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Histone modifications regulated by HDAC5 in PDAC cells

ABSTRACT: Histone modifications regulated by HDAC5 in PDAC cells

PROVIDER: PRJNA627431 | ENA |

REPOSITORIES: ENA

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Histone modifications regulated by HDAC5 in PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3. To understand the epignetic regulations by HDAC5, we performed ChIP-seq analysis of H3K4me3, H3K27ac and H3K9ac in PDAC cells overexpressing GFP or HDAC5, and in HDAC5 escaper cells with HDAC5 knockdown or scramble control.

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RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in escaper cells, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells knocking down of HDAC5 or scramble shRNA control.

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HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3 to suppess gene expression. To identify the target genes of HDAC5, we performed ChIP-seq analysis in FLAG-tagged HDAC5 PDAC escaper cells. HDAC5 binding chromatins were pulled down by HDAC5 antibody and FLAG antibody as replicates.

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RNAseq data comparing KRAS*-independent HDAC5 eccaper PDAC cells and KRAS*-dependent iKPC PDAC cells

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells.

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HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

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RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

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Genome-wide gene expression in HDAC5 wildtype and knockout mice treated with chronic cocaine or saline

Project description:Some individuals are more vulnerable than others to chronic psychiatric illnesses, such as drug addiction or depression, but the neural and molecular mechanisms responsible for this are poorly understood. Although addiction and depression are known to have a strong genetic component, recent evidence has suggested that epigenetic mechanisms, such as histone acetylation, may also contribute. However, the mechanisms which integrate drugs of abuse or stress with changes in chromatin structure remain unclear. Here, we identify the activity-dependent class II histone deacetylase, HDAC5, as a central integrator of these stimuli with changes in chromatin structure and gene expression. We found that chronic, but not acute, exposure to cocaine or stress decreases HDAC5 function in the nucleus accumbens (NAc), a major brain reward region, which allows for increased histone acetylation and transcription of HDAC5 target genes. This regulation is behaviorally important, as loss of HDAC5 causes hypersensitive responses to chronic, not acute, cocaine or stress. Coupling gene expression microarrays and several bioinformatic approaches, we have gone on to identify the most likely HDAC5 target genes responsible for the behavioral maladaptations. One HDAC5 target, the Substance P Receptor, is upregulated in HDAC5 knockout mice, has increased histone acetylation on its promoter, and modulates cocaine reward, as measured by conditioned place preference. These findings suggest that proper balance of histone acetylation is a crucial factor in the saliency of a given emotional stimulus, and that disruption of this balance is involved in the transition from normal adaptive responses to chronic psychiatric illness. Keywords: genetic modification and its impact on cocaine responses in the nucleus accumbens

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Project description:Time makes histone H3 modifications drift

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Histone modifications in lung epithelial cells

Project description:Histone modifications in lung epithelial cells

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