GeneChip array of female D. melanogaster expressing tobacco NtFT4
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
SUBMITTER: Philip Känel
PROVIDER: E-MTAB-10730 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:In the present study, genome-wide expression profiling was carried out to analyze gene expression in RNA from 15 human cryotome samples. For this purpose, Affymetrix GeneChip® Human Gene ST 2.0 Arrays were used in combination with random priming and a one-color based hybridization protocol. Microarray signals were detected using the Affymetrix GeneChip® 3000 Scanner.
2024-07-15 | E-MTAB-13220 | biostudies-arrayexpress
Project description:In the present study, genome-wide expression profiling was carried out to identify gene expression enrichment from RNA of 20 human cryotome samples of pairs of tumor-associated myeloid cells (TAM) and total tumor cells. For this purpose, Affymetrix GeneChip® Human Gene ST 2.0 Arrays were used in combination with random priming and a one-color based hybridization protocol. Microarray signals were detected using the Affymetrix GeneChip® 3000 Scanner.
2024-07-15 | E-MTAB-13219 | biostudies-arrayexpress
Project description:In order to find the protein specifically bound by lncRNA-AC016745.3, we identified it through RNA pulldown combined with Protein Mass Spectrometry
2022-02-15 | PXD029141 | Pride
Project description:Livers for tissue preparation and HSC isolation were derived from 2 and 22 months old male Wistar rats from Janvier Labs (France). Samples from three different lobes (median lobe, left lateral lobe, right lateral lobe) of each liver were collected and pooled for tissue analysis by gene expression. To isolate HSC, the livers were digested with enzyme solutions and HSC were enriched by density gradient centrifugation. HSC were purified by fluorescence-activated cell sorting using their typical retinoid fluorescence emitted after UV-light excitation. The sorted HSC were collected in IMDM supplemented with 10% FCS and 1 % antibiotic-antimycotic solution and cultured for 24 hours. Total RNA of HSC and whole liver tissue from 3 young and 3 old rats was extracted using the Qiagen RNeasy Mini Kit. RNA samples obtained from cultured HSC and whole liver tissues were sent to IMGM Laboratories (Martinsried, Germany) for gene expression analyses by microarrays (Affymetrix, GeneChip Rat Gene 2.0 ST Array, Thermo Fisher Scientific) in triplicates for each age group. The array data were processed by the Transcriptome Analysis Console 3.0 (Thermo Fisher Scientific).
2020-03-12 | E-MTAB-7423 | biostudies-arrayexpress
Project description:Coronary artery disease (CAD) and its complication myocardial infarction (MI) are the leading cause of death worldwide.Our genome-wide association studies (GWAS) in the Chinese population identified a genomic variant, rs6903956, in intron 1 of the C6orf105 gene (later named as ADTRP) as a significant risk factor for CAD and MI. Based on itscell membrane localization and its function on regulation of TFPI, we hypothesize that ADTRP acts as a cell signaling molecule that affects function and expression of many downstream genes/proteins. We performed global gene expression profiling in cells with knockdown of ADTRP expression to identify other downstream targets of ADTRP. To identify other downstream targets of ADTRP, we performed global gene expression profiling in cells with knockdown of ADTRP expression. Because ADTRP downstream genes include those involved in cell cycle regulation and apoptosis as well as multiple histone genes, we carried out cellular studies on cell cycle, cell proliferation and apoptosis to further characterize the function of ADTRP. Global gene expression of ADTRP siRNA sampels and negative controls were profiled by Affymetrix GeneChip PrimeView arrays in HepG2 cells, top downstream genes with differntial expression levels were selected for validation in HepG2, HUVEC, and EAhy926 endothelial cells. Because ADTRP downstream genes include those involved in cell cycle regulation and apoptosis as well as multiple histone genes, we carried out cellular studies on cell cycle, cell proliferation and apoptosis to further characterize the function of ADTRP.
2016-09-07 | E-GEOD-80469 | biostudies-arrayexpress
Project description:Multiple sclerosis is a common inflammatory and degenerative disease that causes neurological disability. It affects young adults and its prevalence is higher in women. The most common form is manifested as a series of acute episodes of neurological disability (relapses) followed by a recovery phase (remission). Recently, non-coding RNAs have emerged as new players in transcriptome regulation, and in turn, they could have a significant role in MS pathogenesis. In this context, our aim was to investigate the involvement of microRNAs and snoRNAs in the relapse-remission dynamics of MS in peripheral blood leucocytes, to shed light on the molecular and regulatory mechanisms that underlie this complex process. With this approach, we found that a subset of small non-coding RNAs (sncRNA) is altered in relapse and remission, revealing unexpected opposite changes that are sex dependent. Furthermore, we found that a relapse-related miRNA signature regulated general metabolism processes in leucocytes, and miRNA altered in remission are involved in the regulation of innate immunity. We observed that sncRNA dysregulation is different in relapse and remission leading to differences in transcriptome regulation, and that this process is sex dependent. In conclusion, relapse and remission have a different molecular background in men and women. 24 multiple sclerosis patients with samples both in remission and relapse (2 samples for each patient; 48 blood samples in total) and 24 healthy controls were included in the study, for a total of 72 samples.
2015-11-03 | E-GEOD-74579 | biostudies-arrayexpress
Project description:Genomes pervasively produce long non-coding RNAs (lncRNAs) of largely unknown functions. Some of these lncRNAs have been implicated in roles related to ageing and associated diseases. Here we characterize aal1 (ageing-associated lncRNA 1) which is induced in non-dividing, ageing cells of fission yeast. Deletion of aal1 shortens the chronological lifespan of non-dividing cells, while ectopic overexpression of aal1 from a plasmid prolongs their lifespan, indicating that this lncRNA acts in trans. We find that aal1 genetically interacts with coding genes functioning in processes related to protein translation, and aal1 overexpression leads to repression of ribosomal protein genes and inhibition of cell growth. The aal1 RNA localizes to the cytoplasm and associates with ribosomes. Notably, aal1 deletion or overexpression is sufficient to increase or decrease the cellular ribosome content, respectively. We identify the mRNA rpl1901, encoding a ribosomal protein, as a binding target of aal1. The expression of rpl1901 is moderately repressed by aal1, and such moderate repression is critical and sufficient to extend the chronological lifespan. Remarkably, expression of the yeast aal1 lncRNA in the fly gut triggers a significant extension of the lifespan in flies. Based on these findings, we propose that the aal1 RNA can reduce the ribosome content by decreasing the levels of the Rpl1901 ribosomal protein, thus attenuating protein translation and promoting longevity. Although the aal1 lncRNA itself is not conserved, its effects in the fly raise the possibility that other organisms feature related mechanisms involving conserved ribosome-associated processes to control ageing.
2024-09-05 | PXD045625 | Pride
Project description:Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, can cause diverse neurodevelopmental diseases (NDD). The NDD FOXG1-syndrome lacks full understanding of the mechanistic role of its eponymous gene product. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that FOXG1 localisation is regulated at selected loci through the lncRNA Pantr1. We identified FOXG1 as an upstream transcriptional activator of Pantr1 in human and mice. Further, we discovered that FOXG1 has the ability to associate with RNAs. Both, transcriptional regulation of Pantr1 by FOXG1 and association of both partners, build up a regulative network that impacts the localisation of FOXG1 at selected genomic loci. Specifically, Pantr1 facilitates cooperative presence of FOXG1/NEUROD1 at specific sites, and Pantr1 reduction leads to redistribution of FOXG1 to comparably more generic binding sites. The rescue of impaired dendritic outgrowth upon FOXG1 reduction by simultaneous overexpression of Pantr1 underlines the importance of the FOXG1/Pantr1 regulative network.
2025-06-03 | PXD056060 | Pride
Project description:Environmental enrichment (EE) conditions have profound beneficial effects for reinstating cognitive ability in neuropathological disorders like Alzheimerâs disease (AD). While EE benefits involve epigenetic gene control mechanisms that comprise histone acetylation, the histone acetyltransferases (HATs) involved remain largely unknown. Here, we examine a role for Tip60 HAT action in mediating activity- dependent beneficial neuroadaptations to EE using the Drosophila CNS mushroom body (MB) as a well-characterized cognition model. We show that flies raised under EE conditions display enhanced MB axonal outgrowth, synapse protein production, histone acetylation induction and transcriptional activation of cognition linked genes when compared to their genotypically identical siblings raised under isolated conditions. Further, these beneficial changes are impaired in both Tip60 HAT mutant flies and APP neurodegenerative flies. While EE conditions provide only slight beneficial neuroadaptive changes in the APP neurodegenerative fly MB, such positive changes are significantly enhanced by increasing MB Tip60 HAT levels. Our results implicate Tip60 as a critical mediator of EE-induced benefits, and provide insight into synergistic behavioral and epigenetic based approaches for treatment of cognitive disorders. EE has been shown to positively impact gene expression profiles in the mouse brain that are enriched in functions such as neuronal structure, synaptic plasticity and neurotransmission. Thus, we asked whether the EE induced beneficial MB structural and synaptic changes we observe are accompanied by neuroadaptive transcriptional benefits in the Drosophila MB, and if so, is Tip60 HAT action required for this process. To address this question, we accessed EE induced beneficial transcriptional changes using microarray. We crossed our UAS-mCD8-GFP;Tip60E431Q flies or control UAS-mCD8-GFP flies to MB GAL4 OK-107 to simultaneously induce Tip60 HAT loss in the MB while tagging MB cells with GFP. Adult progeny were exposed to EE or ISO conditions. After conditioning, the GFP tagged MB Kenyon neurons were FACs purified from conditioned fly brains from each genotype to enrich for detection of an EE induced MB transcriptional response. RNA was isolated from the purified Kenyon MB neurons and transcriptional changes for each genotype were assessed using microarray analysis
2016-01-07 | E-GEOD-76612 | biostudies-arrayexpress
Project description:Long non-coding Rnas (lncRNAs) can act as oncogenes or tumor suppressors to regulate cancer development. We found that CYP1B1-AS1 was down-regulated in breast cancer tissues and correlated with the prognosis of patients. Lentiviral vectors were used to overexpress CYP1B1-AS1 in MCF7 cells, and the target proteins bound to CYP1B1-AS1 were detected by pulldown assay and mass spectrometry. The function of CYP1B1-AS1 is unknown. Our study revealed the molecular mechanism of CYP1B1-AS1 inhibiting breast cancer proliferation in breast cancer, and provided a new strategy for the treatment of breast cancer targeting lncRNA.
2023-10-24 | PXD037317 | Pride