ReviewCell death & disease2021
Stress granules, RNA-binding proteins and polyglutamine diseases: too much aggregation?
Review in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
148 citing papers in PubMed, 214 citations in OpenAlex.
- Article
- Importin-8 silencing reduces Ataxin-3 aggregation and alleviates Machado-Joseph disease/spinocerebellar ataxia type 3.iScience · 2026Article
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Review
- A Dimeric Protein-RNA Glue Promotes Multivalent eIF4A-RNA Assembly.ACS central science · 2026Article
- The Interactions of Tau, RNA, and Stress Granules in Neurodegenerative Disease: A Comprehensive Review.Cells · 2026Review
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- Alphavirus nsP3 as a multifunctional orchestrator of virus-host interplay.Journal of virology · 2026Review
- Article
- Comparative transcriptomic analysis identifies conserved abiotic stress-responsive hub genes in Sorghum bicolor.BMC plant biology · 2026Article
- Stress granule dynamics orchestrate colitis-to-cancer transition via TOM1-mediated disassembly and driven oncogenesis in response to inflammatory oxidative stress.Redox biology · 2026Article
- Pan-biological characteristics of ataxin-2 protein.Neural regeneration research · 2026Article
- Article
- 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
- Liquid-liquid phase separation and the formation of amyloid fibrils from DcpS scavenger enzymes.Scientific reports · 2026Article
- TSC2 is a stress granule suppressor.bioRxiv : the preprint server for biology · 2026Article
- Temperature-specific regulation of the NDR kinase Orb6 by the MAPK Sty1 to promote heat stress resilience.Journal of cell science · 2026Article
- Astrocytic TIA1-Mediated Stress Granules Promote the Demyelination of Optic Neuritis by Sequestering mRNA of Cholesterol Synthesis Genes in an Experimental Autoimmune Encephalomyelitis Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The dynamic and heterogeneous composition of biomolecular condensates and its functional relevance.Nature reviews. Molecular cell biology · 2026Review
- Single-Cell RNA Analysis of Murine Osteosarcoma Uncovers Skp2 Function in Metastasis, Genomic Instability, and Immune Activation and Reveals Additional Target Pathways.Cancer research communications · 2026Article
88 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Stress granules (SGs) are membraneless cell compartments formed in response to different stress stimuli, wherein translation factors, mRNAs, RNA-binding proteins (RBPs) and other proteins coalesce together. SGs assembly is crucial for cell survival, since SGs are implicated in the regulation of translation, mRNA storage and stabilization and cell signalling, during stress. One defining feature of SGs is their dynamism, as they are quickly assembled upon stress and then rapidly dispersed after the stress source is no longer present. Recently, SGs dynamics, their components and their functions have begun to be studied in the context of human diseases. Interestingly, the regulated protein self-assembly that mediates SG formation contrasts with the pathological protein aggregation that is a feature of several neurodegenerative diseases. In particular, aberrant protein coalescence is a key feature of polyglutamine (PolyQ) diseases, a group of nine disorders that are caused by an abnormal expansion of PolyQ tract-bearing proteins, which increases the propensity of those proteins to aggregate. Available data concerning the abnormal properties of the mutant PolyQ disease-causing proteins and their involvement in stress response dysregulation strongly suggests an important role for SGs in the pathogenesis of PolyQ disorders. This review aims at discussing the evidence supporting the existence of a link between SGs functionality and PolyQ disorders, by focusing on the biology of SGs and on the way it can be altered in a PolyQ disease context.
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What OpenQuestion holds
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.