ArticlePloS one2014
BCR-ABL affects STAT5A and STAT5B differentially.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 31 citations in OpenAlex.
- Stafib-2-CR: an Improved Nanomolar and Selective Inhibitor of the Transcription Factor STAT5b Developed by Conformational Restriction of Stafib-2.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- Fusion Molecules Between the STAT5b Inhibitor Stafib-2-CR and a Cereblon Ligand.ChemistryOpen · 2026Article
- Stafiba: A STAT5-Selective Small-Molecule Inhibitor.Chembiochem : a European journal of chemical biology · 2023Article
- Asymmetrically Substituted m-Terphenyl Phosphates Inhibit the Transcription Factor STAT5a.Chembiochem : a European journal of chemical biology · 2022Article
- Short loop functional commonality identified in leukaemia proteome highlights crucial protein sub-networks.NAR genomics and bioinformatics · 2021Article
- The Selectivity of Fosfosal for STAT5b over STAT5a is Mediated by Arg566 in the Linker Domain.Chembiochem : a European journal of chemical biology · 2020Article
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- A Novel Inhibitor of STAT5 Signaling Overcomes Chemotherapy Resistance in Myeloid Leukemia Cells.Cancers · 2019Article
- Review
- Structural and functional consequences of the STAT5BNature communications · 2019Article
- BioSITe: A Method for Direct Detection and Quantitation of Site-Specific Biotinylation.Journal of proteome research · 2018Article
- Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018Review
- Investigating critical genes and gene interaction networks that mediate cyclophosphamide sensitivity in chronic myelogenous leukemia.Molecular medicine reports · 2017Article
- Rational development of Stafib-2: a selective, nanomolar inhibitor of the transcription factor STAT5b.Scientific reports · 2017Article
- c-Kit-Positive Adipose Tissue-Derived Mesenchymal Stem Cells Promote the Growth and Angiogenesis of Breast Cancer.BioMed research international · 2017Article
- Ursolic acid-mediated apoptosis of K562 cells involves Stat5/Akt pathway inhibition through the induction of Gfi-1.Scientific reports · 2016Article
- Nanomolar inhibitors of the transcription factor STAT5b with high selectivity over STAT5a.Angewandte Chemie (International ed. in English) · 2015Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducers and activators of transcription (STATs) are latent cytoplasmic transcription factors linking extracellular signals to target gene transcription. Hematopoietic cells express two highly conserved STAT5-isoforms (STAT5A/STAT5B), and STAT5 is directly activated by JAK2 downstream of several cytokine receptors and the oncogenic BCR-ABL tyrosine kinase. Using an IL-3-dependent cell line with inducible BCR-ABL-expression we compared STAT5-activation by IL-3 and BCR-ABL in a STAT5-isoform specific manner. RNAi targeting of STAT5B strongly inhibits BCR-ABL-dependent cell proliferation, and STAT5B but not STAT5A is essential for BCL-XL-expression in the presence of BCR-ABL. Although BCR-ABL induces STAT5-tyrosine phosphorylation independent of JAK2-kinase activity, BCR-ABL is less efficient in inducing active STAT5A:STAT5B-heterodimerization than IL-3, leaving constitutive STAT5A and STAT5B-homodimerization unaffected. In comparison to IL-3, nuclear accumulation of a STAT5A-eGFP fusion protein is reduced by BCR-ABL, and BCR-ABL tyrosine kinase activity induces STAT5A-eGFP translocation to the cell membrane and co-localization with the IL-3 receptor. Furthermore, BCR-ABL-dependent phosphorylation of Y682 in STAT5A was detected by mass-spectrometry. Finally, RNAi targeting STAT5B but not STAT5A sensitizes human BCR-ABL-positive cell lines to imatinib-treatment. These data demonstrate differences between IL-3 and BCR-ABL-mediated STAT5-activation and isoform-specific effects, indicating therapeutic options for isoform-specific STAT5-inhibition in BCR-ABL-positive leukemia.
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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.