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Single-Cell multi-omics reveals disrupted gene regulatory landscape and cell differentiation by Wilms tumor-associated ENL mutation in the developing kidney (snATAC-Seq)

ABSTRACT: Single-Cell multi-omics reveals disrupted gene regulatory landscape and cell differentiation by Wilms tumor-associated ENL mutation in the developing kidney (snATAC-Seq)

PROVIDER: PRJNA1020186 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26152456_1.fastq.gz	Fastqsanger.gz
	SRR26152456_2.fastq.gz	Fastqsanger.gz
	SRR26152457_1.fastq.gz	Fastqsanger.gz
	SRR26152457_2.fastq.gz	Fastqsanger.gz

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Single-Cell multi-omics reveals disrupted gene regulatory landscape and cell differentiation by Wilms tumor-associated ENL mutation in the developing kidney (snATAC-Seq)

Project description:ENL is an epigenetic acetylation reader and represents the most frequently mutated epigenetic regulator in Wilms tumor. In this study, we established an in vivo mouse model with the ENL hotspot mutation Enl-T1. We performed single-nuclei ATAC sequencing (snATAC-seq) analysis for the Enl-WT and T1 embryonic kidney to study the open chromatin dynamics and gene regulatory mechanism underlying the kidney developing defeat induced by the Enl mutation.

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Project description:ENL is an epigenetic acetylation reader and represents the most frequently mutated epigenetic regulator in Wilms tumor. In this study, we established an in vivo mouse model with the ENL hotspot mutation Enl-T1. Here we performed ChIP sequencing (ChIP-seq) analysis for human embryonuc kidney cell line HEK293 with ENL-WT or T1 to study the genomic binding site alterations induced by ENL mutation and whether those alterations can be rescued by treating the cells with the specific ENL inhibitor TDI-11055.

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