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ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

ABSTRACT: ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

PROVIDER: PRJNA1233327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32613147_1.fastq.gz	Fastqsanger.gz
	SRR32613147_2.fastq.gz	Fastqsanger.gz
	SRR32613148_1.fastq.gz	Fastqsanger.gz
	SRR32613148_2.fastq.gz	Fastqsanger.gz
	SRR32613149_1.fastq.gz	Fastqsanger.gz

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ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

Project description:Endocrine-disrupting chemicals (EDCs) can modulate estrogen receptor (ER) signaling by altering its transcriptional activity. To investigate these effects, we performed chromatin immunoprecipitation sequencing (ChIP-seq) on cells treated with 5α-Dihydrotestosterone (5α-DTT), Flutamide, Estradiol, and Bisphenol B. This dataset includes raw sequencing reads, processed peak files, and metadata, enabling the identification of ER binding sites influenced by each EDC. Gene ontology (GO) analysis of ChIP-enriched regions revealed that these compounds affect key pathways, including antibody-dependent cytotoxicity, BMP signaling in cardiac induction, and hepatocyte growth factor receptor signaling. This dataset provides insights into EDC-induced transcriptional regulation and contributes to the understanding of their role in endocrine disruption.

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Bisphenol A alternatives can effectively substitute for estradiol in promoting cell growth through estrogen receptor alpha in human breast cancer cells

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Expression Analysis of Bisphenol A (0.1 uM), 17beta-estradiol (0.1 uM), and GSK4716 (0.1 uM) Exposure in Embryonic Zebrafish

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Project description:Identification of Estrogen Receptor alpha (ERa) binding sites by ChIP-seq in MCF-7 breast cancer cells following an estrogen treatment. This study describes molecular effects of estradiol treatment and subsequent regulation by ER for a single gene/locus. A public ER chipseq (available in SRA as ERR011973), in addition to our own data, guided us to regulatory regions were ER was binding that were then analyzed in detail using "manual" ChIP. MCF-7 cells were treated for 1 h either 10 nm estradiol (E2) or vehicle (ethanol) and subjected to ChIP using antibodies against ERa or IgG.

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Project description:Investigation of whole genome expression pattern of 24 hours post fertilization Danio rerio embryos exposed to bisphenol A, 17Î²-estradiol, or 0.1% DMSO vehicle control This data represents 2 experiments using 2 separate microarrays. Microarray 1 [Low]: Embryos were exposed to 0.1 ÂµM BPA, 0.1 ÂµM E2, or control from 8 hpf to 24 hpf. Three biological replicates were collected for each treatment. 40 embryos were pooled to comprise a replicate. Microarray 2 [High]: Embryos were exposed to 80 ÂµM BPA, 15 ÂµM E2, or control from 8 hpf to 24 hpf. Two biological replicates were collected for each treatment. 40 embryos were pooled to comprise a replicate. These 2 microarray experiments are cross-comparable, as described in the associated publication.

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Expression data from MCF-7 cells stimulated by Estrogen or IGF-I

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