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dc.contributor.author Martin, Alberto J.M.
dc.date.accessioned 2024-09-26T00:43:38Z
dc.date.available 2024-09-26T00:43:38Z
dc.date.issued 2023-07
dc.identifier.issn 1661-6596
dc.identifier.uri https://repositorio.uss.cl/handle/uss/13277
dc.description Publisher Copyright: © 2023 by the authors.
dc.description.abstract Huntington’s disease (HD) is a disorder caused by an abnormal expansion of trinucleotide CAG repeats within the huntingtin (Htt) gene. Under normal conditions, the CREB Binding Protein interacts with CREB elements and acetylates Lysine 27 of Histone 3 to direct the expression of several genes. However, mutant Htt causes depletion of CBP, which in turn induces altered histone acetylation patterns and transcriptional deregulation. Here, we have studied a differential expression analysis and H3K27ac variation in 4- and 6-week-old R6/2 mice as a model of juvenile HD. The analysis of differential gene expression and acetylation levels were integrated into Gene Regulatory Networks revealing key regulators involved in the altered transcription cascade. Our results show changes in acetylation and gene expression levels that are related to impaired neuronal development, and key regulators clearly defined in 6-week-old mice are proposed to drive the downstream regulatory cascade in HD. Here, we describe the first approach to determine the relationship among epigenetic changes in the early stages of HD. We determined the existence of changes in pre-symptomatic stages of HD as a starting point for early onset indicators of the progression of this disease. en
dc.language.iso eng
dc.relation.ispartof vol. 24 Issue: no. 13 Pages:
dc.source International Journal of Molecular Sciences
dc.title Transcriptional and Histone Acetylation Changes Associated with CRE Elements Expose Key Factors Governing the Regulatory Circuit in the Early Stage of Huntington’s Disease Models en
dc.type Artículo
dc.identifier.doi 10.3390/ijms241310848
dc.publisher.department Facultad de Ingeniería y Tecnología
dc.publisher.department Facultad de Ingeniería, Arquitectura y Diseño


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