ArticleMolecular and cellular biology1996
Activation of different Stat5 isoforms contributes to cell-type-restricted signaling in response to interferons.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 171 citations in OpenAlex.
- Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons.International journal of molecular sciences · 2026Article
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- Cytokine Signaling in Pediatric Kidney Tumor Cell Lines WT-CLS1, WT-3ab and G-401.International journal of molecular sciences · 2024Article
- Interleukin-22 facilitates the interferon-λ-mediated production of tripartite motif protein 25 to inhibit replication of duck viral hepatitis A virus type 1.Veterinary research · 2023Article
- Interferons and Resistance Mechanisms in Tumors and Pathogen-Driven Diseases-Focus on the Major Histocompatibility Complex (MHC) Antigen Processing Pathway.International journal of molecular sciences · 2023Review
- Cytokines Activate JAK-STAT Signaling Pathway in MG-63 Cells on Titanium and Zirconia.Materials (Basel, Switzerland) · 2022Article
- MARCH3 negatively regulates IL-3-triggered inflammatory response by mediating K48-linked polyubiquitination and degradation of IL-3Rα.Signal transduction and targeted therapy · 2022Article
- Robust innate immune responses at the placenta during early gestation may limit in utero HIV transmission.PLoS pathogens · 2021Article
- Deconvoluting global cytokine signaling networks in natural killer cells.Nature immunology · 2021Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Rapidly Switchable Universal CAR-T Cells for Treatment of CD123-Positive Leukemia.Molecular therapy oncolytics · 2020Article
- Importance of Type I and III Interferons at Respiratory and Intestinal Barrier Surfaces.Frontiers in immunology · 2020Review
- JAK2 Inhibition Impairs Proliferation and Sensitises Cervical Cancer Cells to Cisplatin-Induced Cell Death.Cancers · 2019Article
- STAT5: a Target of Antagonism by Neurotropic Flaviviruses.Journal of virology · 2019Article
- Review
- Balancing STAT Activity as a Therapeutic Strategy.Cancers · 2019Review
- Differential Regulation of Type I and Type III Interferon Signaling.International journal of molecular sciences · 2019Review
- Protective Roles of Interferon-γ in Cardiac Hypertrophy Induced by Sustained Pressure Overload.Journal of the American Heart Association · 2018Article
- 17Journal of the Endocrine Society · 2018Article
- Interferon-Gamma at the Crossroads of Tumor Immune Surveillance or Evasion.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine phosphorylation and activation of the transcription factor Stat5 occur in response to stimuli like granulocyte-macrophage colony-stimulating factor, interleukin-3, or erythropoietin that stimulate both proliferation and differentiation of hematopoietic cells. It is unclear whether Stat5 is part of a proliferative response or part of the events leading to cellular differentiation. Here we report that agents promoting differentiation but not proliferation of hematopoietic cells, like phorbol ester or both types of interferons (IFNs), activate Stat5 in promonocytic U937 cells. Both IFN types caused tyrosine phosphorylation and DNA binding of predominantly one Stat5 isoform (Stat5a) despite expression of both Stat5a and Stat5b proteins. Monocytic differentiation of U937 cells led to a strong decrease in IFN-gamma-mediated activation of Stat5 but not of Stat1. Transactivation of Stat5-target genes occurred in response to IFN-gamma, which activates both Stat5 and Stat1, but not in response to granulocyte-macrophage colony-stimulating factor, which activates only Stat5. Tyrosine phosphorylation of Stat5 is not generally part of the IFN response. IFN-gamma did not cause Stat5 activation in HeLa cells, despite the expression of both Stat5 isoforms at similar levels. By contrast, IFN-alpha caused tyrosine phosphorylation and DNA binding of exclusively the b isoform of Stat5, and activated Stat5b formed a DNA binding activity previously found in HeLa cells and designated IFN-alpha activation factor 2. Taken together, our results demonstrate that ligand binding of IFN receptors leads to an isoform-specific activation of Stat5 in a restricted number of cell lineages. Moreover, they suggest that Stat5 might be part of the differentiation response of myeloid cells.
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Registered trials
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