ArticleDisease models & mechanisms2014
Huntingtin is required for ER-to-Golgi transport and for secretory vesicle fusion at the plasma membrane.
Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- Generating a Cell Model to Study ER Stress in iPSC-Derived Medium Spiny Neurons from a Patient with Huntington's Disease.International journal of molecular sciences · 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
- Regulation of Mutant Huntingtin Mitochondrial Toxicity by Phosphomimetic Mutations within Its N-Terminal Region.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Navigating the neuronal recycling bin: Another look at huntingtin in coordinating autophagy.Autophagy reports · 2025Review
- The role of Golgi complex proteins in cell division and consequences of their dysregulation.Frontiers in cell and developmental biology · 2024Review
- Unraveling the Intricate Link: Deciphering the Role of the Golgi Apparatus in Breast Cancer Progression.International journal of molecular sciences · 2023Review
- Impact of ER Stress and ER-Mitochondrial Crosstalk in Huntington's Disease.International journal of molecular sciences · 2022Review
- Amyloid Prefibrillar Oligomers: The Surprising Commonalities in Their Structure and Activity.International journal of molecular sciences · 2021Review
- The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021Review
- Huntingtin: A Protein with a Peculiar Solvent Accessible Surface.International journal of molecular sciences · 2021Article
- Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease.Nature communications · 2021Article
- Increasing brain palmitoylation rescues behavior and neuropathology in Huntington disease mice.Science advances · 2021Article
- Article
- Mutant Huntingtin Is Cleared from the Brain via Active Mechanisms in Huntington Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Huntingtin and the Synapse.Frontiers in cellular neuroscience · 2021Review
- Quantitative Flow Cytometry-Based Assays for Measuring Constitutive Secretion.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Identification of Full-Length Wild-Type and Mutant Huntingtin Interacting Proteins by Crosslinking Immunoprecipitation in Mice Brain Cortex.Journal of Huntington's disease · 2021Article
- Lipid headgroups alter huntingtin aggregation on membranes.Biochimica et biophysica acta. Biomembranes · 2021Article
- Wild-type huntingtin regulates human macrophage function.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Huntingtin is a large membrane-associated scaffolding protein that associates with endocytic and exocytic vesicles and modulates their trafficking along cytoskeletal tracks. Although the progression of Huntington's disease is linked to toxic accumulation of mutant huntingtin protein, loss of wild-type huntingtin function might also contribute to neuronal cell death, but its precise function is not well understood. Therefore, we investigated the molecular role of huntingtin in exocytosis and observed that huntingtin knockdown in HeLa cells causes a delay in endoplasmic reticulum (ER)-to-Golgi transport and a reduction in the number of cargo vesicles leaving the trans-Golgi network. In addition, we found that huntingtin is required for secretory vesicle fusion at the plasma membrane. Similar defects in the early exocytic pathway were observed in primary fibroblasts from homozygous Htt(140Q/140Q) knock-in mice, which have the expansion inserted into the mouse huntingtin gene so lack wild-type huntingtin expression. Interestingly, heterozygous fibroblasts from a Huntington's disease patient with a 180Q expansion displayed no obvious defects in the early secretory pathway. Thus, our results highlight the requirement for wild-type huntingtin at distinct steps along the secretory pathway.
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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.