E-GEOD-60780
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-60780 | ExpressionAtlas | 2015-07-29
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-60780-analysis-methods.tsv | Tabular | |||
| E-GEOD-60780-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-60780-configuration.xml | Xml | |||
| E-GEOD-60780-percentile-ranks.tsv | Tabular | |||
| E-GEOD-60780.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 65 |
Similar Datasets
Project description:Gene expression profiling in mice overexpressing human wild type (WT) keratin 8 (K8) or K8 variants (G62C and R341H).
| PRJNA259537 | ENA
Project description:We aim to investigate the role of renal Sirt1 on albuminuria. To further development of our gene expression approach to biodosimetry, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between wild type(C57BL/6J) mice treated with streptozotocin (WT+STZ) and Sirt1-overexpressing transgenic mice treated with streptozotocin (TG+STZ) mice. To elucidate the molecular mechanisms underlying the amelioration of albuminuria by our TG (Sirt1-overexpressing transgenic) mice, we performed DNA microarray analysis using micro-dissected glomerular regions to examine the differences in gene expression between WT+STZ and TG+STZ mice.
2018-03-08 | GSE50140 | GEO
Project description:Transcriptional profiling of wild-type (WT) and RDD4 overexpressing plants (RDD4-OX) to examine function of RDD4 in rice
2023-01-31 | GSE160908 | GEO
Project description:Transcriptional profiling of wild-type (WT) and RDD2 overexpressing plants (RDD2-OX) to examine function of RDD2 in rice
2021-08-31 | GSE119907 | GEO
Project description:We wanted to know how introduction of H1047R oncogenic mutation of PIK3CA (p110a subunit of PI3K) in HER2-overexpressing MCF10A human non-transformed mammary epitheial cell lines introduces change in gene expression levels. Our control was HER2-overexpressing MCF10A cell line with wild-type (WT) PIK3CA. Mutated oncogene-induced gene expression signature was measured and compared with that induced by the WT oncogene from cell lines harvested at 70-80% confluency.
2021-03-16 | GSE117389 | GEO
Project description:Endothelin-1 (ET-1), an endothelium-derived vasoconstrictor peptide, plays a role in the pathophysiology of cardiovascular disease. Transgenic mice that overexpress human preproET-1 selectively in the endothelium (eET-1) exhibit endothelial dysfunction, hypertrophic remodeling and vascular inflammation of resistance-size arteries in the absence of blood pressure elevation. To understand the mechanisms whereby ET-1 induces vascular damage, vascular gene expression using DNA microarrays was employed. RNA from mesenteric arteries of female and male young (6-7 weeks) and mature (6-8 months) eET-1 and wild type (WT) mice was isolated and changes in gene expression were determined by genome-wide expression profiling using Illumina microarray. This study revealed a set of genes potentially regulated by ET-1, which might be implicated in ET-1 induced-vascular damage. Samples 1-8: Total RNA obtained from the entire mesenteric arterial tree of young (6-7 weeks) female preproendothelin-1 overexpressing mice compared to age and sex matched wild type littermate controls. Samples 9-16: Total RNA obtained from the entire mesenteric arterial tree of mature (6-8 months) female preproendothelin-1 overexpressing mice compared to age and sex matched wild type littermate controls. Samples 17-24: Total RNA obtained from the entire mesenteric arterial tree of young (6-7 weeks) male preproendothelin-1 overexpressing mice compared to age and sex matched wild type littermate controls. Samples 25-32: Total RNA obtained from the entire mesenteric arterial tree of mature (6-8 months) male preproendothelin-1 overexpressing mice compared to age and sex matched wild type littermate controls.
2010-09-01 | E-GEOD-19624 | biostudies-arrayexpress
Project description:Mitofusin-2 (MFN2) is an outer mitochondrial membrane protein essential for mitochondrial networking in most cells. Autosomal dominant mutations in the MFN2 gene cause Charcot-Marie-Tooth type 2A disease (CMT2A), a severe and disabling sensory-motor neuropathy with impact on the entire nervous system. To date, no curative treatment is available. In the paper we propose a novel therapeutic strategy tailored to correct the root genetic defect of CMT2A. In our approach, while mutant and wild-type MFN2 mRNA are inhibited by RNA interference (RNAi), the wild-type protein is restored by overexpressing a cDNA encoding a functional MFN2, modified to be resistant to RNAi. This strategy allows proper MFN2 molecular correction in vivo in the MitoCharc1 CMT2A transgenic mouse model after cerebrospinal fluid (CSF) delivery of the constructs via adenoassociated virus 9 (AAV9) in newborn mice. To identify the therapeutic molecular mechanisms and the pathway that are modulated, we have compared the bulk RNA expression profile of spinal cord from one month old wild type (WT) mice and MitoCharc1 transgenic mice (B6;D2-Tg(Eno2-MFN2*R94Q)L51Ugfm/J) which encode the mutant human MFN2*R94Q under the neuron specific rat enolase (Eno2) promoter, as potential mouse model to test the therapeutic approach. We performed gene expression profiling analysis using data (RNA-seq) obtained from 4 wild type mice and 8 MitoCharch1 transgenic mice at one time point.
2023-11-29 | GSE201264 | GEO
Project description:<p>BACKGROUND: The gut microbiome and the host immune system interact synergistically to maintain intestinal health and defend against infections. Toll-like receptor 5 (TLR5), known for recognizing bacterial flagellin, plays a pivotal role in this regulatory network. Despite significant advances in understanding the gut microbiome and TLR5, the precise role of TLR5 in gut health and infection resistance remains unclear. This study aimed to elucidate the role of TLR5 in regulating gut microbiota and metabolites and their impact on resistance to Salmonella infection using a TLR5 intestinal-specific overexpression mouse model. </p><p>METHODS: Fecal microbiota and metabolite transplantation experiments were conducted using feces from TLR5-overexpressing mice (TLR5+/+ group) and wild-type mice (WT group) into C57 mice, creating four experimental groups: Flora-TLR5-C57, Metabolite-TLR5-C57, Flora-WT-C57 and Metabolite-WT-C57. Mice were infected with Salmonella, and various parameters including survival time, fecal Salmonella load, and alterations in gut microbiota and metabolites were assessed. </p><p>RESULTS: Despite notable shifts in gut microbiota composition and metabolite profiles induced by TLR5 overexpression, no significant differences in fecal Salmonella load or survival time were observed across the experimental groups. TLR5-overexpressing mice exhibited an enrichment of beneficial bacterial taxa and significant changes in metabolites; however, these alterations did not correlate with enhanced resistance to Salmonella infection. </p><p>CONCLUSION: Our findings suggest that while TLR5 overexpression significantly modifies gut microbiota and metabolite profiles, these changes do not directly enhance resistance to Salmonella infection. The immune response to Salmonella is multifaceted and involves various components beyond the gut microbiota and metabolites. Further research is required to elucidate the detailed molecular pathways through which TLR5 influences infection outcomes and to explore potential combined therapeutic strategies for enhancing host defenses against enteric pathogens.</p>
2024-07-25 | MTBLS10592 | MetaboLights
Project description:Gene expression profiling of YAP wild-type or mutants overexpressing MCF10A cells
| PRJNA109455 | ENA