ReviewCritical reviews in biochemistry and molecular biology
Defining the limits: Protein aggregation and toxicity in vivo.
Review in Critical reviews in biochemistry and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
30 citing papers in PubMed.
- Study of blood linear RNA nominates CD55 and DLD as early-stage biomarkers for Parkinson's disease.Brain : a journal of neurology · 2026Article
- Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Actually, what is a gain-of-function mutation?Genetics · 2026Article
- Dysbiosis and Neurodegeneration in ALS: Unraveling the Gut-Brain Axis.Neuromolecular medicine · 2025Review
- iPAR: a new reporter for eukaryotic cytoplasmic protein aggregation.BMC methods · 2025Article
- Design of an Arabidopsis thaliana reporter line to detect heat-sensing and signaling mutants.Plant methods · 2023Article
- Challenges of repurposing tetracyclines for the treatment of Alzheimer's and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Minimal Yet Powerful: The Role of Archaeal Small Heat Shock Proteins in Maintaining Protein Homeostasis.Frontiers in molecular biosciences · 2022Review
- Hsf1 activation by proteotoxic stress requires concurrent protein synthesis.Molecular biology of the cell · 2021Article
- Sis1 potentiates the stress response to protein aggregation and elevated temperature.Nature communications · 2020Article
- Trehalose alleviates the phenotype of Machado-Joseph disease mouse models.Journal of translational medicine · 2020Article
- Therapeutic Approaches Targeting Protein Aggregation in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2020Review
- Article
- Causative Genes in Amyotrophic Lateral Sclerosis and Protein Degradation Pathways: a Link to Neurodegeneration.Molecular neurobiology · 2018Review
- NAA10-related syndrome.Experimental & molecular medicine · 2018Review
- Truncating Variants in NAA15 Are Associated with Variable Levels of Intellectual Disability, Autism Spectrum Disorder, and Congenital Anomalies.American journal of human genetics · 2018Article
- Prion-Like Characteristics of Polyglutamine-Containing Proteins.Cold Spring Harbor perspectives in medicine · 2018Review
- Pathways of cellular proteostasis in aging and disease.The Journal of cell biology · 2018Review
- The Insoluble Protein Deposit (IPOD) in Yeast.Frontiers in molecular neuroscience · 2018Article
- Antisense Oligonucleotide-Mediated Removal of the Polyglutamine Repeat in Spinocerebellar Ataxia Type 3 Mice.Molecular therapy. Nucleic acids · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Abstract others complementary, to resolve mis-folded proteins when they arise, ranging from refolding through the action of molecular chaperones to elimination through regulated proteolytic mechanisms. These protein quality control pathways are sufficient, under normal conditions, to maintain a functioning proteome, but in response to diverse environmental, genetic and/or stochastic events, protein mis-folding exceeds the corrective capacity of these pathways, leading to the accumulation of aggregates and ultimately toxicity. Particularly devastating examples of these effects include certain neurodegenerative diseases, such as Huntington's Disease, which are associated with the expansion of polyglutamine tracks in proteins. In these cases, protein mis-folding and aggregation are clear contributors to pathogenesis, but uncovering the precise mechanistic links between the two events remains an area of active research. Studies in the yeast Saccharomyces cerevisiae and other model systems have uncovered previously unanticipated complexity in aggregation pathways, the contributions of protein quality control processes to them and the cellular perturbations that result from them. Together these studies suggest that aggregate interactions and localization, rather than their size, are the crucial considerations in understanding the molecular basis of toxicity.
Indexed as
Identifiers
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.