ArticleHuman molecular genetics2023
G3BP1-dependent mechanism suppressing protein aggregation in Huntington's models and its demise upon stress granule assembly.
Article in Human molecular genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Stress granules at the crossroads of the proteostasis network.RNA biology · 2026Review
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- G3BP1 depletion, observed in Parkinson's Disease, drives Golgi-lysosome-autophagy defects.Cell death and differentiation · 2026Article
- Shuttle and stabilize: H1.2-FUS complex in amyotrophic lateral sclerosis pathogenesis.Neural regeneration research · 2026Article
- Resveratrol offers therapeutic potential in obesity-related osteoarthritis by targeting ferroptosis via G3BP1-SGs/mTOR modulation.Communications biology · 2026Article
- Modulation of the Stress Granule Component Carhsp1 Mitigates Disease-Associated Deficits in Spinocerebellar Ataxia Type 3 Mouse Models.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Expression Patterns of T-Cell Intracellular Antigen 1 in Neurodegenerative Disorders and Stroke.International journal of molecular sciences · 2026Review
- Stress granules as a central hub linking organelle stress, aging, and neurodegeneration.BMB reports · 2026Review
- RNA Granules at the Crossroads of Synaptic Dysfunction and Neurodegeneration.Journal of neurochemistry · 2025Review
- Partial Reprogramming in Senescent Schwann Cells Enhances Peripheral Nerve Regeneration via Restoration of Stress Granule Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The aging factor EPS8 induces disease-related protein aggregation through RAC signaling hyperactivation.Nature aging · 2025Article
- Repeated activation of Gαq has a detrimental impact on C. elegans in an age-dependent manner.The Journal of biological chemistry · 2025Article
- CellPHIE: Integrating Pathway Discovery With Pooled Profiling of Perturbations Uncovers Pathways of Huntington's Disease, Including Genetic Modifiers of Neuronal Development and Morphology.bioRxiv : the preprint server for biology · 2025Article
- Stress granules: emerging players in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Huntingtin is an RNA binding protein and participates inScience advances · 2024Article
- Article
- Mutant-Huntingtin Molecular Pathways Elucidate New Targets for Drug Repurposing.International journal of molecular sciences · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress granules are membrane-less ribonucleoprotein organelles that assemble upon exposure to stress conditions, but rapidly disassemble upon removal of stress. However, chronic stress can lead to persistent stress granules, a feature of distinct age-related neurodegenerative disorders. Among them, Huntington's disease (HD), which is caused by mutant expansion of the polyglutamine (polyQ) repeats of huntingtin protein (HTT), leading to its aggregation. To identify modulators of mutant HTT aggregation, we define its interactome in striatal neurons differentiated from patient-derived induced pluripotent stem cells (HD-iPSCs). We find that HTT interacts with G3BP1, a characteristic component of stress granules. Knockdown of G3BP1 increases mutant HTT protein levels and abolishes the ability of iPSCs as well as their differentiated neural counterparts to suppress mutant HTT aggregation. Moreover, loss of G3BP1 hastens polyQ-expanded aggregation and toxicity in the neurons of HD C. elegans models. Likewise, the assembly of G3BP1 into stress granules upon distinct stress conditions also reduces its interaction with HTT in human cells, promoting mutant HTT aggregation. Notably, enhancing the levels of G3BP1 is sufficient to induce proteasomal degradation of mutant HTT and prevent its aggregation, whereas the formation of stress granules blocks these ameliorative effects. In contrast, a mutant G3BP1 variant that cannot accumulate into granules retains its capacity to prevent mutant HTT aggregation even when the cells assemble stress granules. Thus, our findings indicate a direct role of G3BP1 and stress granule assembly in mutant HTT aggregation that may have implications for HD.
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