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High throughput screen identifies novel small molecules that derepress genes repressed by DNA methylation

ABSTRACT: High throughput screen identifies novel small molecules that derepress genes repressed by DNA methylation

PROVIDER: PRJNA417267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6260970.fastq.gz	Fastqsanger.gz
	SRR6260980.fastq.gz	Fastqsanger.gz
	SRR6260990.fastq.gz	Fastqsanger.gz
	SRR6260971.fastq.gz	Fastqsanger.gz
	SRR6260981.fastq.gz	Fastqsanger.gz

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High throughput screen identifies novel small molecules that derepress genes repressed by DNA methylation

Project description:Genes repressed by DNA methylation can be derepressed by various compounds targeting DNA methyltransferases, histone deacetylases, etc. Here, we report a high throughput screen against a 308,251-member chemical library aiming to identify novel small molecules that derepress an EGFP reporter gene silenced by DNA methylation. RNA-seq was used to measure mRNA abundance in control and compound-treated cells.

2018-03-12 | GSE106573 | GEO

High-throughput Oligopaint screen identifies druggable 3D genome regulators

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High-Throughput Screen Identifies Non-Inflammatory Small Molecule Inducers of Trained Immunity

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A genome-wide screen identifies silencers with distinct chromatin properties and mechanisms of repression [repressed STARR-seq]

Project description:A genome-wide screen identifies silencers with distinct chromatin properties and mechanisms of repression [repressed STARR-seq]

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High-throughput small molecule screen identifies inhibitors of aberrant chromatin accessibility

Project description:Mutations in chromatin modifying proteins are associated with a variety of cancers. These mutations may result in characteristic patterns of accessible chromatin indicative of altered nucleosome positioning and depletion at regulatory elements. We describe the adaptation of Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE), a chemical method to enrich for nucleosome-depleted genomic regions, as a high-throughput, automated assay. We applied this method in a screen of epigenetically targeted small molecules by evaluating regions of aberrant nucleosome depletion mediated by EWS-FLI1, the chimeric transcription factor critical for the bone and soft tissue tumor Ewing Sarcoma. We identified a novel compound, UNC0621, which exhibited a dose-dependent reduction in chromatin accessibility, decreased Ewing Sarcoma cell viability, and inhibited anchorage-independent growth. We demonstrate that chromatin accessibility can be exploited for drug discovery efforts offering the advantage that it does not depend on the a priori selection of a single molecular target. Identified compounds can then be used for biological target discovery and potential therapeutic validation. HT-FAIRE was performed on Human Umbilical Vein Endothelial Cells (HUVEC) in duplicate. No reference/control experiment is necessary.

2015-09-24 | E-GEOD-61735 | biostudies-arrayexpress

A High-Throughput Screen Identifies DYRK inhibitor ID-8 that Stimulates Human Kidney Tubular Proliferation

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An RNAi Screen of Chromatin Proteins Identifies Tip60-p400 as a Regulator of Embryonic Stem Cell Identity

Project description:This SuperSeries is composed of the following subset Series: GSE11240: An RNAi Screen of Chromatin Proteins Identifies Tip60-p400 as a Regulator of Embryonic Stem Cell Identity, Experiment A GSE11241: An RNAi Screen of Chromatin Proteins Identifies Tip60-p400 as a Regulator of Embryonic Stem Cell Identity, Experiment B Keywords: SuperSeries Refer to individual Series

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A High-Throughput Flow Cytometry Screen Identifies Molecules That Inhibit Hantavirus Cell Entry.

Project description:Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), which infects more than 200,000 people worldwide. Sin Nombre virus (SNV) and Andes virus (ANDV) cause the most severe form of HCPS, with case fatality ratios of 30%-40%. There are no specific therapies or vaccines for SNV. Using high-throughput flow cytometry, we screened the Prestwick Chemical Library for small-molecule inhibitors of the binding interaction between UV-inactivated and fluorescently labeled SNVR18 particles, and decay-accelerating factor (DAF) expressed on Tanoue B cells. Eight confirmed hit compounds from the primary screen were investigated further in secondary screens that included infection inhibition, cytotoxicity, and probe interference. Antimycin emerged as a bona fide hit compound that inhibited cellular infection of the major HCPS (SNV)- and HCPS (Hantaan)-causing viruses. Confirming our assay's ability to detect active compounds, orthogonal testing of the hit compound showed that antimycin binds directly to the virus particle and blocks recapitulation of physiologic integrin activation caused by SNV binding to the integrin PSI domain.

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A high-throughput small molecule screen identifies synergism between DNA methylation and Aurora kinase pathways for X-chromosome reactivation

Project description:X-chromosome inactivation is a mechanism of dosage compensation in which one of the two X chromosomes in female mammals is transcriptionally silenced. Once established, silencing of the inactive X (Xi) is robust and difficult to reverse pharmacologically. Yet, the Xi is a reservoir of >1000 functional genes that could be potentially tapped to treat X-linked disease. To identify compounds that could reactivate the Xi, here we screened ~367,000 small molecules in an automated high-content screen using an Xi-linked GFP reporter in mouse fibroblasts. Given the robust nature of silencing, we sensitized the screen by “priming” cells with the DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine (5azadC). Compounds that elicited GFP activity include VX680, MLN8237, and 5azadC,, which are known to target the Aurora kinase and DNA methylation pathways. We demonstrate that the combinations of VX680 and 5azadC, as well as MLN8237 and 5azadC, synergistically upregulated genes on the Xi. Thus, our work identifies a synergism between the DNA methylation and Aurora kinase pathways as being one of interest for possible pharmacological reactivation of the Xi.

2017-02-10 | GSE85103 | GEO

High-throughput Oligopaint screen identifies druggable 3D genome regulators

Project description:Although the molecular rules governing chromatin folding are being quickly elucidated, relatively few proteins regulating genome organization have been identified. To address this, we developed HiDRO (high-throughput labeling of DNA or RNA with optimized Oligopaint probes). Combined with automated image analysis, we used HiDRO to conduct a novel FISH-based screen of ~3,000 druggable genes that alter inter-TAD interactions. We isolated several enzymes that alter the integrity of architectural boundaries, including our top hit Glycogen synthase kinase alpha (GSK3A). We demonstrated using chemical and genetic inhibition that this ubiquitously expressed kinase enhances chromatin looping by regulating the chromatin binding of cohesin regulators. Finally, our data demonstrate that a GSK3A inhibitor can rescue both chromatin misfolding and gene misexpression at a sensitive locus after partial cohesin loss. These results illustrate a noncanonical role for GSK3A in cohesin regulation and highlight the broader utility of HiDRO-based screening to identify novel genome organizing factors.

2023-05-05 | GSE199607 | GEO

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