ArticleBlood2010
Stat5a serine 725 and 779 phosphorylation is a prerequisite for hematopoietic transformation.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Unexpected functional role of the transactivation domain for nuclear import of STAT5.Communications biology · 2026Article
- Age-associated myeloid malignancies - the role of STAT3 and STAT5 in myelodysplastic syndrome and acute myeloid leukemia.FEBS letters · 2024Review
- Genomic Mutations of the STAT5 Transcription Factor Are Associated with Human Cancer and Immune Diseases.International journal of molecular sciences · 2022Review
- Group I p21-activated kinases in leukemia cell adhesion to fibronectin.Cell adhesion & migration · 2021Article
- STAT proteins: a kaleidoscope of canonical and non-canonical functions in immunity and cancer.Journal of hematology & oncology · 2021Review
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- JAK-STAT in Early Hematopoiesis and Leukemia.Frontiers in cell and developmental biology · 2021Review
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- Oncogenic D816V-KIT signaling in mast cells causes persistent IL-6 production.Haematologica · 2020Article
- Review
- Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018Review
- Mediator Kinase Phosphorylation of STAT1 S727 Promotes Growth of Neoplasms With JAK-STAT Activation.EBioMedicine · 2017Article
- O-GlcNAcylation of STAT5 controls tyrosine phosphorylation and oncogenic transcription in STAT5-dependent malignancies.Leukemia · 2017Article
- Expansion of BCR/ABL1British journal of haematology · 2017Article
- SEL120-34A is a novel CDK8 inhibitor active in AML cells with high levels of serine phosphorylation of STAT1 and STAT5 transactivation domains.Oncotarget · 2017Article
- Mechanisms and consequences of Jak-STAT signaling in the immune system.Nature immunology · 2017Review
- Three Tyrosine Residues in the Erythropoietin Receptor Are Essential for Janus Kinase 2 V617F Mutant-induced Tumorigenesis.The Journal of biological chemistry · 2017Article
- STAT5A/5B-specific expansion and transformation of hematopoietic stem cells.Blood cancer journal · 2017Article
- Stat5 Exerts Distinct, Vital Functions in the Cytoplasm and Nucleus of Bcr-Abl+ K562 and Jak2(V617F)+ HEL Leukemia Cells.Cancers · 2015Article
- Article
Corrections and comments
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Authors and funding
15 authors at 9 institutions in 3 countries.
Funding
Abstract
Stat5 transcription factors are essential gene regulators promoting proliferation, survival, and differentiation of all hematopoietic cell types. Mutations or fusions of oncogenic tyrosine kinases often result in constitutive Stat5 activation. We have modeled persistent Stat5 activity by using an oncogenic Stat5a variant (cS5). To analyze the hitherto unrecognized role of Stat5 serine phosphorylation in this context, we have generated cS5 constructs with mutated C-terminal serines 725 and 779, either alone or in combination. Genetic complementation assays in primary Stat5(null/null) mast cells and Stat5(DeltaN) T cells demonstrated reconstitution of proliferation with these mutants. Similarly, an in vivo reconstitution experiment of transduced Stat5(null/null) fetal liver cells transplanted into irradiated wild-type recipients revealed that these mutants exhibit biologic activity in lineage differentiation. By contrast, the leukemogenic potential of cS5 in bone marrow transplants decreased dramatically in cS5 single-serine mutants or was completely absent upon loss of both serine phosphorylation sites. Our data suggest that Stat5a serine phosphorylation is a prerequisite for cS5-mediated leukemogenesis. Hence, interference with Stat5a serine phosphorylation might provide a new therapeutic option for leukemia and myeloid dysplasias without affecting major functions of Stat5 in normal hematopoiesis.
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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.