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H3K27ac ChIP upon NeuroD1 overexpression

ABSTRACT: H3K27ac ChIP upon NeuroD1 overexpression

PROVIDER: PRJNA714252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13959204.fastq.gz	Fastqsanger.gz
	SRR13959205.fastq.gz	Fastqsanger.gz
	SRR13959206.fastq.gz	Fastqsanger.gz
	SRR13959207.fastq.gz	Fastqsanger.gz
	SRR13959208.fastq.gz	Fastqsanger.gz

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H3K27ac ChIP upon NeuroD1 overexpression

Project description:Cell-fate specification relies on a close cooperation of distinct transcription factors and their crosstalk with the epigenetic landscape during embryonic development. NeuroD1 is known to be essential for eliciting neurogenesis and is able to reprogram other cell types into neurons. Despite progress, its global impact on the epigenome and cooperativity with other transcription factors during neurogenesis remains unknown. Here we show that despite NeuroD1 binding and a gain of active chromatin, only sites that show high local density of adjacent bHLH motifs, higher minor groove width and propeller twist as well as enrichment of another novel bHLH motif were able to get transcriptionally induced. Transcription factor activity analysis on the epigenome timecourse following NeuroD1 induction further identified this bHLH factor among top factors that gained activity during this process. Importantly, this bHLH factor was induced simultaneously to NeuroD1 as cells transit from an apical to a basal progenitor state during cortical development. Moreover, this bHLH factor interacts with NeuroD1 and co-occupies NeuroD1 target distinct genomic regions. We further show that the loss of this bHLH factor during cortical development severely impairs neurogenesis. Our study not only reveals the mechanistic basis underlying a productive transcriptional response of NeuroD1 during neurogenesis but also identified a novel bHLH transcription factor that partners with NeuroD1 and plays a critical role during cortical development.

2022-02-03 | GSE168853 | GEO

Distinct Function for ASCL1 and NEUROD1 in Pulmonary Neuroendocrine Tumors (ChIP-seq)

Project description:Small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC) are high-grade pulmonary neuroendocrine tumors. The neural basic helix-loop-helix (bHLH) transcription factors ASCL1 and NEUROD1 have been shown to play crucial roles in promoting the malignant behavior and survival of human SCLC cell lines. In this study, we find ASCL1 and NEUROD1 identify distinct neuroendocrine tumors, bind distinct genomic loci, and regulate mostly distinct genes. ASCL1 and NEUROD1 are often bound in super-enhancers that are associated with highly expressed genes in their respective SCLC cell lines suggesting different cell lineage of origin for these tumors. ASCL1 targets oncogenic genes such as MYCL1, RET, and NFIB, while NEUROD1 targets the oncogenic gene MYC. Although ASCL1 and NEUROD1 regulate different genes, many of these gene targets commonly contribute to neuroendocrine and cell migration function. ASCL1 in particular also regulates genes in the NOTCH pathway and genes important in cell-cycle dynamics. Finally, we demonstrate ASCL1 but not NEUROD1 is required for SCLC and LCNEC tumor formation in current in vivo genetic mouse models of pulmonary neuroendocrine tumors ChIP-seq analysis performed on three ASCL1high and two NEUROD1high human SCLC cell lines to identify ASCL1 and/or NEUROD1 binding sites in these two types of cells. Also, we performed ChIP-seq for Ascl1 binding sites in mouse neuroendocrine lung tumors obtained from Trp53;Rb1;Rbl2 triple knockout model mice treated with Adeno-CMVCRE intratracheally.

2016-07-21 | E-GEOD-69394 | biostudies-arrayexpress

ChIP-seq of NeuroD1 and H3K4me3 in SCLC cells

Project description:We hypothesized that functional polymorphisms in NEUROD1 target genes may also affect the clinical outcomes of patients with SCLC, as NEUROD1 plays a crucial role in SCLC carcinogenesis. To test this hypothesis, we performed ChIP-seq of NeuroD1 and H3K4me3 in SCLC cells. Then we evaluated the association between putative functional polymorphisms in NEUROD1 target genes and the chemotherapy response and survival outcomes of patients with SCLC.

2022-08-19 | GSE211475 | GEO

H3K27ac ChIP-seq analysis for zebrafish normal thymus and tumors driven by overexpression of human IRF4

Project description:H3K27ac ChIP-seq analysis was performed using zebrafish normal thymus and primary tumors to analyze potential regulatory elements activated by IRF4 overexpression.

2022-03-14 | GSE166644 | GEO

H3K27ac changes upon overexpression of the active NOTCH1 intracellular domain (N1ICD) in human adipose tissue endothelial cells.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes, and is involved in the development of a multitude of diseases. Here we investigate by ChIP-Seq the effects of overexpression of the active NOTCH1 intracellular domain (N1ICD) on H3K27ac in human adipose tissue endothelial cells.

2023-06-16 | GSE195537 | GEO

H3K4me3 and H3K27ac ChIp-seq

Project description:H3K4me3 and H3K27ac ChIp-seq

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BET Inhibitors Target the SCLC-N subtype of Small Cell Lung Cancer by Blocking NEUROD1 Transactivation

Project description:Small cell lung cancer can be divided into several molecular subtypes based on the expression of four master transcription factors (ASCL1, NEUROD1, POU2F3, and YAP1). These master factors have not been directly druggable, and we hypothesized that targeting their transcriptional coactivator(s) could provide an alternative approach. Here, we identify that BET bromodomain proteins physically interact with NEUROD1 and function as transcriptional coactivators. Using CRISPR knockout and ChIP-seq, we demonstrate that NEUROD1 plays a critical role in defining the landscapes of BET bromodomain proteins in the SCLC genome. Targeting BET bromodomain proteins by BET inhibitors leads to broad suppression of the NEUROD1-target genes, especially those associated with superenhancers, and reduces SCLC growth in vitro and in vivo. LSAMP, a membrane protein in the IgLON family, was identified as one of the NEUROD1-target genes mediating BET inhibitor sensitivity in SCLC. Altogether, our study reveals that targeting transcriptional coactivators could be a novel approach to blocking the master transcription factors in SCLC for therapeutic purposes. The goal of this experiment was to characterize the genome-wide binding profiles of BET proteins, RPII, and H3K27Ac upon NEUORD1 knockout in H446 cells.

2022-11-23 | GSE210113 | GEO

Genome-wide profiling of H3K27ac (ChIP-seq) in IMR90 cells

Project description:To determine the genome-wide pattern of H3K27ac in IMR90 (ATCC CCL-186) cells we performed ChIP-seq upon hormone treatment (1.5 h, 1 M dexamethasone).

2018-04-12 | E-MTAB-5355 | biostudies-arrayexpress

YRA1 overexpression microarray and ChIP-chip

Project description:YRA1 overexpression microarray and ChIP-chip

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H3K27ac ChIP-Seq in LOUCY

Project description:H3K27ac ChIP-Seq data of the T-ALL cell line LOUCY was obtained to find active regions in the genome and to correlate that with expression profiling of lncRNAs in the LOUCY cell line. ChIP-sequencing data was generated for H3K27ac in the T-ALL cell line LOUCY.

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