ArticleCell systems2022
Dynamics of huntingtin protein interactions in the striatum identifies candidate modifiers of Huntington disease.
Article in Cell systems, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Uncovering hidden protein networks in Huntington's disease: implications for pathogenesis and therapy.Molecular biology reports · 2026Review
- Huntingtin (HTT) interactome in regulation of DNA repair/remodeling and RNA processing pathways.Life science alliance · 2026Article
- Structural-functional analyses of the huntingtin/HAP40 complex inJournal of biomolecular structure & dynamics · 2026Article
- Aberrant medial ganglionic eminence (MGE) GABAergic neurogenesis contributes to Huntington's disease pathogenesis.Neurobiology of disease · 2026Article
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- High-affinity, structure-validated and selective macrocyclic peptide tools for chemical biology studies of Huntingtin.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ALS and Huntington Disease: Unraveling the Connections between TDP-43 and Huntingtin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Proximal proteomics reveals a landscape of human nuclear condensates.Nature cell biology · 2025Article
- Dysregulation of huntingtin interacting protein networks in human juvenile Huntington's disease brain.Journal of Huntington's disease · 2025Article
- Revolutionizing Huntington's Disease Treatment: Breakthroughs in AAV-Mediated Gene Therapy.Cells · 2025Review
- Structure of the Huntingtin F-actin complex reveals its role in cytoskeleton organization.Science advances · 2025Article
- Huntingtin reduction results in altered nuclear structure and heterochromatic instability.Human molecular genetics · 2025Article
- High-Affinity, Structure-Validated and Selective Macrocyclic Peptide Tools for Chemical Biology Studies of Huntingtin.bioRxiv : the preprint server for biology · 2025Article
- Multi-epitope immunocapture of huntingtin reveals striatum-selective molecular signatures.Molecular systems biology · 2025Article
- Opposing roles for GSK3β and ERK1-dependent phosphorylation of huntingtin during neuronal dysfunction and cell death in Huntington's disease.Cell death & disease · 2025Article
- Challenges and advances for huntingtin detection in cerebrospinal fluid: in support of relative quantification.Biomarker research · 2025Article
- Insights into RNA-mediated pathology in new mouse models of Huntington's disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Structural and Dynamical Properties of Nucleic Acid Hairpins Implicated in Trinucleotide Repeat Expansion Diseases.Biomolecules · 2024Review
- I'm Walking into Spiderwebs: Making Sense of Protein-Protein Interaction Data.Journal of proteome research · 2024Review
- Role of TFEB in Huntington's Disease.Biology · 2024Review
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13 authors at 6 institutions in 2 countries.
Funding
Abstract
Huntington disease (HD) is a monogenic neurodegenerative disorder with one causative gene, huntingtin (HTT). Yet, HD pathobiology is multifactorial, suggesting that cellular factors influence disease progression. Here, we define HTT protein-protein interactions (PPIs) perturbed by the mutant protein with expanded polyglutamine in the mouse striatum, a brain region with selective HD vulnerability. Using metabolically labeled tissues and immunoaffinity purification-mass spectrometry, we establish that polyglutamine-dependent modulation of HTT PPI abundances and relative stability starts at an early stage of pathogenesis in a Q140 HD mouse model. We identify direct and indirect PPIs that are also genetic disease modifiers using in-cell two-hybrid and behavioral assays in HD human cell and Drosophila models, respectively. Validated, disease-relevant mHTT-dependent interactions encompass mediators of synaptic neurotransmission (SNAREs and glutamate receptors) and lysosomal acidification (V-ATPase). Our study provides a resource for understanding mHTT-dependent dysfunction in cortico-striatal cellular networks, partly through impaired synaptic communication and endosomal-lysosomal system. A record of this paper's Transparent Peer Review process is included in the supplemental information.
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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.