Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide H3K4me3 and H3K27me3 occupancy Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we combined chromatin-immunoprecipitation and deep-sequencing analysis to identify H3K4me3-marks and H3K27me3-marks in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: H3K4me3 and H3K27me3-marks showed a rapid global increase at specific sites throughout the genome under hypoxia, both genic and inter-genic, that was partly restored upon reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates the epigenetic state of the genome.
Project description:To find the genes with significant expression changes after liver ischemia-reperfusion injury,we established a hypoxia-reoxygenation model using AML12 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq under normoxia and hypoxia-reoxygenation conditions.
Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide gene expression Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we performed a transcriptomics analysis in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: Global downregulation upon hypoxia; partial restore on reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates gene transcription.
Project description:The molecular signature at histone H3K4me3 and H3K27me3 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3, associated with active chromatin, and H3K27me3, associated with repressed chromatin, histone modifications to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. histone H3K4me3 and H3K27me3 ChIP-seq normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells Please note that the 'H3K4me3' and 'input' data are duplicated records of the samples represented in GSE69377 for the convenient retrieval of the complete raw data from SRA.
Project description:This study describes the epigenetic profiling of the X chromosome during X inactivation. It includes H3K4me3 and H3K27me3 ChIP-Seq profiles of male (E14) and female (LF2 and XT67E1) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). It also includes ChIP-chip profiles around the Xic on chromosome X of H3K4me3, H3K27me3, H3K9me2, H3K36me3, Pol II, TBP, H3-Core as well as expression, using male (E14) and female (LF2) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). Examination of two different histone modifications in 3 cell lines under 3 conditions using ChIP-Seq. Examination of five different histone modifications two transcription factors and gene expression under three conditions in 2 cell lines using ChIP-chip.
Project description:This study describes the epigenetic profiling of the X chromosome during X inactivation. It includes H3K4me3 and H3K27me3 ChIP-Seq profiles of male (E14) and female (LF2 and XT67E1) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). It also includes ChIP-chip profiles around the Xic on chromosome X of H3K4me3, H3K27me3, H3K9me2, H3K36me3, Pol II, TBP, H3-Core as well as expression, using male (E14) and female (LF2) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). Examination of two different histone modifications in 3 cell lines under 3 conditions using ChIP-Seq. Examination of five different histone modifications two transcription factors and gene expression under three conditions in 2 cell lines using ChIP-chip.
Project description:Purpose: Study hypoxia induced changes in genome-wide H3K27me3 occupancy Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we combined chromatin-immunoprecipitation and deep-sequencing analysis to identify H3K27me3-marks in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia). Results: H3K27me3-marks showed a rapid global increase at specific sites throughout the genome under hypoxia, both genic and inter-genic. Conclusions: Our data show that oxygen availability dynamically regulates the epigenetic state of the genome. Genome-wide H3K27me3-mark profiles were generated by combining ChIP analysis with deep sequencing using Illumina GAIIx.
Project description:In this study, we performed temporal profiling of transcriptome and chromatin accessibility in HL-1 cells for understanding the molecular mechanisms underlying cardiac responses to hypoxia. We collected HL-1 cells under four conditions (4 h and 8 h of hypoxia exposure, 24 h reoxygenation and the normal condition), applied RNA-seq and ATAC-seq to them and performed pairwise comparison of gene expression and open chromatin status on a genome-wide scale.