Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA238673 | ENA |
REPOSITORIES: ENA
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Project description:Pervasive genomic transcription during oxidative stress generates thousands of previously uncharacterized lncRNAs
| PRJNA238663 | ENA
Project description:Pervasive genomic transcription during oxidative stress generates thousands of previously uncharacterized lncRNAs (RNA-Seq)
| PRJNA238674 | ENA
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress. Chromatin immunoprecipitation coupled sequencing of 2 histone modifications in BJ (hTert/sT) and total levels of RNA polymerase II after 0, 30 and 120 minutes of treatment with H2O2 in MRC5 cells.
2015-05-27 | E-GEOD-55171 | biostudies-arrayexpress
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress. RNA-Sequencing profiles of nuclear and cytosolic fractions of fibroblast cell lines after 0, 30 and 120 minutes of treatment with H2O2.
2015-05-27 | E-GEOD-55169 | biostudies-arrayexpress
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress.
2015-05-27 | GSE55169 | GEO
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress.
2015-05-27 | GSE55171 | GEO
Project description:Recent studies have uncovered thousands of long non-coding RNAs (lncRNAs) in human pancreatic β cells. β cell lncRNAs are often cell type specific and exhibit dynamic regulation during differentiation or upon changing glucose concentrations. Although these features hint at a role of lncRNAs in β cell gene regulation and diabetes, the function of β cell lncRNAs remains largely unknown. In this study, we investigated the function of β cell-specific lncRNAs and transcription factors using transcript knockdowns and co-expression network analysis. This revealed lncRNAs that function in concert with transcription factors to regulate β cell-specific transcriptional networks. We further demonstrate that the lncRNA PLUTO affects local 3D chromatin structure and transcription of PDX1, encoding a key β cell transcription factor, and that both PLUTO and PDX1 are downregulated in islets from donors with type 2 diabetes or impaired glucose tolerance. These results implicate lncRNAs in the regulation of β cell-specific transcription factor networks.
| EGAS00001002865 | EGA
Project description:Long non-coding RNAs (lncRNAs) exhibit a poor interspecies conservation and often show spatial- and temporal-specific expression patterns. What, if any, role they have in oxidative stress remains unknown. To identify potential roles for lncRNAs, we examined their expression in normal and H2O2-treated human umbilical vein endothelial cells. Oxidative stress related lncRNAs were generated by deep sequencing, using Illumina HiSeq 2000 or 2500 platform. Sequencing of the cDNA libraries from H2O2-treated HUVECs generated 12.5 million uniquely valid reads, meanwhile, 10.2 million valid fragments were obtained from control group in our experiment. A total of 10, 765 known and 30, 629 novel putative lncRNAs were identified according to RNA-Seq. Among them, 2, 091 of known and 25, 800 of novel lncRNAs were differentially expressed in H2O2-treated HUVECs compared with control HUVECs, and 12 of these were validated with qRTâPCR. Taken together, our findings provide evidence differentially expressed lncRNAs were mediated by oxidative stress in HUVECs, it is, therefore, likely that aberrant expression of lncRNAs, at least in part, participate in the process of endothelial injury caused by oxidative stress. Examination of lncRNAs in the oxidative-stressed human umbilical vein endothelial cells
2016-02-25 | E-GEOD-78275 | biostudies-arrayexpress
Project description:Metabolically-engineered Escherichia coli has been used previously to degrade the ubiquitous pollutant cis-1,2-dichloroethylene (cis-DCE), and the impact of the metabolic engineering was assessed by investigating the changes in the proteome. Here, genome-wide transcriptome analysis was performed to confirm that a strong heat shock and/or oxidative stress occurs during enhanced cis-DCE mineralization. Also, seven new stress proteins (YchH, YdeI, YodD, YodC, YgiW, YhcN, and YjaA) that were previously uncharacterized have been identified.
2009-11-24 | GSE13698 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE41936: Rho and NusG suppress pervasive antisense transcription in Escherichia coli [ChIP-chip]. GSE41938: Rho and NusG suppress pervasive antisense transcription in Escherichia coli [tiling array]. GSE41939: Rho and NusG suppress pervasive antisense transcription in Escherichia coli [RNA-seq]. Refer to individual Series
2012-11-01 | E-GEOD-41940 | biostudies-arrayexpress