ReviewCells2018
Unconventional Secretion and Intercellular Transfer of Mutant Huntingtin.
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed.
- HDDF2-A Novel Patient-Derived Fibroblast Line from Huntington's Disease with Prominent Cellular Senescence and polyQ Pathology.Biomedicines · 2026Article
- Unraveling Lysosomal Exocytosis: From Molecular Mechanisms to Physiological Functions.Traffic (Copenhagen, Denmark) · 2026Review
- Small Extracellular Vesicles in Neurodegenerative Disease: Emerging Roles in Pathogenesis, Biomarker Discovery, and Therapy.International journal of molecular sciences · 2025Review
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Article
- The HSPB1-p62/SQSTM1 functional complex regulates the unconventional secretion and transcellular spreading of the HD-associated mutant huntingtin protein.Human molecular genetics · 2023Article
- Transmission-selective muscle pathology induced by the active propagation of mutant huntingtin across the human neuromuscular synapse.Frontiers in molecular neuroscience · 2023Article
- Exosomal RNAs in diagnosis and therapies.Non-coding RNA research · 2022Article
- Striatal Induction and Spread of the Huntington's Disease Protein: A Novel Rhes Route.Journal of Huntington's disease · 2022Review
- Tunneling Nanotubes Facilitate Intercellular Protein Transfer and Cell Networks Function.Frontiers in cell and developmental biology · 2022Review
- Brain Exosomes: Friend or Foe in Alzheimer's Disease?Molecular neurobiology · 2021Review
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Shedding a new light on Huntington's disease: how blood can both propagate and ameliorate disease pathology.Molecular psychiatry · 2021Article
- Systemic manifestation and contribution of peripheral tissues to Huntington's disease pathogenesis.Ageing research reviews · 2021Review
- Structural insight into transmissive mutant huntingtin species by correlative light and electron microscopy and cryo-electron tomography.Biochemical and biophysical research communications · 2021Article
- Peering into tunneling nanotubes-The path forward.The EMBO journal · 2021Review
- The phasor FLIM method reveals a link between a change in energy metabolism and mHtt protein spread in healthy Mammalian cells when co-cultured with Huntington diseased cells.Methods and applications in fluorescence · 2021Article
- Super-resolution imaging of the dynamic cleavage of intercellular tunneling nanotubes.Frontiers of optoelectronics · 2020Article
- Trafficking Unconventionally via UPS.Cells · 2020Article
- Stress-Sensitive Protein Rac1 and Its Involvement in Neurodevelopmental Disorders.Neural plasticity · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of intercellular transmission of pathological agents in neurodegenerative diseases has received much recent attention. Huntington's disease (HD) is caused by a monogenic mutation in the gene encoding Huntingtin (HTT). Mutant HTT (mHTT) harbors a CAG repeat extension which encodes an abnormally long polyglutamine (polyQ) repeat at HTT's N-terminus. Neuronal pathology in HD is largely due to the toxic gain-of-function by mHTT and its proteolytic products, which forms both nuclear and cytoplasmic aggregates that perturb nuclear gene transcription, RNA splicing and transport as well cellular membrane dynamics. The neuropathological effects of mHTT have been conventionally thought to be cell-autonomous in nature. Recent findings have, however, indicated that mHTT could be secreted by neurons, or transmitted from one neuronal cell to another via different modes of unconventional secretion, as well as via tunneling nanotubes (TNTs). These modes of transmission allow the intercellular spread of mHTT and its aggregates, thus plausibly promoting neuropathology within proximal neuronal populations and between neurons that are connected within neural circuits. Here, the various possible modes for mHTT's neuronal cell exit and intercellular transmission are discussed.
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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.