Ontology highlight
ABSTRACT:
PROVIDER: PRJNA658796 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12503320.fastq.gz | Fastqsanger.gz | |||
| SRR12503321.fastq.gz | Fastqsanger.gz | |||
| SRR12503322.fastq.gz | Fastqsanger.gz | |||
| SRR12503323.fastq.gz | Fastqsanger.gz | |||
| SRR12503324.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 15 |
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Project description:RNA-sequencing of Drosophila expressing mutant Huntingtin in neurons or glia
| PRJNA660766 | ENA
Project description:Transcriptional profiling of C.elegans purified touch receptor neuron precursors, comparing cells expressing mutant Huntingtin N-terminal fragment to normal Huntingtin N-terminal fragment, both fused to GFP under mec-3 promoter. As a control the same experiment has been done with comparing cell expressing normal Huntingtin to GFP only. Goal was to determine the specific effect of expanded polyglutamines on gene expression in purified cell population. Three-condition experiment: mutant Huntingtin (128Q) versus normal Huntingtin (19Q), and normal Huntingtin versus GFP only, 3 biological replicates of each. Cells were purified based on GFP fluorescence using a cell sorter.
2015-02-01 | E-GEOD-35939 | biostudies-arrayexpress
Project description:Transcriptional profiling of C.elegans purified touch receptor neuron precursors, comparing cells expressing mutant Huntingtin N-terminal fragment to normal Huntingtin N-terminal fragment, both fused to GFP under mec-3 promoter. As a control the same experiment has been done with comparing cell expressing normal Huntingtin to GFP only. Goal was to determine the specific effect of expanded polyglutamines on gene expression in purified cell population.
2015-02-01 | GSE35939 | GEO
Project description:Huntington disease is a severe neurological disorder caused by an abnormal polyglutamine expansion in the N-terminal of the huntingtin protein. Here we show that breast tumours appear earlier when mutant huntingtin is expressed in an activated polyomavirus middle T antigen (PyVT) mouse breast cancer model as compared to the control mice expressing wild-type huntingtin. Tumours bearing mutant huntingtin have a modified gene expression pattern revealing increases in the IGF-1/Akt signalling, epithelial-mesenchymal transition and metastatic properties. Indeed, polyQ-huntingtin expressing tumours show hyper-activation of Akt pathway. Also, when mutant huntingtin is expressed, cancer cells in culture change morphology and the levels of cell adhesion and mesenchymal markers are affected in primary tumour or corresponding derived cells. As a consequence, PyVT induced lung metastasis is higher in Huntington disease mice than in the control mice. Finally, analysis of cases of Huntington disease patients developing breast cancer may suggest an increased aggressiveness of breast cancer when compared to the control population.
2014-04-14 | GSE28685 | GEO
Project description:Huntington disease is a severe neurological disorder caused by an abnormal polyglutamine expansion in the N-terminal of the huntingtin protein. Here we show that breast tumours appear earlier when mutant huntingtin is expressed in an activated polyomavirus middle T antigen (PyVT) mouse breast cancer model as compared to the control mice expressing wild-type huntingtin. Tumours bearing mutant huntingtin have a modified gene expression pattern revealing increases in the IGF-1/Akt signalling, epithelial-mesenchymal transition and metastatic properties. Indeed, polyQ-huntingtin expressing tumours show hyper-activation of Akt pathway. Also, when mutant huntingtin is expressed, cancer cells in culture change morphology and the levels of cell adhesion and mesenchymal markers are affected in primary tumour or corresponding derived cells. As a consequence, PyVT induced lung metastasis is higher in Huntington disease mice than in the control mice. Finally, analysis of cases of Huntington disease patients developing breast cancer may suggest an increased aggressiveness of breast cancer when compared to the control population. 8 Total samples were analyzed: 4 x MMTV-PyVT/HdhQ7/Q7 breast tumours; 4 x MMTV-PyVT/HdhQ111/Q111 breast tumours;
2014-04-14 | E-GEOD-28685 | biostudies-arrayexpress
Project description:Expressing a mutant fragment of huntingtin (Htt) in yeast produces several HD-relevant phenotypes. We used microarrays to study global change in expression induced by this mutant htt fragment. Expression was also analysed in three suppressor deletion strains expressing a toxic mutant htt fragment: bna4Δ, mbf1Δ, and ume1Δ.
2010-11-09 | GSE18644 | GEO
Project description:To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. Although changes in the brains of knock-in and full-length transgenic models of HD took longer to appear, 15- and 22-month CHL2(Q150/Q150), 18-month Hdh(Q92/Q92) and 2-year-old YAC128 animals also exhibited significant HD-like mRNA signatures. Whereas it was expected that the expression of full-length huntingtin transprotein might result in unique gene expression changes compared with those caused by the expression of an N-terminal huntingtin fragment, no discernable differences between full-length and fragment models were detected. In addition, very high correlations between the signatures of mice expressing normal levels of wild-type huntingtin and mice in which the wild-type protein is absent suggest a limited effect of the wild-type protein to change basal gene expression or to influence the qualitative disease-related effect of mutant huntingtin. The combined analysis of mouse and human HD transcriptomes provides important temporal and mechanistic insights into the process by which mutant huntingtin kills striatal neurons. In addition, the discovery that several available lines of HD mice faithfully recapitulate the gene expression signature of the human disorder provides a novel aspect of validation with respect to their use in preclinical therapeutic trials. Experiment Overall Design: Striatal samples from 3 Hdh4/Q80 mutant mice (12 months-old) and 3 age-matched wild-type littermates.
2008-06-16 | E-GEOD-9375 | biostudies-arrayexpress
Project description:To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. Although changes in the brains of knock-in and full-length transgenic models of HD took longer to appear, 15- and 22-month CHL2(Q150/Q150), 18-month Hdh(Q92/Q92) and 2-year-old YAC128 animals also exhibited significant HD-like mRNA signatures. Whereas it was expected that the expression of full-length huntingtin transprotein might result in unique gene expression changes compared with those caused by the expression of an N-terminal huntingtin fragment, no discernable differences between full-length and fragment models were detected. In addition, very high correlations between the signatures of mice expressing normal levels of wild-type huntingtin and mice in which the wild-type protein is absent suggest a limited effect of the wild-type protein to change basal gene expression or to influence the qualitative disease-related effect of mutant huntingtin. The combined analysis of mouse and human HD transcriptomes provides important temporal and mechanistic insights into the process by which mutant huntingtin kills striatal neurons. In addition, the discovery that several available lines of HD mice faithfully recapitulate the gene expression signature of the human disorder provides a novel aspect of validation with respect to their use in preclinical therapeutic trials. Experiment Overall Design: Striatal samples from 5 R6/2 mutant mice (12 weeks-old) and 4 age-matched wild-type mice.
2008-06-16 | E-GEOD-9804 | biostudies-arrayexpress