ArticleThe Journal of biological chemistry2013
HDAC6 regulates mutant SOD1 aggregation through two SMIR motifs and tubulin acetylation.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 69 citations in OpenAlex.
- Proteomic analysis reveals differentially regulated protein acetylation in human amyotrophic lateral sclerosis spinal cord.PloS one · 2013Trial
- The HDAC Inhibitor Butyrate Reduces SOD1 Aggregation and Improves Motor Function inInternational journal of cell biology · 2026Article
- Histone Deacetylase 6 Brain PET in Amyotrophic Lateral Sclerosis-Frontotemporal Spectrum Disorder.Annals of clinical and translational neurology · 2025Article
- Exploring epigenetic modifications as potential biomarkers and therapeutic targets in amyotrophic lateral sclerosis.Journal of neurology · 2025Review
- Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.Results and problems in cell differentiation · 2025Review
- Epigenetic Explorations of Neurological Disorders, the Identification Methods, and Therapeutic Avenues.International journal of molecular sciences · 2024Review
- Screens in aging-relevant human ALS-motor neurons identify MAP4Ks as therapeutic targets for the disease.Cell death & disease · 2024Article
- Linking acetylated α-Tubulin redistribution to α-Synuclein pathology in brain of Parkinson's disease patients.NPJ Parkinson's disease · 2024Article
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Disruption of axonal transport in neurodegeneration.The Journal of clinical investigation · 2023Review
- Modeling gain-of-function and loss-of-function components of SPAST-based hereditary spastic paraplegia using transgenic mice.Human molecular genetics · 2022Article
- The role of altered protein acetylation in neurodegenerative disease.Frontiers in aging neuroscience · 2022Review
- A perspective on therapies for amyotrophic lateral sclerosis: can disease progression be curbed?Translational neurodegeneration · 2021Review
- Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis.British journal of pharmacology · 2021Review
- Epigenetics and Communication Mechanisms in Microglia Activation with a View on Technological Approaches.Biomolecules · 2021Review
- Epigenetic Regulation of ALS and CMT: A Lesson fromInternational journal of molecular sciences · 2021Review
- Potential Therapeutic Role of HDAC Inhibitors in FUS-ALS.Frontiers in molecular neuroscience · 2021Review
- Autophagy regulation by acetylation-implications for neurodegenerative diseases.Experimental & molecular medicine · 2021Review
- Regulation of Functional Protein Aggregation by Multiple Factors: Implications for the Amyloidogenic Behavior of the CAP Superfamily Proteins.International journal of molecular sciences · 2020Review
- The impact of proteostasis dysfunction secondary to environmental and genetic causes on neurodegenerative diseases progression and potential therapeutic intervention.Environmental science and pollution research international · 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase 6 (HDAC6) is a tubulin deacetylase that regulates protein aggregation and turnover. Mutations in Cu/Zn superoxide dismutase (SOD1) linked to familial amyotrophic lateral sclerosis (ALS) make the mutant protein prone to aggregation. However, the role of HDAC6 in mutant SOD1 aggregation and the ALS etiology is unclear. Here we report that HDAC6 knockdown increased mutant SOD1 aggregation in cultured cells. Different from its known role in mediating the degradation of poly-ubiquitinated proteins, HDAC6 selectively interacted with mutant SOD1 via two motifs similar to the SOD1 mutant interaction region (SMIR) that we identified previously in p62/sequestosome 1. Expression of the aggregation-prone mutant SOD1 increased α-tubulin acetylation, and the acetylation-mimicking K40Q α-tubulin mutant promoted mutant SOD1 aggregation. Our results suggest that ALS-linked mutant SOD1 can modulate HDAC6 activity and increase tubulin acetylation, which, in turn, facilitates the microtubule- and retrograde transport-dependent mutant SOD1 aggregation. HDAC6 impairment might be a common feature in various subtypes of ALS.
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.