ArticleMolecular and cellular biology2009
Mutant huntingtin impairs vesicle formation from recycling endosomes by interfering with Rab11 activity.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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61 citing papers in PubMed, 116 citations in OpenAlex.
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- Decanoic Acid Treatment Alleviates Non-cell Autonomous Transfer of HD Pathology by Secretome of Mutant Huntingtin Expressing Cells.Neurochemical research · 2026Article
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- The profiling of extracellular vesicle subtypes in Huntington's disease brains identifies Alix as a novel marker of neuropathology.Acta neuropathologica communications · 2025Article
- Article
- Impaired XK recycling for importing manganese underlies striatal vulnerability in Huntington's disease.The Journal of cell biology · 2022Article
- CAG Repeat Instability in the Peripheral and Central Nervous System of Transgenic Huntington's Disease Monkeys.Biomedicines · 2022Article
- Therapeutic Targeting of Rab GTPases: Relevance for Alzheimer's Disease.Biomedicines · 2022Review
- Nuclear and Cytoplasmatic Players in Mitochondria-Related CNS Disorders: Chromatin Modifications and Subcellular Trafficking.Biomolecules · 2022Review
- Defective repair of topoisomerase I induced chromosomal damage in Huntington's disease.Cellular and molecular life sciences : CMLS · 2022Article
- Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.Matrix biology plus · 2021Review
- Article
- Huntingtin CAG expansion impairs germ layer patterning in synthetic human 2D gastruloids through polarity defects.Development (Cambridge, England) · 2021Article
- Gene targeting techniques for Huntington's disease.Ageing research reviews · 2021Review
- Correlative light and electron microscopy suggests that mutant huntingtin dysregulates the endolysosomal pathway in presymptomatic Huntington's disease.Acta neuropathologica communications · 2021Article
- Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases.Frontiers in neuroscience · 2021Review
- Disposition of Proteins and Lipids in Synaptic Membrane Compartments Is Altered in Q175/Q7 Huntington's Disease Mouse Striatum.Frontiers in synaptic neuroscience · 2021Article
- Vps54 regulatesBiology open · 2020Article
- MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Loss of Hap1 selectively promotes striatal degeneration in Huntington disease mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Huntingtin (Htt) localizes to endosomes, but its role in the endocytic pathway is not established. Recently, we found that Htt is important for the activation of Rab11, a GTPase involved in endosomal recycling. Here we studied fibroblasts of healthy individuals and patients with Huntington's disease (HD), which is a movement disorder caused by polyglutamine expansion in Htt. The formation of endocytic vesicles containing transferrin at plasma membranes was the same in control and HD patient fibroblasts. However, HD fibroblasts were delayed in recycling biotin-transferrin back to the plasma membrane. Membranes of HD fibroblasts supported less nucleotide exchange on Rab11 than did control membranes. Rab11-positive vesicular and tubular structures in HD fibroblasts were abnormally large, suggesting that they were impaired in forming vesicles. We used total internal reflection fluorescence imaging of living fibroblasts to monitor fluorescence-labeled transferrin-carrying transport intermediates that emerged from recycling endosomes. HD fibroblasts had fewer small vesicles and more large vesicles and long tubules than did control fibroblasts. Dominant active Rab11 expressed in HD fibroblasts normalized the recycling of biotin-transferrin. We propose a novel mechanism for cellular dysfunction by the HD mutation arising from the inhibition of Rab11 activity and a deficit in vesicle formation at recycling endosomes.
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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.