ArticleNature communications2020
G3BP1 controls the senescence-associated secretome and its impact on cancer progression.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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Who cites it
56 citing papers in PubMed, 85 citations in OpenAlex.
- Heat stress promotes GTBP-1 association with perinuclear P-bodies in the C. elegans germline.PLoS genetics · 2026Article
- Stress granules and RNA-binding proteins in cellular senescence: a modular perspective on stress adaptation and inflammation.Molecular biology reports · 2026Review
- cGAS-STING signaling in aging and age-related diseases: therapeutic promise and precaution.Archives of pharmacal research · 2026Review
- G3BP1 Succinylation at K413 is Critical for Cardiac Function by Modulating PI3K-AKT-mTOR Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction.European heart journal · 2026Article
- G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs.Bioscience reports · 2026Article
- 5'untranslated regions provide a versatile toolkit for tunable exogenous protein expression.Molecular biology of the cell · 2026Article
- Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.Aging cell · 2026Article
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- TREM2 Drives Neutrophil Extracellular Traps-Induced Dendritic Cell Maturation and Contributes to Lupus Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RECQL4 promotes the malignant progression of lung adenocarcinoma through the YBX1/G3BP1-mediated NF-κB signaling pathway.Cell death discovery · 2026Article
- Design of CellProfiler-Based Pipelines Enabling the Attribution of Molecular Stress Markers to Specific Tissue and Subcellular Compartments of the Colonic Mucosa.Cellular and molecular gastroenterology and hepatology · 2026Article
- Pharmacological modulation of stress granulesFrontiers in pharmacology · 2026Review
- Therapy-induced senescent glioblastoma cells sustain a procancer immune microenvironment by activating DDX58-mediated STAT1 signaling.Neuro-oncology · 2025Article
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- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- TNFAIP2 promotes NF-κB signaling mediate lymph node metastasis of oral squamous cell carcinoma by protecting IKKβ from ubiquitin proteasome degradation.Cell communication and signaling : CCS · 2025Article
- The transcription factor STAT3 and aging: an intermediate medium.Biogerontology · 2025Review
- Senescent human fibroblasts have increased FasL expression and impair the tumor immune response.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular senescence is a known driver of carcinogenesis and age-related diseases, yet senescence is required for various physiological processes. However, the mechanisms and factors that control the negative effects of senescence while retaining its benefits are still elusive. Here, we show that the rasGAP SH3-binding protein 1 (G3BP1) is required for the activation of the senescent-associated secretory phenotype (SASP). During senescence, G3BP1 achieves this effect by promoting the association of the cyclic GMP-AMP synthase (cGAS) with cytosolic chromatin fragments. In turn, G3BP1, through cGAS, activates the NF-κB and STAT3 pathways, promoting SASP expression and secretion. G3BP1 depletion or pharmacological inhibition impairs the cGAS-pathway preventing the expression of SASP factors without affecting cell commitment to senescence. These SASPless senescent cells impair senescence-mediated growth of cancer cells in vitro and tumor growth in vivo. Our data reveal that G3BP1 is required for SASP expression and that SASP secretion is a primary mediator of senescence-associated tumor growth.
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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.