Ontology highlight
ABSTRACT:
PROVIDER: PRJNA990812 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25117700_1.fastq.gz | Fastqsanger.gz | |||
| SRR25117700_2.fastq.gz | Fastqsanger.gz | |||
| SRR25117701_1.fastq.gz | Fastqsanger.gz | |||
| SRR25117701_2.fastq.gz | Fastqsanger.gz | |||
| SRR25117702_1.fastq.gz | Fastqsanger.gz |
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Project description:HS-induced proteome changes in WT and DNAJA1-KO cells were quantified using label free-based quantitative proteomic analysis. Four groups:wild type HUVECs group, DNAJA1 knockout HUVECs group, WT HUVECs with heat stress group, DNAJA1 knockout HUVECs with heat stress group,were conducted label free-based quantitative proteomic analysis to detect the mechanism of DNAJA1's protective effects on heat stress.
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Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. In this study we assayed for genome-wide localization of HSF1 enrichment in the HCT116 FBXW7 KO colon cells and their wild type counterpart in untreated cells and upon heat shock. These results revealed that accumulation of nuclear HSF1 in FBXW7 KO cells results in rewiring of the HSF1 transcriptional program. Five million cells were used for the ChIP and precipitated using 5 micrograms of antibody (cell signaling, 4356) against human HSF1
2015-02-20 | E-GEOD-57398 | biostudies-arrayexpress
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. In this study we assayed for genome-wide localization of HSF1 enrichment in the HCT116 FBXW7 KO colon cells and their wild type counterpart in untreated cells and upon heat shock. These results revealed that accumulation of nuclear HSF1 in FBXW7 KO cells results in rewiring of the HSF1 transcriptional program.
2015-02-20 | GSE57398 | 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. hsfa2 (the KO mutant of HSFA2, Col-0 background) and A2QK-10 (CaMV 35S:HSFA2 in QK mutant; QK is HSFA1a/b/d/e quadruple KO mutant) were used to compare the difference of heat shock response when plants lack HSFA1s or HSFA2. The aim is to find the HSFA1s- and HSFA2-preferred regulating genes after heat stress. As the control samples, wild type is the plant with normal heat shock response, and QK (HSFA1s KO mutant, Col-0 and Ws mixed background) is the plant that lost the heat shock response controlled by HSFA1s.
2013-04-09 | E-GEOD-44655 | biostudies-arrayexpress
Project description:We utilized precicion run-on sequencing (PRO-seq) to analyze the roles of HSF1 and HSF2 in the reprogramming of transcription under oxidative stress and heat shock. PRO-seq was performed in wild-type (WT), HSF1 knock-out (HSF1 KO) and HSF2 knock-out (HSF2 KO) mouse embryonic fibroblasts (MEFs) that were treated with heat shock (HS) or oxidative stress induced by menadione (MD).
2022-06-10 | GSE183243 | GEO
Project description:To identify transcripts that are regulated by putative transcriptional co-activators, WT (Col) and KO of heat responsive transcriptional co-activator (Multiprotein Bridging Factor 1c) in Arabidopsis were subjeted to heat stress. These plants were compared to find transcripts that are regulated by the transcriptional co-activator during heat stress.
2011-06-09 | E-MEXP-2760 | biostudies-arrayexpress
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7. Whole RNA was extracted from 1 million HCT116 WT or FBXW7KO cells using the RNAeasy kit (Qiagen) according to the manufacturer’s protocol. Poly-A+ (magnetic oligodT-containing beads (Invitrogen)) or Ribominus RNA was used for library preparation. cDNA preparation and strand-specific library construction was performed using the dUTP method. Libraries were sequenced on the Illumina HiSeq 2000 using 50bp single-read method. Differential gene expression analysis was performed for each matched recovery versus heat-shock pairs, separately in each biological replicate and cell line (WT or KO). Two types of comparisons were tested: (a) WT recovery vs WT heat shock, (b) FBXW7 KO recovery vs heat shock.
2015-02-20 | E-GEOD-57397 | biostudies-arrayexpress
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7.
2015-02-20 | GSE57397 | GEO
Project description:au08-06_mpk6_heat_stressed - au08-06_mpk6_heat_stressed - Mitogen Activated Protein Kinase (MAPK) signaling pathways are key regulators of cell proliferation, differentiation and stress effectors. The core of the MAP kinase signal transduction cascade is composed of a three-kinase module consisting of a MAP kinase kinase kinase (MAPKKK), a MAP kinase kinase (MAPKK), and a MAP kinase (MAPK). The signaling pathway is activated upon stimulation by a phosphorylation cascade. In previous studies, it was shown that the mpk6 KO mutant plants are significantly more tolerant to heat stress in comparison to wt and that after 3h treatment at 37°C, an activation of heat-shock proteins occures in the mpk6 mutant. To better understand the changes occuring in the mpk6 mutant upon heat stress at the gene expression level, we would like to perform a microarray transcriptomic analysis. - Mitogen Activated Protein Kinase (MAPK) signaling pathways are key regulators of cell proliferation, differentiation and stress effectors. The core of the MAP kinase signal transduction cascade is composed of a three-kinase module consisting of a MAP kinase kinase kinase (MAPKKK), a MAP kinase kinase (MAPKK), and a MAP kinase (MAPK). The signaling pathway is activated upon stimulation by a phosphorylation cascade. In previous studies, it was shown that the mpk6 KO mutant plants are significantly more tolerant to heat stress in comparison to wt and that after 3h treatment at 37°C, an activation of heat-shock proteins occures in the mpk6 mutant. To better understand the changes occuring in the mpk6 mutant upon heat stress at the gene expression level, we would like to perform a microarray transcriptomic analysis. Keywords: treated vs untreated comparison 4 dye-swap - CATMA arrays
2010-06-28 | E-GEOD-22568 | 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