The role of LANP and ataxin 1 in E4F‐mediated transcriptional repression
Open accessAbstract
The leucine-rich acidic nuclear protein (LANP) belongs to the INHAT family of corepressors that inhibits histone acetyltransferases. The mechanism by which LANP restricts its repression to specific genes is unknown. Here, we report that LANP forms a complex with transcriptional repressor E4F and modulates its activity. As LANP interacts with ataxin 1--a protein mutated in the neurodegenerative disease spinocerebellar ataxia type 1 (SCA1)--we tested whether ataxin 1 can alter the E4F-LANP interaction. We show that ataxin 1 relieves the transcriptional repression induced by the LANP-E4F complex by competing with E4F for LANP. These results provide the first functional link, to our knowledge, between LANP and ataxin 1, and indicate a potential mechanism for the transcriptional aberrations observed in SCA1.
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Alterations in gene expression is the earliest pathological finding in SCA1 disease.
“alterations in gene expression is the earliest pathological finding in SCA1 disease (Lin et al., 2000; Serra et al., 2004; Cvetanovic et al., 2007; Crespo-Barreto et al., 2010; Cvetanovic et al., 2011; Fryer et al., 2011)”
From Polyglutamine Disease Toxicity Is Regulated by Nemo-like Kinase in Spinocerebellar Ataxia Type 1 (2013) · cites this paper as Cvetanovic et al., 2007
The Introduction calls transcriptional misregulation the earliest pathological change identified in SCA1 mice. The cited sentence extends that finding to SCA1 disease generally, without the mouse-model qualifier. (LLM, conf=0.85)
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Polyglutamine expansion down-regulates specific neuronal genes before pathologic changes in SCA1
Lin, X., Antalffy, B., Kang, D., Orr, H. T., & Zoghbi, H. Y. (2000) · Nature Neuroscience · doi:10.1038/72101 · Cited by 374 · see citing works
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Polyglutamine Disease Toxicity Is Regulated by Nemo-like Kinase in Spinocerebellar Ataxia Type 1
Ju, H., Kokubu, H., Todd, T. W., Kahle, J. J., Kim, S., Richman, R., Chirala, K., Orr, H. T., Zoghbi, H. Y., & Lim, J. (2013) · The Journal of Neuroscience · doi:10.1523/jneurosci.3465-12.2013 · Cited by 31 · see citing works
“Because alterations in gene expression is the earliest pathological finding in SCA1 disease (Lin et al., 2000; Serra et al., 2004; Cvetanovic et al., 2007, 2011; Crespo-Barreto et al., 2010; Fryer et al., 2011) and the CIC family proteins play a key role in modulating ATXN1 functions and SCA1…”
BackgroundSelf-citation
- Authors
- Cvetanovic, M., Rooney, R. J., Garcia, J. J., Toporovskaya, N., Zoghbi, H. Y., & Opal, P.
- Affiliations
- Duke Medical Center (US)
- Howard Hughes Medical Institute (US)
- Northwestern University (US)
- Corresponding author
- Opal, Puneet
- Venue
- The EMBO Reports
- Published
- 2007-06-08
- Volume
- 8
- Issue
- 7
- Pages
- 671-677
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC1905893
- OpenAlex
- W2059717396
- Cited by
- 52
- References
- 1
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 4 · 2019: 2 · 2018: 1 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 6 · 2012: 5
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- EMBO Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- National Organization for Rare Disorders
- National Ataxia Foundation
- National Institute of Neurological Disorders and Stroke
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- ataxin-1, transcriptional repression, corepressors, histone acetyltransferase inhibition, spinocerebellar ataxia type 1, protein-protein interaction, neurodegenerative diseases
- MeSH terms
- Ataxins, Ataxin-1, Animals, Cell Line, Chlorocebus aethiops, HeLa Cells, Humans, Immunohistochemistry, Luciferases, Mutation, Nerve Tissue Proteins, Neuroblastoma, Nuclear Proteins, Phosphoproteins, Precipitin Tests, Repressor Proteins, Genes, Reporter, Molecular Chaperones, Spinocerebellar Ataxias, Two-Hybrid System Techniques, Ubiquitin-Protein Ligases, Cell Line, Tumor, Chromatin Immunoprecipitation, Mice
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