ArticleNature communications2025
Fbxo42 promotes the degradation of Ataxin-2 granules to trigger terminal Xbp1 signaling.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Ataxin-2 regulates the synaptonemal complex to ensure chromosome pairing during female meiosis.Genetics · 2026Article
- Ubiquitin and ubiquitin-like modifications in the endoplasmic reticulum stress response.The FEBS journal · 2026Review
- Dual IRE1 targets: Determinants of the cell fate?The FEBS journal · 2026Review
- The regulation of protein phosphatase 4 by FBXO42 is required for cancer cell survival.EMBO reports · 2026Article
- HNRNPD Induces Radioresistance in Nasopharyngeal Carcinoma by Sequestering GRAMD4 mRNA in Stress Granules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Bioinformatic Analyses of the Ataxin-2 Family Since Algae Emphasize Its Small Isoforms, Large Chimerisms, and the Importance of Human Exon 1B as Target of Therapies to Prevent Neurodegeneration.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
The Unfolded Protein Response (UPR) is activated by the accumulation of misfolded proteins in the Endoplasmic Reticulum (ER), a condition known as ER stress. Prolonged ER stress and UPR activation cause cell death, by mechanisms that remain poorly understood. Here, we report that regulation of Ataxin-2 by Fbxo42 is a crucial step during UPR-induced cell death. From a genetic screen in Drosophila, we identify loss of function mutations in Fbxo42 that suppress cell death and retinal degeneration induced by the overexpression of Xbp1
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Registered trials
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