ArticleNature cell biology2008
Drosophila STAT is required for directly maintaining HP1 localization and heterochromatin stability.
Article in Nature cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.
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Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 140 citations in OpenAlex.
- The Prognostic Role of STAT5B Across Cancer Types and Comparative Analysis with STAT5A: A Systematic Review.Biomolecules · 2025Pooled it
- Expression and prognostic role of STAT5a across cancer types.Bioscience reports · 2023Pooled it
- The JAK/STAT pathway: key mechanism in gene activation, disease regulation, and emerging therapeutic targets.Molecular biology reports · 2026Review
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- JAK inhibition in PD-1 immunotherapy and tumor microenvironment.Frontiers in immunology · 2026Review
- CRIF counteracts oncogenic Ras and regulates heterochromatin.Molecular genetics and genomics : MGG · 2025Article
- ETS transcription factor pointed controls germline survival in Drosophila.PLoS genetics · 2025Article
- E-cadherin endocytosis promotes non-canonical EGFR:STAT signalling to induce cell death and inhibit heterochromatinisation.PLoS genetics · 2025Article
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Ruxolitinib-dependent reduction of seizure load and duration is accompanied by spatial memory improvement in the rat pilocarpine model of temporal lobe epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- The emerging role of SARS-CoV-2 nonstructural protein 1 (nsp1) in epigenetic regulation of host gene expression.FEMS microbiology reviews · 2024Review
- Computational simulation of JAK/STAT signaling in somatic versus germline stem cells.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- Canonical and non-canonical functions of STAT in germline stem cell maintenance.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Review
- The JAK-STAT Signaling Pathway in Epilepsy.Current neuropharmacology · 2023Review
- The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021Review
- Interactions and Feedbacks in E-Cadherin Transcriptional Regulation.Frontiers in cell and developmental biology · 2021Article
29 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
7 authors at 1 institution in 1 country.
Funding
Abstract
STAT (Signal transducer and activator of transcription) is a potent transcription factor and its aberrant activation by phosphorylation is associated with human cancers. We have shown previously that overactivation of JAK, which phosphorylates STAT, disrupts heterochromatin formation globally in Drosophila melanogaster. However, it remains unclear how this effect is mediated and whether STAT is involved. Here, we demonstrate that Drosophila STAT (STAT92E) is involved in controlling heterochromatin protein 1 (HP1) distribution and heterochromatin stability. We found, unexpectedly, that loss of STAT92E, had the same effects as overactivation of JAK in disrupting heterochromatin formation and heterochromatic gene silencing, whereas overexpression of STAT92E had the opposite effects. We have further shown that the unphosphorylated or 'transcriptionally inactive' form of STAT92E is localized on heterochromatin in association with HP1, and is required for stabilizing HP1 localization and histone H3 Lys 9 methylation (H3mK9) . However, activation by phosphorylation reduces heterochromatin-associated STAT92E, causing HP1 displacement and heterochromatin destabilization. Thus, reducing levels of unphosphorylated STAT92E, either by loss of STAT92E or increased phosphorylation, causes heterochromatin instability. These results suggest that activation of STAT by phosphorylation controls both access to chromatin and activity of the transcription machinery.
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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.