Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112959 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Experiment Overall Design: Primary neurons samples infected with TRE-Htt-N853-18Q or -82Q.
2008-10-25 | E-GEOD-12481 | biostudies-arrayexpress
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study
2008-09-01 | GSE12481 | GEO
Project description:In this study, we conducted a comprehensive transcriptional profiling of the hippocampus utilizing a zQ175 knock-in (KI) mouse model of Huntington's disease, which was treated with either HTT-10150 siRNA specifically designed to target the full-length huntingtin (Htt) mRNA or combination of HTT-634 and HTT-486 siRNAs targeting HTT1a. Our investigation aimed to assess the impact of this intervention across different time points.
2026-05-05 | GSE284500 | GEO
Project description:Knee osteoarthritis (KOA), as a degenerative multifactorial disease, affects the quality of life and mental health of patients, and also brings a huge socioeconomic burden. Treating synovitis have shown promise as anti-inflammatory therapeutics in mitigating OA symptoms and disease progression. Here, by analysing synovial single-cell sequencing (scRNA-seq) data from KOA, we found that synovial fibroblasts (FLS) in OA synovium showed a distinct pro-inflammatory phenotype. We collected synovial tissue from patients with clinical OA as well as from healthy donors, and histological examination was consistent with findings in scRNA-seq. Inspired by recent cross-tissue fibroblast lineage studies, we identified by sequencing that healthy FLS in synovial tissues share transcriptome-level similarities with dermal fibroblasts (DFb). Subsequently, we revealed the local as well as systemic distribution of intra-articular injected DFbs by constructing/extracting two types of rat fibroblasts (luciferase DFbs as well as GFP DFbs). The results demonstrate that DFbs can be locally retained in the synovium for up to three weeks following targeted engrafting on it. And intra-articular injection does not result in DFbs migration to vital organs or the occurrence of histological changes in these organs. A rat model of KOA was constructed by anterior cruciate ligament transection (ACLT) in order to study the therapeutic effect of DFbs on KOA. After injection, the rats showed improvement in painful gait. In addition, histological as well as imaging results showed reduced synovitis and improvement in articular cartilage. Finally we verified the protective effect of DFbs on cytokine-stimulated chondrocytes in a co-culture system.
2026-06-24 | GSE304724 | GEO
Project description:In this study we conducted a comprehensive transcriptional profiling of the striatum utilizing a zQ175 knock-in (KI) mouse model of Huntington's disease, which was treated with HTT-10150 siRNA specifically designed to target the full-length huntingtin (Htt) mRNA. Our investigation aimed to assess the impact of this intervention across different time points.
2026-05-05 | GSE284497 | GEO
Project description:Huntington's disease (HD) is characterized by the aggregation of polyglutamine-expanded huntingtin (HTT), proceeding from soluble oligomers to end-stage inclusions. The molecular mechanisms of how protein aggregation leads to neuronal dysfunction are not well understood. We employed mass spectrometry-based quantitative proteomics to dissect spatiotemporal mechanisms of neurodegeneration using the R6/2 mouse model of HD. We show that extensive remodeling of the soluble brain proteome correlates with changes in insoluble aggregate formation during disease progression. In-depth characterization of HTT inclusion bodies uncovered an unprecedented complexity of several hundred proteins. Sequestration to inclusions was dependent on protein expression levels and the presence of aggregation-prone amino acid sequence features, such as low-complexity regions or coiled-coil domains. Overexpression of several sequestered proteins ameliorated HTT toxicity and modified the aggregation behavior in an in vitro model of HD. Our study provides a comprehensive and spatiotemporally-resolved proteome resource of HD progression, indicating that widespread loss of protein function contributes to aggregate-mediated toxicity.
2017-11-24 | PXD004973 | Pride
Project description:Transcriptional changes are an early feature of Huntington's disease (HD). We profiled genome-wide interaction sites for the huntingtin protein (HTT) using ChIP-sequencing from mouse striatal tissue at 4 months of age. We include replicate samples from CAG-expanded murine Htt (heterozygous Q111/+) and wildtype littermate controls.
2018-12-01 | GSE102750 | GEO
Project description:We used microarrays to investigate whether transcriptional dysregulation in hypothalamus is caused by expression of the huntingtin (HTT) protein We used two different Huntington's disease mouse models: BACHD mice with ubiquitous full-length mutant HTT expression (97 CAG repeats) and wild-type mice with targeted bilateral injections of wild-type or mutant HTT (853 amino acids length, wild-type HTT: 18 CAG repeats, mutant HTT: 79 CAG repeats) in hypothalamus.
2022-10-18 | GSE215217 | GEO
Project description:Despite growing descriptions of wild-type Huntingtin's (wt-HTT) roles in both adult brain function and, more recently, development, several clinical trials are exploring HTT-lowering approaches that target both wt-HTT and the mutant isoforms (mut-HTT) responsible for Huntington's disease (HD). This non-selective targeting is based on the autosomal dominant inheritance of HD, supporting the idea that mutant HTT exerts its harmful effects through a toxic gain-of-function or a dominant-negative mechanism. However, the precise amount of wt-HTT needed for healthy neurons in adults and during development remains unclear. In this study, we address this question by examining how wt-HTT loss affects human neuronal network formation, synaptic maturation, and homeostasis in vitro. Our findings establish a role of wt-HTT in the maturation of dendritic arborization and the acquisition of network-wide synchronized activity by human cortical neuronal networks modeled in vitro. Interestingly, the network synchronization defects only became apparent when more than two-thirds of the wt-HTT protein was depleted. Our study underscores the critical need to precisely understand wt-HTT's role in neuronal health. It also emphasizes the potential risks of excessive wt-HTT loss associated with non-selective therapeutic approaches targeting both wt and mutant HTT isoforms in HD patients.
2025-03-25 | PXD053150 | Pride