Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA261153 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of genes regulated by HSF1 in control and heat-shocked cells
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Project description:To examine the expressions of HSF1 and SSBP1-mediated gene in control and heat shock conditions, we performed DNA microarray analysis. mRNA levels in control and heat-shocked MEF cells, which were infected with adenovirus expressing scramble RNA, or shRNA against HSF1 and SSBP1, were analyzed by DNA microarray analysis using GeneChip Mouse Gene 1.0 ST Array (Affymetrix).
2015-01-27 | E-GEOD-61456 | biostudies-arrayexpress
Project description:To examine the regulation of HSF1-mediated gene expression in control and heat shock conditions, we performed DNA microarray analysis. mRNA levels in control and heat-shocked MEF cells, which were infected with adenovirus expressing scramble RNA or HSF1 short hairpin RNA, were analyzed by DNA microarray analysis using GeneChip Mouse Gene 1.0 ST Array (Affymetrix).
2014-11-01 | E-GEOD-54060 | biostudies-arrayexpress
Project description:Genome-wide HSF1 binding sites in control and heat shocked spermatocytes and hepatocytes
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Project description:Heat shock transcription factor 1(HSF1) is an important transcription factor which regulates the expression of a wide array of genes including heat shock proteins and oncogenes. Here, we report that HSF1 as a target of WNT/β-catenin signaling, regulates parts of target genes of WNT/β-catenin signaling. To explore the biological relevance of HSF1 activation to WNT/β-catenin signaling, we profiled gene expression of wild type mouse embryonic fibroblasts (WT MEF) and HSF1 knock out MEF (HSF1 KO MEF) before and after lithium chloride (LiCl) treatment which was a potent GSK3β inhibitor and increased the expression of β-catenin.
2020-08-31 | GSE151119 | GEO
Project description:Identification of genes regulated by knockdown of HSF1 or RPA1
| PRJNA167801 | ENA
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.
2012-08-22 | GSE40248 | GEO
Project description:External stressors, especially heat stress, always lead to DNA damage and genome instability in cells. However, how cells rapidly response to these DNA damage remains largely unknown. In this study, we found that the major transcription factor in heat shock response, HSF1, activated several NHEJ pathway related genes, especially NHEJ1, through the puncta it formed, thereby promoting the NHEJ pathway, reducing the DNA double-strand break upon heat stress. Furthermore, RNA m6A modification and its reader YTHDC1 were also found to play a role in this process, promoting the splicing of the NHEJ1 gene. Depletion of HSF1 or YTHDC1 led to increased nuclear γH2AX intensities in the heat shocked cells, which was rescued by overexpression of NHEJ1. Besides, overexpression of HSF1 or YTHDC1 both caused increased NHEJ pathway level in the heat shocked cells, indicating the HSF1/YTHDC1 – NHEJ1 – DNA double-strand repair axis. Our findings investigate an approach through which cells repair their damaged DNAs in the heat shock response, offering a new insight of how cells maintain a bare-minimum genome stability when exposed to external stressors.
2026-05-05 | GSE291973 | 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.
2012-08-28 | GSE40390 | GEO