ArticleNeurobiology of disease2008
Expression of expanded polyglutamine targets profilin for degradation and alters actin dynamics.
Article in Neurobiology of disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases.BMC medical genomics · 2013Pooled it
- Profilin and Non-Canonical Wnt Signaling: Coordinating Cytoskeletal Dynamics from Development to Disease.Journal of developmental biology · 2025Review
- Single-nuclei transcriptome analysis of Huntington disease iPSC and mouse astrocytes implicates maturation and functional deficits.iScience · 2023Article
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Huntingtin fibrils with different toxicity, structure, and seeding potential can be interconverted.Nature communications · 2021Article
- Polyphasic linkage and the impact of ligand binding on the regulation of biomolecular condensates.Biophysics reviews · 2021Review
- Pluripotent stem cell-derived models of neurological diseases reveal early transcriptional heterogeneity.Genome biology · 2021Article
- Profilin Isoforms in Health and Disease - All the Same but Different.Frontiers in cell and developmental biology · 2021Review
- Profilin choreographs actin and microtubules in cells and cancer.International review of cell and molecular biology · 2020Article
- Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases.International journal of molecular sciences · 2018Review
- Cofilin and profilin: partners in cancer aggressiveness.Biophysical reviews · 2018Review
- Caspase-2 promotes cytoskeleton protein degradation during apoptotic cell death.Cell death & disease · 2013Article
- Polyglutamine domain flexibility mediates the proximity between flanking sequences in huntingtin.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Multiple phenotypes in Huntington disease mouse neural stem cells.Molecular and cellular neurosciences · 2012Article
- Neurogenic and myogenic contributions to hereditary motor neuron disease.Neuro-degenerative diseases · 2012Review
- Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Journal of genetics · 2010Review
- F-actin binding regions on the androgen receptor and huntingtin increase aggregation and alter aggregate characteristics.PloS one · 2010Article
- Animal models of polyglutamine diseases and therapeutic approaches.The Journal of biological chemistry · 2009Review
- Phosphorylation of profilin by ROCK1 regulates polyglutamine aggregation.Molecular and cellular biology · 2008Article
- The role of the cofilin-actin rod stress response in neurodegenerative diseases uncovers potential new drug targets.BioarchitectureArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease is caused by polyglutamine expansion in the huntingtin protein. Huntingtin directly interacts with profilin, a major actin monomer sequestering protein and a key integrator of signals leading to actin polymerization. We observed a progressive loss of profilin in the cerebral cortex of Huntington's disease patients, and in cell culture and Drosophila models of polyglutamine disease. This loss of profilin is likely due to increased degradation through the ubiquitin proteasome system. Profilin loss reduces the F/G actin ratio, indicating a shift in actin polymerization. Overexpression of profilin abolishes mutant huntingtin toxicity in cells and partially ameliorates the morphological and functional eye phenotype and extends lifespan in a transgenic polyglutamine Drosophila model. These results indicate a link between huntingtin and profilin and implicate profilin in Huntington's disease pathogenesis.
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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.