Transcriptome-wide changes in HeLa cell line investigated in response to Heat-shock stress
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE26776 | GEO | 2011/11/09
SECONDARY ACCESSION(S): PRJNA136287
REPOSITORIES: GEO
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Project description:The repertoire of transcripts that are differentially regulated in response to Heat-shock were studied using Illumina WG-6 v2.0 BeadChip. Study was undertaken with 3 biological replicates for each condition of Heat-Shock Treated and Untreated condition.
2011-11-09 | E-GEOD-26776 | biostudies-arrayexpress
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Project description:To investigate the effect of HSATIII lncRNA on m6A modification, we performed m6A-RIP(RNA immuno precipitation) RNA-seq from heat shock-exposed HeLa cells upon HSATIII knockdown.
2021-04-30 | GSE164200 | GEO
Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules).
2011-11-09 | GSE24197 | GEO
Project description:Recombinant Escherichia coli cultures are used to manufacture numerous therapeutic proteins and industrial enzymes, where many of these processes use elevated temperatures to induce recombinant protein production. The heat-shock response in wild-type E. coli has been well studied. In this study, the transcriptome profiles of recombinant E. coli subjected to a heat-shock and to a dual heat-shock recombinant protein induction were examined. Most classical heat-shock protein genes were identified as regulated in both conditions. The major transcriptome differences between the recombinant and reported wild-type cultures were heavily populated by hypothetical and putative genes, which indicates recombinant cultures utilize many unique genes to respond to a heat-shock. Comparison of the dual stressed culture data with literature recombinant protein induced culture data revealed numerous differences. The dual stressed response encompassed three major response patterns: induced-like, in-between, and greater than either individual stress response. Also, there were no genes that only responded to the dual stress. The most interesting difference between the dual stressed and induced cultures was the amino acid-tRNA gene levels. The amino acid-tRNA genes were elevated for the dual cultures compared to the induced cultures. Since tRNAs facilitate protein synthesis via translation, this observed increase in amino acid-tRNA transcriptome levels, in concert with elevated heat-shock chaperones, might account for improved productivities often observed for thermo-inducible systems. Most importantly, the response of the recombinant cultures to a heat-shock was more profound than wild-type cultures, and further, the response to recombinant protein induction was not a simple additive response of the individual stresses. The objective of the present work is to gain a better understanding of the heat-shock response in recombinant cultures and how this response might impact recombinant protein production. To accomplish this objective, the transcriptome response of recombinant cultures subjected to a heat-shock and a dual heat-shock recombinant protein induction were analyzed. The transcriptome levels were determined using Affymetrix E. coli Antisense DNA microarrays, such that the entire genome was evaluated. These two transcriptome responses were also compared to recombinant cultures at normal growth temperature that were not over-expressing the recombinant protein and a set of literature recombinant culture data that were chemically induced to over-express the recombinant protein. Additionally, the heat-shock response of the recombinant cultures was compared to the literature report of the heat-shock response in wild-type cultures. The results of the global transcriptome analysis demonstrated that recombinant cultures respond differently to a heat-shock stress than wild-type cultures, where the transcriptome response of the recombinant cultures is further modified by production of a recombinant protein.
2009-08-07 | GSE17507 | GEO
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:HSFA1s are a gene family of HSFA1 with four members, HSFA1a, HSFA1b, HSFA1d, and HSFA1e. HSFA1s are the master regulators of heat shock response. As a part of the heat shock response, HSFA2 can prolong the heat shock response and amplify the heat shock response in response to repeat heat shock. To identify the heat-shock-responsive genes differentially regulated by HSFA1s and HSFA2, we compared the transcriptomic differences of plants containing only constitutively expressed HSFA1s or HSFA2 after heat stress.
2013-04-09 | GSE44655 | GEO
Project description:The heat-shock stress response was studied at the level of exons using Affymetrix Exon-array profiling for both sense and anti-sense transcripts. Sense transcript profiling was done as per the protocol of Affymetrix Exon 1.0 ST array and anti-sense transcript array profiling was done using a modified protocol (Xijin Ge et al., BMC Genomics. 2008 Jan 22;9:27). In short, for profiling antisense transcripts, first cycle cDNA synthesis and IVT step is skipped. This modified protocol starts directly from the second cycle cDNA synthesis step. The labelled target DNA fragments are in reverse orientation of original mRNAs. Thus the hybridization signals will represent transcripts from the same exonic regions but from the opposite DNA strand. Study was undertaken with 2 biological replicates each for - a) Heat-shock treated Sense b) Heat-shock treated Anti-sense c) Untreated control Sense d) Untreated control Anti-Sense
2011-07-31 | E-GEOD-27127 | biostudies-arrayexpress
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:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In this study, we demonstrate that the RNAPII interactor RPRD1B is required for proper transcription of heat shock induced genes and for survival to heat shock.
2022-09-08 | GSE197993 | GEO