ArticleLeukemia2014
PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- Unexpected functional role of the transactivation domain for nuclear import of STAT5.Communications biology · 2026Article
- Stromal STAT5-Mediated Trophic Activity Regulates Hematopoietic Niche Factors.Stem cells (Dayton, Ohio) · 2023Article
- Blocking STAT3/5 through direct or upstream kinase targeting in leukemic cutaneous T-cell lymphoma.EMBO molecular medicine · 2022Article
- p21-Activated kinases as promising therapeutic targets in hematological malignancies.Leukemia · 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
- Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets.Leukemia · 2021Article
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- Opioids drive breast cancer metastasis through the δ-opioid receptor and oncogenic STAT3.Neoplasia (New York, N.Y.) · 2021Article
- Quantitative Phosphoproteomic Analysis Reveals Dendritic Cell- Specific STAT Signaling After α2-3-Linked Sialic Acid Ligand Binding.Frontiers in immunology · 2021Article
- Dasatinib overcomes stroma-based resistance to the FLT3 inhibitor quizartinib using multiple mechanisms.Leukemia · 2020Article
- Activation of STAT transcription factors by the Rho-family GTPases.Biochemical Society transactions · 2020Review
- Coordinated dysregulation of cancer progression by the HER family and p21-activated kinases.Cancer metastasis reviews · 2020Review
- Review
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- Review
- Review
- A kinase-independent role for CDK8 in BCR-ABL1Nature communications · 2019Article
- Combined inhibition of receptor tyrosine and p21-activated kinases as a therapeutic strategy in childhood ALL.Blood advances · 2018Article
- Aggressive B-cell lymphomas in patients with myelofibrosis receiving JAK1/2 inhibitor therapy.Blood · 2018Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
The transcription factor STAT5 (signal transducer and activator of transcription 5) is frequently activated in hematological malignancies and represents an essential signaling node downstream of the BCR-ABL oncogene. STAT5 can be phosphorylated at three positions, on a tyrosine and on the two serines S725 and S779. We have investigated the importance of STAT5 serine phosphorylation for BCR-ABL-induced leukemogenesis. In cultured bone marrow cells, expression of a STAT5 mutant lacking the S725 and S779 phosphorylation sites (STAT5(SASA)) prohibits transformation and induces apoptosis. Accordingly, STAT5(SASA) BCR-ABL(+) cells display a strongly reduced leukemic potential in vivo, predominantly caused by loss of S779 phosphorylation that prevents the nuclear translocation of STAT5. Three distinct lines of evidence indicate that S779 is phosphorylated by group I p21-activated kinase (PAK). We show further that PAK-dependent serine phosphorylation of STAT5 is unaffected by BCR-ABL tyrosine kinase inhibitor treatment. Interfering with STAT5 phosphorylation could thus be a novel therapeutic approach to target BCR-ABL-induced malignancies.
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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.