ArticleScientific reports2018
Spermine increases acetylation of tubulins and facilitates autophagic degradation of prion aggregates.
Article in Scientific reports, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Insulin signaling engages divergent transcriptional mechanisms in neural and metabolic tissues.BMC molecular and cell biology · 2026Article
- Tubastatin A attenuates impaired autophagic degradation and promotes myogenic program in skeletal muscle following downhill running.Journal of muscle research and cell motility · 2025Article
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- The Yeast-Fermented Garlic and a Balance of Spermine/Spermidine Activates Autophagy via EGR1 Transcriptional Factor.Molecular nutrition & food research · 2025Article
- Acetylation modification in the regulation of macroautophagy.Advanced biotechnology · 2024Review
- Metformin ameliorates valve interstitial cell calcification by promoting autophagic flux.Scientific reports · 2023Article
- Metabolism of Polyamines and Kidney Disease: A Promising Therapeutic Target.Kidney diseases (Basel, Switzerland) · 2023Review
- p53 Regulates Mitochondrial Dynamics in Vascular Smooth Muscle Cell Calcification.International journal of molecular sciences · 2023Article
- Prion therapeutics: Lessons from the past.Prion · 2022Review
- The autophagy inducer SMER28 attenuates microtubule dynamics mediating neuroprotection.Scientific reports · 2022Article
- Altered Brain Arginine Metabolism and Polyamine System in a P301S Tauopathy Mouse Model: A Time-Course Study.International journal of molecular sciences · 2022Article
- Investigating the Role of Spermidine in a Model System of Alzheimer's Disease Using Correlative Microscopy and Super-resolution Techniques.Frontiers in cell and developmental biology · 2022Article
- Beyond Antioxidant Effects: Nature-Based Templates Unveil New Strategies for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Spermidine Is Critical for Growth, Development, Environmental Adaptation, and Virulence inFrontiers in microbiology · 2021Article
- Loss of Deacetylation Enzymes Hdac6 and Sirt2 Promotes Acetylation of Cytoplasmic Tubulin, but Suppresses Axonemal Acetylation in Zebrafish Cilia.Frontiers in cell and developmental biology · 2021Article
- Acetylation Modification During Autophagy and Vascular Aging.Frontiers in physiology · 2021Review
- An Update on Autophagy in Prion Diseases.Frontiers in bioengineering and biotechnology · 2020Review
- Full restoration of specific infectivity and strain properties from pure mammalian prion protein.PLoS pathogens · 2019Article
- Altered brain arginine metabolism in a mouse model of tauopathy.Amino acids · 2019Article
- Autophagy pathways in the treatment of prion diseases.Current opinion in pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Autolysosomal dysfunction and unstable microtubules are hallmarks of chronic neurodegenerative diseases associated with misfolded proteins. Investigation of impaired protein quality control and clearance systems could therefore provide an important avenue for intervention. To investigate this we have used a highly controlled model for protein aggregation, an in vitro prion system. Here we report that prion aggregates traffic via autolysosomes in the cytoplasm. Treatment with the natural polyamine spermine clears aggregates by enhancing autolysosomal flux. We demonstrated this by blocking the formation of mature autophagosomes resulting in accumulation of prion aggregates in the cytoplasm. Further we investigated the mechanism of spermine's mode of action and we demonstrate that spermine increases the acetylation of microtubules, which is known to facilitate retrograde transport of autophagosomes from the cellular periphery to lysosomes located near the nucleus. We further report that spermine facilitates selective autophagic degradation of prion aggregates by binding to microtubule protein Tubb6. This is the first report in which spermine and the pathways regulated by it are applied as a novel approach towards clearance of misfolded prion protein and we suggest that this may have important implication for the broader family of protein misfolding diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.