ArticleLife science alliance2019
The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
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- Temperature-specific regulation of the NDR kinase Orb6 by the MAPK Sty1 to promote heat stress resilience.Journal of cell science · 2026Article
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- Stress granule dynamics govern TOR reactivation and growth recovery during post-heat stress adaptation.Science advances · 2025Article
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- A Charge-Driven Strategy for Covalent Modification and Modulation of Biomolecular Condensates.Journal of the American Chemical Society · 2025Article
- Membraneless Organelles and Phase Separation in Tumours: Mechanisms and Prospects.Cell proliferation · 2025Review
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- iPSC-Derived Liver Organoids as a Tool to Study Medium Chain Acyl-CoA Dehydrogenase Deficiency.Journal of inherited metabolic disease · 2025Article
- Regulation of innate immunity by liquid-liquid phase separation: a focus on veterinary viruses.Frontiers in microbiology · 2025Review
- Precision-cut liver slices as an ex vivo model to assess impaired hepatic glucose production.Communications biology · 2024Article
- Metal-polyphenol-network coated R612F nanoparticles reduce drug resistance in hepatocellular carcinoma by inhibiting stress granules.Cell death discovery · 2024Article
- Myeloid PTEN loss affects the therapeutic response by promoting stress granule assembly and impairing phagocytosis by macrophages in breast cancer.Cell death discovery · 2024Article
- Pifithrin-µ Induces Stress Granule Formation, Regulates Cell Survival, and Rewires Cellular Signaling.Cells · 2024Article
- Apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) promotes stress granule formation via YBX1 phosphorylation in ovarian cancer.Cellular and molecular life sciences : CMLS · 2024Article
- Personalised modelling of clinical heterogeneity between medium-chain acyl-CoA dehydrogenase patients.BMC biology · 2023Article
- Signaling Pathways Leading to mTOR Activation Downstream Cytokine Receptors in Lymphocytes in Health and Disease.International journal of molecular sciences · 2023Review
- GePI: large-scale text mining, customized retrieval and flexible filtering of gene/protein interactions.Nucleic acids research · 2023Article
- SREBP signaling is essential for effective B cell responses.Nature immunology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All cells and organisms exhibit stress-coping mechanisms to ensure survival. Cytoplasmic protein-RNA assemblies termed stress granules are increasingly recognized to promote cellular survival under stress. Thus, they might represent tumor vulnerabilities that are currently poorly explored. The translation-inhibitory eIF2α kinases are established as main drivers of stress granule assembly. Using a systems approach, we identify the translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regulator mammalian target of rapamycin complex 1 (mTORC1) to promote stress granule assembly. When highly active, PI3K is the main driver of stress granules; however, the impact of p38 becomes apparent as PI3K activity declines. PI3K and p38 thus act in a hierarchical manner to drive mTORC1 activity and stress granule assembly. Of note, this signaling hierarchy is also present in human breast cancer tissue. Importantly, only the recognition of the PI3K-p38 hierarchy under stress enabled the discovery of p38's role in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation.
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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.