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Epigenetic inhibitors

ABSTRACT: Epigenetic inhibitors

PROVIDER: PRJNA670966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12884777_1.fastq.gz	Fastqsanger.gz
	SRR12884777_2.fastq.gz	Fastqsanger.gz
	SRR12884778_1.fastq.gz	Fastqsanger.gz
	SRR12884778_2.fastq.gz	Fastqsanger.gz
	SRR12884779_1.fastq.gz	Fastqsanger.gz

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Epigenetic inhibitors

Project description:The project aims to looks at differential gene targets in the human Sezary syndrome HuT78 cell line when treated with epigenetic inhibitors romidepsin, F5446, and chaetocin compared to the vehicle treated cells (DMSO) for 72hrs.

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Unraveling epigenetic changes in A. thaliana calli: Impact of HDAC inhibitors

Project description:The aim was to characterize epigenetic changes in histone proteins during callus formation from roots and shoots of Arabidopsis thaliana seedlings using mass spectrometry-based approach. Increased level of histone H3.3 variant was found to be the most prominent feature of 20-day-old calli, associated with chromatin relaxation. Methylation status in root- and shoot-derived calli reached the same level during long-term propagation, whereas differences in acetylation levels provided a long-lasting imprint of root and shoot origin. On the other hand, epigenetic signs of origin completely disappeared during 20 days of calli propagation in the presence of histone deacetylase inhibitors (HDACi), sodium butyrate and trichostatin A, although each HDACi affected the state of post-translational histone modifications in a specific manner.

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Polycomb Deficiency Drives a FOXP2-high Aggressive State Targetable by Epigenetic Inhibitors

Project description:Polycomb Deficiency Drives a FOXP2-high Aggressive State Targetable by Epigenetic Inhibitors

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Polycomb Deficiency Drives a FOXP2-high Metastatic State Targetable by Epigenetic Inhibitors

Project description:Polycomb Deficiency Drives a FOXP2-high Metastatic State Targetable by Epigenetic Inhibitors

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An epigenetic vulnerability in PI3K/AKT inhibition resistant cancers is targetable by both bromodomain and HDAC inhibitors

Project description:Acquisition of resistance to PI3K/AKT-targeted monotherapy regardless of cancer types implies the existence of common mechanisms. Here we demonstrate that while causing glycolysis crisis, acetyl-CoA shortage and global decrease of histone acetylation, PI3K/AKT inhibitors induce drug resistance by selectively augmenting CBP/p300, H3K27 acetylation and BRD4 binding at genomic loci of a subset of growth factor and receptor (GF/R) genes. BRD4 occupation at these loci and drug resistant cell growth are vulnerable to both bromodomain and HDAC inhibitors. Little or none occupation of HDACs at the GF/R gene loci underscores the paradox that cells respond equivalently to the two classes of inhibitors with opposite modes of action. Targeting this unique epigenetic vulnerability offers a general solution to overcome PI3K/AKT inhibitor resistance in different cancers.

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A Combination of Epigenetic BET and CDK9 Inhibitors for Treatment of Human Melanoma

Project description:A Combination of Epigenetic BET and CDK9 Inhibitors for Treatment of Human Melanoma

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Analysis of differential miRNA expression in mineralising DPCs treated with pharmacological epigenetic inhibitors.

Project description:Analysis of differential miRNA expression in mineralising DPCs treated with pharmacological epigenetic inhibitors.

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Growth Inhibition and Induction of Innate Immune Signaling of Chondrosarcomas with Epigenetic Inhibitors

Project description:Growth Inhibition and Induction of Innate Immune Signaling of Chondrosarcomas with Epigenetic Inhibitors

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A Combination of Epigenetic BET and CDK9 Inhibitors for Treatment of Human Melanoma

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