Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA121577 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Yeast Artificial Chomosome (YAC) 128 model of Huntington's disease shows substantial deficits in motor, learning and memory tasks and alterations in its transcriptional profile. We examined the changes in the transcriptional profile in the YAC 128 mouse model of HD at 6, 12, and 18 weeks
2016-07-07 | GSE70656 | GEO
Project description:The Yeast Artificial Chomosome (YAC) 128 model of Huntington's disease shows substantial deficits in motor, learning and memory tasks and alterations in its transcriptional profile. We examined the changes in the transcriptional profile in the YAC 128 mouse model of HD at 6, 12, and 18 weeks Brain striatal tissue from Wild Type and YAC 128 mice were sampled at the three age groups
2016-07-07 | E-GEOD-70656 | biostudies-arrayexpress
Project description:An integrated model of stress-dependent gene expression in yeast
| PRJNA130707 | ENA
Project description:Huntington's disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions. Gene expression profiles were analyzed to examine the effects of p62 depletion in mouse with or without mutant huntingtin exon 1 To examine the effect of p62 depletion on the transcriptome of Huntington's disease model mice, we crossed p62 knockout mice with HD model mice. We extracted total RNA from the striatum of these mice at 8 weeks and used for a microaaray analysis. The samples are HD transgenic mice with p62 knockout (HD_p62KO), HD mice with normal p62 (HD_p62WT), non-HD-transgenic mice with p62 knockout (NT_p62KO), and non-HD-transgenic mice with normal p62 (NT_p62WT).
2014-10-10 | E-GEOD-62210 | biostudies-arrayexpress
Project description:Rescue of alpha-synuclein toxicity in a yeast model of Parkinson's disease
| PRJNA106153 | ENA
Project description:Functional Genomic Analysis of Commercial Baker’s Yeast during Initial Stages of Model Dough-Fermentation
| PRJNA93059 | ENA
Project description:Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD.
2013-07-18 | GSE48962 | GEO
Project description:Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD.
2013-07-18 | GSE48960 | GEO
Project description:Dysregulation of the kynurenine (Kyn) pathway has been associated with the progression of Huntington's disease (HD). In particular, elevated levels of the kynurenine metabolites 3-hydroxy kynurenine (3-OH-Kyn) and quinolinic acid (Quin), have been reported in the brains of HD patients as well as in rodent models of HD. The production of these metabolites is controlled by the activity of kynurenine mono-oxygenase (KMO), a mitochondrial outer membrane enzyme which catalyzes the synthesis of 3-OH-Kyn from Kyn. Thus inhibiting KMO is expected to produce a beneficial effect in Huntington's Disease (HD) patients, hopefully reversing their phenotype to match healthy subjects. To test this effect, we acutely treated a mouse model of HD (R6/2, a transgenic mouse model of HD which contains a human HTT gene containing 90 CAG repeats) and wild type mice with a KMO inhibitor, and separately used a mock treatment on both the transgenic mice and wild type mice. The goal of this project is to analyze the RNA-seq data and find gene expression changes associated with the KMO inhibitor
2017-10-30 | GSE106161 | GEO
Project description:Dysregulation of the kynurenine (Kyn) pathway has been associated with the progression of Huntington's disease (HD). In particular, elevated levels of the kynurenine metabolites 3-hydroxy kynurenine (3-OH-Kyn) and quinolinic acid (Quin), have been reported in the brains of HD patients as well as in rodent models of HD. The production of these metabolites is controlled by the activity of kynurenine mono-oxygenase (KMO), a mitochondrial outer membrane enzyme which catalyzes the synthesis of 3-OH-Kyn from Kyn. Thus inhibiting KMO is expected to produce a beneficial effect in Huntington's Disease (HD) patients, hopefully reversing their phenotype to match healthy subjects. To test this effect, we chronically treated a mouse model of HD (R6/2, a transgenic mouse model of HD which contains a human HTT gene containing 90 CAG repeats) and wild type mice with a KMO inhibitor for 8 weeks, and separately used a mock treatment on both the transgenic mice and wild type mice. The goal of this project is to analyze the RNA-seq data and find gene expression changes associated with the KMO inhibitor.
2017-10-30 | GSE105158 | GEO