ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016
Are aberrant phase transitions a driver of cellular aging?
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 2 of them syntheses that pooled it.
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
124 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Shift of the insoluble content of the proteome in the aging mouse brain.Proceedings of the National Academy of Sciences of the United States of America · 2023Pooled it
- A comparative meta-analysis of membraneless organelle-associated proteins with age related proteome of C. elegans.Cell stress & chaperones · 2022Pooled it
- Backbone Hydrogen Bonding as a Determinant of Condensate Material States.Journal of the American Chemical Society · 2026Article
- Embracing non-linearity in human ageing.Nature reviews. Genetics · 2026Review
- ATP binding to lysozyme and superfolder GFP amyloid fibrils induces aggregate remodeling and attenuates their cytotoxicity.Cell death discovery · 2026Article
- De novo design of peptides localizing at the interface of biomolecular condensates.Nature communications · 2026Article
- Nucleolar expansion: A biomolecular condensate mortality timer.Geromedicine · 2026Article
- Condensatopathies as a mechanistic framework for disease and integrated theranostic intervention.Theranostics · 2026Review
- Direct interaction between TDP-43 and Tau promotes their co-condensation, while suppressing Tau fibril formation and seeding.The EMBO journal · 2025Article
- Local Protein Synthesis at Synapses: A Driver for Synapse Diversification.Journal of neurochemistry · 2025Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Flexible iron: disorder in the ironome brings order to protein structure and function.Frontiers in molecular biosciences · 2025Article
- Fluorescence Loss After Photoactivation (FLAPh): A Pulse-Chase Cellular Assay for Understanding Kinetics and Dynamics of Viral Inclusions.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Reshuffling Overcrowded Milieu: Stress-Induced Reorganization of the Eukaryotic Membrane-Less Organelles.Sub-cellular biochemistry · 2025Review
- Catalytic Droplets: Enzyme Containing Microcompartments.Sub-cellular biochemistry · 2025Review
- Nucleo-cytoplasmic environment modulates spatiotemporal p53 phase separation.Science advances · 2024Article
- Molecular Mechanisms of Phase Separation and Amyloidosis of ALS/FTD-linked FUS and TDP-43.Aging and disease · 2024Review
- Age-specific and compartment-dependent changes in mitochondrial homeostasis and cytoplasmic viscosity in mouse peripheral neurons.Aging cell · 2024Article
- The role of biomolecular condensates in protein aggregation.Nature reviews. Chemistry · 2024Review
- Roles of Nucleic Acids in Protein Folding, Aggregation, and Disease.ACS chemical biology · 2024Review
64 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Why do cells age? Recent advances show that the cytoplasm is organized into many membrane-less compartments via a process known as phase separation, which ensures spatiotemporal control over diffusion-limited biochemical reactions. Although phase separation is a powerful mechanism to organize biochemical reactions, it comes with the trade-off that it is extremely sensitive to changes in physical-chemical parameters, such as protein concentration, pH, or cellular energy levels. Here, we highlight recent findings showing that age-related neurodegenerative diseases are linked to aberrant phase transitions in neurons. We discuss how these aberrant phase transitions could be tied to a failure to maintain physiological physical-chemical conditions. We generalize this idea to suggest that the process of cellular aging involves a progressive loss of the organization of phase-separated compartments in the cytoplasm.
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Identifiers
What Socratic 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 Socratic graph.