ArticlePloS one2010
F-actin binding regions on the androgen receptor and huntingtin increase aggregation and alter aggregate characteristics.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Structure of the Huntingtin F-actin complex reveals its role in cytoskeleton organization.Science advances · 2025Article
- Perturbed actin cap as a new personalized biomarker in primary fibroblasts of Huntington's disease patients.Frontiers in cell and developmental biology · 2023Article
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Article
- Disposition of Proteins and Lipids in Synaptic Membrane Compartments Is Altered in Q175/Q7 Huntington's Disease Mouse Striatum.Frontiers in synaptic neuroscience · 2021Article
- The MYH9 Cytoskeletal Protein Is a Novel Corepressor of Androgen Receptors.Frontiers in oncology · 2021Article
- The Huntingtin-interacting protein SETD2/HYPB is an actin lysine methyltransferase.Science advances · 2020Article
- Huntingtin associates with the actin cytoskeleton and α-actinin isoforms to influence stimulus dependent morphology changes.PloS one · 2019Article
- Rac1 Activity Is Modulated by Huntingtin and Dysregulated in Models of Huntington's Disease.Journal of Huntington's disease · 2019Article
- Quantitative Proteomic Analysis Reveals Similarities between Huntington's Disease (HD) and Huntington's Disease-Like 2 (HDL2) Human Brains.Journal of proteome research · 2016Article
- Identification of novel polyglutamine-expanded aggregation species in spinal and bulbar muscular atrophy.Brain research · 2015Article
- Polyglutamine domain flexibility mediates the proximity between flanking sequences in huntingtin.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Structure and topology of the huntingtin 1-17 membrane anchor by a combined solution and solid-state NMR approach.Biophysical journal · 2013Article
- An N-terminal nuclear export signal regulates trafficking and aggregation of Huntingtin (Htt) protein exon 1.The Journal of biological chemistry · 2013Article
- Substrate recognition in nuclear protein quality control degradation is governed by exposed hydrophobicity that correlates with aggregation and insolubility.The Journal of biological chemistry · 2013Article
- Mechanisms mediating spinal and bulbar muscular atrophy: investigations into polyglutamine-expanded androgen receptor function and dysfunction.Frontiers in neurology · 2013Article
- Physical chemistry of polyglutamine: intriguing tales of a monotonous sequence.Journal of molecular biology · 2012Review
- Article
- Multiple phenotypes in Huntington disease mouse neural stem cells.Molecular and cellular neurosciences · 2012Article
- Clues to γ-secretase, huntingtin and Hirano body normal function using the model organism Dictyostelium discoideum.Journal of biomedical science · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Protein aggregation is associated with neurodegeneration. Polyglutamine expansion diseases such as spinobulbar muscular atrophy and Huntington disease feature proteins that are destabilized by an expanded polyglutamine tract in their N-termini. It has previously been reported that intracellular aggregation of these target proteins, the androgen receptor (AR) and huntingtin (Htt), is modulated by actin-regulatory pathways. Sequences that flank the polyglutamine tract of AR and Htt might influence protein aggregation and toxicity through protein-protein interactions, but this has not been studied in detail. Here we have evaluated an N-terminal 127 amino acid fragment of AR and Htt exon 1. The first 50 amino acids of ARN127 and the first 14 amino acids of Htt exon 1 mediate binding to filamentous actin in vitro. Deletion of these actin-binding regions renders the polyglutamine-expanded forms of ARN127 and Htt exon 1 less aggregation-prone, and increases the SDS-solubility of aggregates that do form. These regions thus appear to alter the aggregation frequency and type of polyglutamine-induced aggregation. These findings highlight the importance of flanking sequences in determining the propensity of unstable proteins to misfold.
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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.