports · 2023Article
- Integrative multi-omic cancer profiling reveals DNA methylation patterns associated with therapeutic vulnerability and cell-of-origin.Cancer cell · 2023Article
- Rational design and synthesis of 2-(1Journal of enzyme inhibition and medicinal chemistry · 2022Article
- FLT3 Inhibitors as Maintenance Therapy after Allogeneic Stem-Cell Transplantation.Blood and lymphatic cancer : targets and therapy · 2022Review
- Therapeutic Targeting of FLT3 in Acute Myeloid Leukemia: Current Status and Novel Approaches.OncoTargets and therapy · 2022Review
- Review
- Discovery of 5-methyl-Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Conformational restriction of a type II FMS inhibitor leading to discovery of 5-methyl-Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance.International journal of molecular sciences · 2018Review
- Glutaminolysis is a metabolic dependency in FLT3Blood · 2018Article
- Midostaurin: a novel therapeutic agent for patients with FLT3-mutated acute myeloid leukemia and systemic mastocytosis.Therapeutic advances in hematology · 2017Review
- The Future of Targeting FLT3 Activation in AML.Current hematologic malignancy reports · 2017Review
- The Cytokine Flt3-Ligand in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2017Review
- RNA binding protein MSI2 positively regulates FLT3 expression in myeloid leukemia.Leukemia research · 2017Article
- How I treat FLT3-mutated AML.Blood · 2017Article
- Tyrosine kinase inhibitors targeting FLT3 in the treatment of acute myeloid leukemia.Stem cell investigation · 2017Review
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 4 institutions in 1 country.
Funding
Abstract
The receptor tyrosine kinase Flt3 plays an important role in proliferation and survival of hematopoietic stem and progenitor cells. Although some post-receptor signaling events of Flt3 have been characterized, the involvement of the Janus kinase/signal transducer and activator of transcription (Jak/Stat) pathway in Flt3 signaling has not been thoroughly evaluated. To this aim, we examined whether Flt3 activates the Jak/Stat pathway in Baf3/Flt3 cells, a line stably expressing human Flt3 receptor. Stat5a, but not Stats 1-4, 5b, or 6, was potently activated by Flt3 ligand (FL) stimulation. Interestingly, FL did not activate any Jaks. Activation of Stat5a required the kinase activity of Flt3. A selective role for Stat5a in the proliferative response of primary hematopoietic progenitor cells to FL was documented, as FL did not act on progenitors from marrows of Stat5a(-/-) mice, but did stimulate/costimulate proliferation of these cells from Stat5a(+/+), Stat5b(-/-), and Stat5b(+/+) mice. Thus, Stat5a is essential for at least certain effects of FL. Moreover, our data confirm that Stat5a and Stat5b are not redundant, but rather are at least partially distinctive in their function.
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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 Socratic graph.