ArticleNature communications2015
A short N-terminal domain of HDAC4 preserves photoreceptors and restores visual function in retinitis pigmentosa.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- The N-terminal fragment of histone deacetylase 4 (1-669aa) promotes chondrocyte apoptosis via the p53-dependent endoplasmic reticulum stress pathway.Journal of cellular and molecular medicine · 2024Article
- Circ_HIPK3 Inhibits HBiochemical genetics · 2023Article
- The role of epigenetic changes in the pathology and treatment of inherited retinal diseases.Frontiers in cell and developmental biology · 2023Review
- Migration of pre-induced human peripheral blood mononuclear cells from the transplanted to contralateral eye in mice.Stem cell research & therapy · 2021Article
- Metabolic and Redox Signaling of the Nucleoredoxin-Like-1 Gene for the Treatment of Genetic Retinal Diseases.International journal of molecular sciences · 2020Review
- The Role of Histone Acetyltransferases and Histone Deacetylases in Photoreceptor Differentiation and Degeneration.International journal of medical sciences · 2020Review
- Inhibition of HDAC4 Attenuated JNK/c-Jun-Dependent Neuronal Apoptosis and Early Brain Injury Following Subarachnoid Hemorrhage by Transcriptionally Suppressing MKK7.Frontiers in cellular neuroscience · 2019Article
- Epigenetic control of gene regulation during development and disease: A view from the retina.Progress in retinal and eye research · 2018Review
- Nanowire arrays restore vision in blind mice.Nature communications · 2018Article
- DZNep inhibits H3K27me3 deposition and delays retinal degeneration in the rd1 mice.Cell death & disease · 2018Article
- Nrl knockdown by AAV-delivered CRISPR/Cas9 prevents retinal degeneration in mice.Nature communications · 2017Article
- Gene Therapy in a Large Animal Model of PDE6A-Retinitis Pigmentosa.Frontiers in neuroscience · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Retinitis pigmentosa is a leading cause of inherited blindness, with no effective treatment currently available. Mutations primarily in genes expressed in rod photoreceptors lead to early rod death, followed by a slower phase of cone photoreceptor death. Rd1 mice provide an invaluable animal model to evaluate therapies for the disease. We previously reported that overexpression of histone deacetylase 4 (HDAC4) prolongs rod survival in rd1 mice. Here we report a key role of a short N-terminal domain of HDAC4 in photoreceptor protection. Expression of this domain suppresses multiple cell death pathways in photoreceptor degeneration, and preserves even more rd1 rods than the full-length HDAC4 protein. Expression of a short N-terminal domain of HDAC4 as a transgene in mice carrying the rd1 mutation also prolongs the survival of cone photoreceptors, and partially restores visual function. Our results may facilitate the design of a small protein therapy for some forms of retinitis pigmentosa.
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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.