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Bioorthogonal Chemical Epigenetic Modifiers Enable Dose-dependent CRISPR Targeted Gene Activation

ABSTRACT: Bioorthogonal Chemical Epigenetic Modifiers Enable Dose-dependent CRISPR Targeted Gene Activation

PROVIDER: PRJNA771351 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16340000.fastq.gz	Fastqsanger.gz
	SRR16340001.fastq.gz	Fastqsanger.gz
	SRR16340002.fastq.gz	Fastqsanger.gz
	SRR16339987.fastq.gz	Fastqsanger.gz
	SRR16339988.fastq.gz	Fastqsanger.gz

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Bioorthogonal Chemical Epigenetic Modifiers Enable Dose-dependent CRISPR Targeted Gene Activation

Project description:CRISPR-Cas9 systems have been developed to regulate gene expression by using either fusions to epigenetic regulators or, more recently, through the use of chemically mediated strategies. These approaches have armed researchers with new tools to examine the function of proteins by intricately controlling expression levels of specific genes. Here, we present a CRISPR based chemical approach that uses a new Chemical Epigenetic Modifier (CEM) to hone to a gene targeted with a catalytically inactive Cas9 (dCas9) bridged to an FK506-binding protein (FKBP). One arm of the bifunctional CEM recruits BRD4 to the target site and the other arm is composed of a bumped ligand that binds to a mutant FKBP with a compensatory hole at F36V. This bump-and-hole strategy allows for activation of target genes in a dose dependent and reversible fashion with increased specificity and high efficacy.

2022-08-22 | GSE185912 | GEO

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Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells [ATAC-seq]

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miR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

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2019-12-31 | GSE118121 | GEO

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Project description:Measuring dose-dependent effects of drugs on post-translational modifications on a proteome-wide scale reveals how these drugs work in cells. Here, we present a quantitative chemical proteomic approach termed decryptM, able to assess target and pathway engagement as well as the mode of action (MoA) of diverse cancer drugs in cells by measuring their dose- (and time-) resolved modulation of PTMs on a proteomic scale. Data collected for 31 drugs, representing six drug classes in 13 human cell lines, demonstrate that the approach is widely applicable. The body of data represents ~1.8 million quantitative cellular drug assays (dose-response curves) including 47502 regulated p-peptides (of 124660 detected on 11982 proteins), 7316 Ubi-peptides (of 9173 detected on 3006 proteins), and 546 Ac-peptides (of 2478 detected on 1377 proteins). Most PTMs were not regulated by most drugs, which is highly valuable information for understanding which pathways are addressed (or not) by each drug in cells. The decryptM data have been incorporated into ProteomicsDB and can be explored interactively. The raw files, searches, curves files, and result PDFs can be downloaded here. For details, have a look at the Experiment_summary.xlsx.Paper: doi/10.1126/science.ade3925

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Genetic Modifiers of Huntington's Disease

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Targeted randomization dose optimization trials enable fractional dosing of scarce drugs.

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