Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613550 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11354809.fastq.gz | Fastqsanger.gz | |||
| SRR11354810.fastq.gz | Fastqsanger.gz | |||
| SRR11354811.fastq.gz | Fastqsanger.gz | |||
| SRR11354812.fastq.gz | Fastqsanger.gz | |||
| SRR11354813.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:Heat shock transcription factor 1 (HSF1) is responsible for triggering stress-induced activation of the HSP genes. HSF1 is also involved in the regulation of many other genes associated with multiple cellular processes including cell signaling, development, fertility, cell death and metabolism, e.g. NFkappaB transcription factor. Here we aimed to establish a global picture for the association between hyperthermia-modulated expression of NFkappaB-dependent genes and HSF1 binding in regulatory regions of target genes. The global pattern of HSF1 binding was analyzed after 10 and 20 minutes of hyperthermia using the ChIP-Seq approach. The analysis revealed about 25,000 HSF1 binding sites in chromatin of control untreated U-2 OS cells, which nearly doubled in cells subjected to hyperthermia. The presence of hyperthermia-induced HSF1 binding was established in regulatory regions of hyperthermia-affected genes and in TNF-affected genes. In most cases hyperthermia pre-conditioning inhibited cytokine-mediated activation of NF-κB-dependent genes. However, our results also revealed novel gene subsets that included TNFalpha-regulated and hyperthermia-unaffected genes, as well as genes (co)repressed, (co)stimulated, or antagonized by both types of stimuli.
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Project description:This dataset consists of 10 raw MS files and associated peak lists and results files, acquired on AB Sciex TripleTOF 6600 mass spectrometer operated in Data Dependent Acquisition mode.
Samples were generated by Yukari Endo. Mass spectrometry acquisition and data analysis was performed by Cassandra Wong.
The files are associated with a manuscript submitted for publication by Yukari Endo et al. The main goal of this paper was to identify new genetic variants that predisposed individuals to exertional heat illness (EHI) and malignant hyperthermia (MH), both which are life threatening conditions.
James J. Dowling is the corresponding author of the manuscript (james.dowling@sickkids.ca); Karen Colwill should be contacted for questions on this dataset (colwill@lunenfeld.ca)
This submission is associated with 3 Supplementary Files (in addition to this README file)
Table 1 describes the composition of this dataset
Table 2 lists all the peptide identification evidence (as per iProphet)
Table 3 lists the SAINTexpress interactions
2022-05-04 | MSV000089417 | MassIVE