ArticleMolecular and cellular biology2004
Mutant huntingtin impairs axonal trafficking in mammalian neurons in vivo and in vitro.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers.
What it found
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Who cites it
251 citing papers in PubMed, 505 citations in OpenAlex.
- The small giant actor in the pathogenesis of neurodegenerative diseases: Microtubules.Metabolic brain disease · 2026Review
- Review
- Huntingtin polyglutamine expansions misdirect axonal transport by perturbing motor and adaptor recruitment.iScience · 2026Article
- Synaptic mitochondria in aging and neurodegenerative diseases: Functional decline and vulnerability.Neural regeneration research · 2026Article
- SKOOTS: Skeleton-Oriented Object Segmentation for Mitochondria in High-Resolution Cochlear EM Datasets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Quality control of protein import into mammalian mitochondria.Protein science : a publication of the Protein Society · 2026Review
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- Actin depolymerization promotes axon regeneration by restoring axonal mitochondrial transport in mouse models of optic neuropathy.Science translational medicine · 2026Article
- Differential effects of overexpression of mutant huntingtin and TDP-43 in agouti-related protein neurons in the arcuate nucleus of the hypothalamus in mice.Acta neuropathologica communications · 2025Article
- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- SKOOTS: Skeleton-oriented object segmentation for mitochondria.bioRxiv : the preprint server for biology · 2025Article
- G9a an Epigenetic Therapeutic Strategy for Neurodegenerative Conditions: From Target Discovery to Clinical Trials.Medicinal research reviews · 2025Review
- Cholesterol and SREBP2 Dynamics During Spermatogenesis Stages in Rabbits: Effects of High-Fat Diet and Protective Role of Extra Virgin Olive Oil.International journal of molecular sciences · 2025Article
- Optineurin-facilitated axonal mitochondria delivery promotes neuroprotection and axon regeneration.Nature communications · 2025Article
- Crosstalk Between Phase-Separated Membraneless Condensates and Membrane-Bound Organelles in Cellular Function and Disease.Advances in experimental medicine and biology · 2025Review
- Developmental and physiological impacts of pathogenic human huntingtin protein in the nervous system.Neurobiology of disease · 2024Article
- Optineurin-facilitated axonal mitochondria delivery promotes neuroprotection and axon regeneration.bioRxiv : the preprint server for biology · 2024Article
- From Pathogenesis to Therapeutics: A Review of 150 Years of Huntington's Disease Research.International journal of molecular sciences · 2023Review
- Mitochondrial Dysfunction in Repeat Expansion Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- The Role of Mitophagy in Various Neurological Diseases as a Therapeutic Approach.Cellular and molecular neurobiology · 2023Review
191 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 11 institutions in 4 countries.
Funding
Abstract
Recent data in invertebrates demonstrated that huntingtin (htt) is essential for fast axonal trafficking. Here, we provide direct and functional evidence that htt is involved in fast axonal trafficking in mammals. Moreover, expression of full-length mutant htt (mhtt) impairs vesicular and mitochondrial trafficking in mammalian neurons in vitro and in whole animals in vivo. Particularly, mitochondria become progressively immobilized and stop more frequently in neurons from transgenic animals. These defects occurred early in development prior to the onset of measurable neurological or mitochondrial abnormalities. Consistent with a progressive loss of function, wild-type htt, trafficking motors, and mitochondrial components were selectively sequestered by mhtt in human Huntington's disease-affected brain. Data provide a model for how loss of htt function causes toxicity; mhtt-mediated aggregation sequesters htt and components of trafficking machinery leading to loss of mitochondrial motility and eventual mitochondrial dysfunction.
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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.