Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA244384 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1233230.fastq.gz | Fastqsanger.gz | |||
| SRR1233231.fastq.gz | Fastqsanger.gz | |||
| SRR1233232.fastq.gz | Fastqsanger.gz | |||
| SRR1233233.fastq.gz | Fastqsanger.gz | |||
| SRR1233234.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43M-BM-0C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38M-BM-0C. In contrary at 43M-BM-0C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38M-BM-0C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock. On Illumina platform we sequenced DNA immunoprecipitated from isolated spermatocytes using anti-HSF1 antibody or anti-HSF2 antibody. Cells were either untreated (control) or heat shocked for 5-20 minutes. Two PCR-verified ChIP replicates were collected per each sample, and three negative control samples with normal goat serum were included.
2014-10-07 | E-GEOD-56735 | biostudies-arrayexpress
Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43°C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38°C. In contrary at 43°C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38°C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock.
2014-10-07 | GSE56735 | GEO
Project description:We utilized chromatin immunoprecipitation sequencing (ChIP-seq) to analyze the binding of HSF1 and HSF2 to chromatin under oxidative stress and heat shock. ChIP-seq was performed in mouse embryonic fibroblasts (MEFs) that were exposed to heat shock (HS) or oxidative stress induced by menadione (MD). Antibodies against HSF1 and HSF2 were used for immunoprecipitation.
2022-06-10 | GSE183244 | GEO
Project description:Heat shock factor 1 (HSF1) is well known for its role in the heat shock response (HSR), where it drives a transcriptional program comprising heat shock protein (HSP) genes, and in tumorigenesis, where it drives a program comprising HSPs and many non-canonical target genes that support malignancy. Here, we find that HSF2, an HSF1 paralog with no significant role in the HSR, physically and functionally interacts with HSF1 across diverse types of cancer. HSF1 and HSF2 have strikingly similar chromatin occupancy and regulate a common set of genes which include both HSPs and non-canonical transcriptional targets with roles critical in supporting malignancy. Loss of either HSF1 or HSF2 results in a dysregulated response to nutrient stresses in vitro and reduced tumor progression in cancer cell line xenografts. Taken together, these findings establish HSF2 as a critical cofactor of HSF1 in driving a cancer cell transcriptional program to support the anabolic malignant state.
2022-03-15 | GSE194098 | GEO
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:We hypothesized that broad-scale expression profiling would provide insight into the regulatory pathways that control gene expression in response to stress, and potentially identify novel heat-responsive genes. HEp2 cells were heated at 37 to 43 °C for 60 min to gauge the heat shock response, using as a proxy inducible HSP-70 quantified by western blot analysis. Based on these results, microarray experiments were conducted at 37, 40, 41, 42 and 43°C (3 replicates/temperature x 5 groups = 15 U95Aver2 GeneChips). Using linear modeling, we compared the sets of microarrays at 40, 41, 42 and 43°C with the 37°C baseline temperature and took the union of the genes exhibiting differential gene expression signal to create two sets of “heat shock response” genes, each set reflecting either increased or decreased RNA abundance. Leveraging human and mouse orthologous alignments, we used the two lists of co-expressed genes to predict transcription factor binding sites in silico, including those for heat shock factor 1 (HSF1) and heat shock factor 2 (HSF2) transcription factors. We discovered HSF1 and HSF2 binding sites in 15 genes not previously associated with the heat shock response. We conclude that microarray experiments coupled with upstream promoter analysis can be used to identify novel genes that respond to heat shock. Additional experiments are required to validate these putative heat shock proteins and facilitate a deeper understanding of the mechanisms involved during the stress response. Keywords: stress response, temperature, human epithelial cells
2007-04-10 | GSE7458 | GEO
Project description:In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To find out molecular targets of HSF1 in all promoter regions, and to elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide HSF1 binding analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results. On Affymetrix GeneChipM-BM-. Mouse Promoter 1.0R Arrays we analyzed DNA immunoprecipitated (using anty-HSF1 antibody) from spermatocytes or hepatocytes, either untreated (control) or immediately after heat shock performed in vitro for 5-20 minutes. ChIP on chip analyses were done in triplicate.
2012-08-28 | E-GEOD-40390 | biostudies-arrayexpress
Project description:In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide transcriptional analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results. Genes that are differently regulated during hyperthermia in both types of cells have been identified. On Affymetrix gene chip arrays we analyzed RNA isolated from spermatocytes or hepatocytes, either untreated (control) or after heat shock and 2h of recovery at physiological temperature. Analyses were done in triplicate.
2012-08-22 | E-GEOD-40248 | biostudies-arrayexpress
Project description:Genome-wide characterization of binding sites for heat shock transcription factors HSF1 and HSF2 in freely cycling and mitotic K562 cells in optimal growth conditions and upon 30 min heat stress at 42C
2013-08-04 | GSE43579 | GEO
Project description:RNA sequencing (RNA-seq) was used to study the impact of heat shock factors 1 and 2 (HSF1 and HSF2) on gene expression in normal growth conditions, upon Bortezomib-induced proteasome inhibition (25 nM, 6 h or 10 h), and upon heat shock (42∘C, 1 h).
2020-01-14 | GSE115973 | GEO