Ontology highlight
ABSTRACT:
PROVIDER: PRJNA779479 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16914153_1.fastq.gz | Fastqsanger.gz | |||
| SRR16914153_2.fastq.gz | Fastqsanger.gz | |||
| SRR16914154_1.fastq.gz | Fastqsanger.gz | |||
| SRR16914154_2.fastq.gz | Fastqsanger.gz | |||
| SRR16914155_1.fastq.gz | Fastqsanger.gz |
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Project description:Heat shock-induced ribosomal intergenic spacer RNA
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Project description:Cells adapt to environmental stressors such as heat shock and extracellular acidosis through formation of nuclear membrane-less compartments called Amyloid bodies (A-bodies). Stressors activate formation of Amyloid bodies (A-bodies) via induction of ribosomal intergenic spacer RNA (rIGSRNA). RNA-seq on non-ribosome depleted RNA from human MCF7 cells exposed to heat shock (43C, 30 minutes) revealed the heat shock-specific expression profile of rIGSRNA.
2018-08-02 | GSE115731 | GEO
Project description:To realize the gene expression in response to acute heat stress in chicken small yellow follicles, we have employed whole genome microarray expression profiling as we have employed whole genome microarray expression profiling as a tool to identify genes response to acute heat stress. Female B strain Taiwan country chickens were subjected to acute heat stress (38℃) for 2 h, and then exposed to 25℃, with small yellow follicles collected 0, 2, and 6 h after the cessation of heat stress, using non heat-stressed hens as a control group (n = 3 hens per group). Based on a chicken 44K oligo microarray, 69, 51, and 76 genes were upregulated and 58, 15, 56 genes were downregulated after heat treatment of H2R0, H2R2, and H2R6, respectively, using a cutoff value of two-fold or higher in the small yellow follicles of the heat-stressed chickens from those of the control chickens. Upregulation of heat shock protein 25, interleukin 6, metallopeptidase 1, and metalloproteinase 13, and downregulation of type II alpha 1 collagen, discoidin domain receptor tyrosine kinase 2, and Kruppel-like factor 2 were confirmed through quantitative real-time polymerase chain reaction (qRT-PCR).
2015-07-21 | GSE71091 | GEO
Project description:To realize the gene expression in response to acute heat stress in chicken small yellow follicles, we have employed whole genome microarray expression profiling as we have employed whole genome microarray expression profiling as a tool to identify genes response to acute heat stress. Female B strain Taiwan country chickens were subjected to acute heat stress (38℃) for 2 h, and then exposed to 25℃, with small yellow follicles collected 0, 2, and 6 h after the cessation of heat stress, using non heat-stressed hens as a control group (n = 3 hens per group). Based on a chicken 44K oligo microarray, 69, 51, and 76 genes were upregulated and 58, 15, 56 genes were downregulated after heat treatment of H2R0, H2R2, and H2R6, respectively, using a cutoff value of two-fold or higher in the small yellow follicles of the heat-stressed chickens from those of the control chickens. Upregulation of heat shock protein 25, interleukin 6, metallopeptidase 1, and metalloproteinase 13, and downregulation of type II alpha 1 collagen, discoidin domain receptor tyrosine kinase 2, and Kruppel-like factor 2 were confirmed through quantitative real-time polymerase chain reaction (qRT-PCR).
2017-05-20 | GSE99108 | GEO
Project description:HSF1 is a major transcriptional regulator of heat shock responses. Many cells activate HSF1 in response to heat shock temperatures (>42oC) and other cellular stress causing agents. Unlike other cell types, T cells activate HSF1 in response to T cell activation or when exposed to febrile (40oC) temperatures, suggesting a role for HSF1 beyond the heat-shock response. We used microarray analysis and HSF1 knock-out mice to study the HSF1 mediated gene regulation in activated T cells under normal and fever temperatures.
2012-09-20 | GSE41005 | GEO
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels
Project description:Heat Shock Factor 1 drives intergenic association of its target gene loci during heat shock
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Project description:Bacterial and eukaryotic cells survive an otherwise lethal heat shock once they are primed by a mild pre-heat shock. Using B. subtilis as a model organism, we investigated transcriptional changes during thermotolerance development at 37 °C, 48 °C, 53 °C and 48/53 °C and observed a comprehensive upregulation of genes of the general and heat shock response and the downregulation of many translation-related genes. In addition, strains lacking (p)ppGpp (ppGpp0) or with elevated (p)ppGpp levels (ΔrelA) were analyzed at 37 °C and 48 °C, revealing broad and pleiotropic transcripional changes mediated by (p)ppGpp in the ΔrelA mutant. In addition, our data suggests a contribution of the (p)ppGpp-mediated stringent response in the heat-mediated transcripional down-regulation of ribosomal genes and additional processes.
2019-04-15 | GSE125467 | GEO
Project description:The combination of Chromatin Immunoprecipitation and Massively Parallel Sequencing, or ChIP-Seq, has greatly advanced our genome-wide understanding of chromatin and enhancer structures. However, its resolution at any given genetic locus is limited by several factors. In applying ChIP-Seq to study the ribosomal RNA genes we found that a major limitation to resolution was imposed by the often dominant variability in sequence coverage provided by the massively parallel sequencing technology. Here we describe a simple numerical deconvolution approach that in large part corrects for this variability and significantly improves both the resolution and quantitation of protein-DNA interaction maps deduced from ChIP-Seq data. This approach has allowed us to study the in vivo organization of the RNA Polymerase I pre-initiation complexes that form at the promoters of the mouse and human ribosomal RNA genes. The data identify and map a Spacer Promoter and associated stalled polymerase in the intergenic spacer of the human ribosomal genes and show that a very similar Enhancer structure and organization to that found in rodents and even in lower vertebrates also exists in human.
2017-12-31 | E-MTAB-6032 | biostudies-arrayexpress