ArticleNeuro-degenerative diseases2012
Pcaf modulates polyglutamine pathology in a Drosophila model of Huntington's disease.
Article in Neuro-degenerative diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis.International journal of molecular sciences · 2022Article
- The role of altered protein acetylation in neurodegenerative disease.Frontiers in aging neuroscience · 2022Review
- Autophagy regulation by acetylation-implications for neurodegenerative diseases.Experimental & molecular medicine · 2021Review
- Pharmacological blockade of PCAF ameliorates osteoarthritis development via dual inhibition of TNF-α-driven inflammation and ER stress.EBioMedicine · 2019Article
- Hat1 acetylates histone H4 and modulates the transcriptional program in Drosophila embryogenesis.Scientific reports · 2019Article
- Article
- The TinyInternational journal of molecular sciences · 2018Review
- Revealing the protein propionylation activity of the histone acetyltransferase MOF (males absent on the first).The Journal of biological chemistry · 2018Article
- Acetyltransferases (HATs) as targets for neurological therapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Ecdysone induced gene expression is associated with acetylation of histone H3 lysine 23 in Drosophila melanogaster.PloS one · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Huntingtin peptides with elongated polyglutamine domains, the root causes of Huntington's disease, hinder histone acetylation, which leads to transcriptional dysregulation. However, the range of acetyltransferases interacting with mutant Huntingtin has not been systematically evaluated. We used genetic interaction tests in Drosophila to determine whether specific acetyltransferases belonging to distinct protein families influence polyglutamine pathology. We found that flies expressing a mutant form of the Huntingtin protein (Httex1pQ93) exhibit reduced viability, which is further decreased by partial loss of Pcaf or nejire, while the tested MYST family acetyltransferases did not affect pathology. Reduced levels of Pcaf also led to the increased degeneration of photoreceptor neurons in the retina. Overexpression of Pcaf, however, was not sufficient to ameliorate these phenotypes, and the level of soluble Pcaf is unchanged in Httex1pQ93-expressing flies. Thus, our results indicate that while Pcaf has a significant impact on Huntington's disease pathology, therapeutic strategies aimed at elevating its levels are likely to be ineffective in ameliorating Huntington's disease pathology; however, strategies that aim to increase the specific activity of Pcaf remain to be tested.
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