ArticleThe EMBO journal2024
Energy stress promotes P-bodies formation via lysine-63-linked polyubiquitination of HAX1.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- AMPK γ-Subunit Isoform Switching Governs Temozolomide Resistance and Survival in Glioblastoma.Cells · 2026Article
- Identification and Experimental Validation of Key Genes Related to Neuroendocrine in Periodontitis Based on Single-Cell and Bulk Transcriptome Data.Journal of cellular and molecular medicine · 2026Article
- Plant P-bodies in post-transcriptional control: Composition, dynamics, and context-dependent roles.Plant communications · 2026Review
- Reshaping cancer cell plasticity by P-body dynamics and protein translation.Communications biology · 2026Review
- Disruption of the nucleocapsid-RNA condensation by punicalagin is a broad-spectrum antiviral approach.Fundamental research · 2026Article
- Biomolecular phase separation in tumorigenesis: from aberrant condensates to therapeutic vulnerabilities.Molecular cancer · 2025Review
- TRIM23 promotes 5-Fluorouracil resistance in colorectal cancer by upregulating GALNT4 expression.Apoptosis : an international journal on programmed cell death · 2025Article
- Stress sensing and response through biomolecular condensates in plants.Plant communications · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Energy stress, characterized by the reduction of intracellular ATP, has been implicated in various diseases, including cancer. Here, we show that energy stress promotes the formation of P-bodies in a ubiquitin-dependent manner. Upon ATP depletion, the E3 ubiquitin ligase TRIM23 catalyzes lysine-63 (K63)-linked polyubiquitination of HCLS1-associated protein X-1 (HAX1). HAX1 ubiquitination triggers its liquid‒liquid phase separation (LLPS) and contributes to P-bodies assembly induced by energy stress. Ubiquitinated HAX1 also interacts with the essential P-body proteins, DDX6 and LSM14A, promoting their condensation. Moreover, we find that this TRIM23/HAX1 pathway is critical for the inhibition of global protein synthesis under energy stress conditions. Furthermore, high HAX1 ubiquitination, and increased cytoplasmic localization of TRIM23 along with elevated HAX1 levels, promotes colorectal cancer (CRC)-cell proliferation and correlates with poor prognosis in CRC patients. Our data not only elucidate a ubiquitination-dependent LLPS mechanism in RNP granules induced by energy stress but also propose a promising target for CRC therapy.
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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 Socratic graph.