ArticleNucleic acids research2012
Evolution and function of CAG/polyglutamine repeats in protein-protein interaction networks.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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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.
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Who cites it
122 citing papers in PubMed, 203 citations in OpenAlex.
- Discovery of a mutation-containing circRNA in polyglutamine disease through systematic analysis of RNAs with CAG repeats.RNA biology · 2026Article
- CRISPR screening identifies TRIM27 as a destabilizer of the Smith-Magenis syndrome protein RAI1.Genetics · 2026Article
- Structural bases of signal generation and transduction by the SPS amino acid sensor of Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- Short CAG repeat variation as a regulatory factor in health and disease.Frontiers in genetics · 2026Review
- Insights into Noncanonical and Diversified Functions of ABCF1: From Health to Disease.Journal of molecular biology · 2025Review
- The HTT gene influences plasma neurofilament light chain and brain metabolism in prodromal Alzheimer's disease.Journal of neurology · 2025Article
- Fitness landscapes of human microsatellites.PLoS genetics · 2024Article
- Predicting the involvement of polyQ- and polyA in protein-protein interactions by their amino acid context.Heliyon · 2024Article
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- The hypoxia response pathway in the Antarctic fish Notothenia coriiceps is functional despite a poly Q/E insertion mutation in HIF-1α.Comparative biochemistry and physiology. Part D, Genomics & proteomics · 2024Article
- Homorepeat variability within the human population.NAR genomics and bioinformatics · 2024Article
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- Article
- Pathogen-specific structural features ofmBio · 2023Article
- Evolutionary Study of Protein Short Tandem Repeats in Protein Families.Biomolecules · 2023Article
- On the identification of potential novel therapeutic targets for spinocerebellar ataxia type 1 (SCA1) neurodegenerative disease using EvoPPI3.Journal of integrative bioinformatics · 2023Article
- Native functions of short tandem repeats.eLife · 2023Article
- Identification of subfunctionalized aggregate-remodeling J-domain proteins in Arabidopsis thaliana.Journal of experimental botany · 2023Article
- Mutation and selection processes regulating short tandem repeats give rise to genetic and phenotypic diversity across species.Journal of evolutionary biology · 2023Review
- The nucleotide landscape of polyXY regions.Computational and structural biotechnology journal · 2023Article
62 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expanded runs of consecutive trinucleotide CAG repeats encoding polyglutamine (polyQ) stretches are observed in the genes of a large number of patients with different genetic diseases such as Huntington's and several Ataxias. Protein aggregation, which is a key feature of most of these diseases, is thought to be triggered by these expanded polyQ sequences in disease-related proteins. However, polyQ tracts are a normal feature of many human proteins, suggesting that they have an important cellular function. To clarify the potential function of polyQ repeats in biological systems, we systematically analyzed available information stored in sequence and protein interaction databases. By integrating genomic, phylogenetic, protein interaction network and functional information, we obtained evidence that polyQ tracts in proteins stabilize protein interactions. This happens most likely through structural changes whereby the polyQ sequence extends a neighboring coiled-coil region to facilitate its interaction with a coiled-coil region in another protein. Alteration of this important biological function due to polyQ expansion results in gain of abnormal interactions, leading to pathological effects like protein aggregation. Our analyses suggest that research on polyQ proteins should shift focus from expanded polyQ proteins into the characterization of the influence of the wild-type polyQ on protein interactions.
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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.