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Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

ABSTRACT: Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

PROVIDER: PRJNA548964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9305140.fastq.gz	Fastqsanger.gz
	SRR9305139.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

2020-01-01 | GSE132784 | GEO

Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

Project description:Mutations in NIPBL are the major cause of Cornelia de Lange Syndrome (CdLS). NIPBL is the cohesin loading factor and has recently been associated with the BET (Bromodomains and Extra Terminal (ET) domain) proteins BRD2 and BRD4. Related to this, a CdLS-like phenotype has been described associated to BRD4 mutations. To understand the relationship between NIPBL and BET proteins, we have performed RNA-Seq expression analysis following depletion of the different proteins in mouse P19 teratocarcinoma cells. Results indicate that genes regulated by NIPBL largely overlap with those regulated by BRD4 but not with those regulated by BRD2.

2020-01-01 | GSE132785 | GEO

Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

Project description:Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

| PRJNA548966 | ENA

Calcium Signaling Prompts NIPBL Recruitment at Active Enhancers and Promoters via Distinct Mechanisms to Reconstruct Genome Compartmentalization

Project description:During developmental progression the genomes of immune cells undergo large-scale changes in chromatin folding. However, insights into the signals and epigenetics that induce alterations in nuclear architecture remain rudimentary. Here, we found that calcium influx rapidly recruited the cohesin-loading factor NIPBL to thousands of binding sites to dictate widespread changes in compartment segregation. The induction of NIPBL-binding was coordinate with increased P300, BRG1 and RNA Polymerase II co-occupancy, via different kinetics at active enhancers and promoters. Through acute degradation system, we found that enhancers, rather than promoters, are dependent on BAF complexes to induce NIPBL recruitment. Finally, we found that calcium signaling acts universally to orchestrate rapid redistribution of NIPBL in both primary innate and adaptive immune cells. Collectively, these data reveal how calcium signaling regulates NIPBL occupancy to orchestrate nuclear architecture.

2020-10-10 | GSE154051 | GEO

Decreasing Wapl dosage partially corrects transcriptome phenotypes in Nipbl-/+ embryonic mouse brain

Project description:Cohesin rings interact with DNA and modulate expression of thousands of genes. NIPBL loads cohesin onto chromosomes and WAPL takes it off. Heterozygous mutations in NIPBL lead to a developmental disorder called Cornelia de Lange syndrome. Nipbl heterozygous mice are a good model for this disease. Mutations in WAPL were not known to cause disease or gene expression changes in mammals. Here we show dysregulation of >1000 genes in Wapl-/+embryonic mouse brains. The patterns of dysregulation are highly similar in Wapl and Nipbl heterozygotes, suggesting that Wapl mutations may cause disease in humans. Since WAPL and NIPBL have opposite effects on cohesin’s association with DNA, we asked whether a heterozygous Wapl mutation could correct phenotypes seen in Nipbl heterozygous mice. In fact, both gene expression and embryonic growth are partially corrected. Our data are consistent with the view that cohesin dynamics play a key role in regulating gene expression.

2022-10-11 | GSE203014 | GEO

Peptide mapping of SRSF7_RRM isoforms in murine P19 cells

Project description:Here we mapped peptides of mouse SRSF7_RRM purified from P19 cells.

2020-05-27 | PXD016884 | Pride

Gastrulation-stage gene expression in Nipbl+/- mouse embryos foreshadows the development of syndromic birth defects

Project description:In animal models, Nipbl-deficiency phenocopies gene expression changes and birth defects seen in Cornelia de Lange Syndrome (CdLS), the most common cause of which is Nipbl-haploinsufficiency. Previous studies in Nipbl+/- mice identified aberrant gene expression and heart defects as early as cardiac crescent (CC) stage. Here, we performed single-cell RNA-sequencing on wildtype (WT) and Nipbl+/- mouse embryos at CC- and earlier (gastrulation) stages. Nipbl+/- embryos had fewer mesoderm cells than WT and altered proportions of mesodermal cell subpopulations. These findings were associated with an underexpression of genes implicated in driving specific mesodermal lineages. Nipbl+/- embryos also misexpressed developmentally-critical genes, including the transcription factor, Nanog, and genes governing left-right and anterior-posterior patterning. These events of cell misallocation and transcriptional dysregulation foreshadowed defects in tissue composition and patterning that arise later in Nipbl+/- mice, offering insights into early developmental contributions to birth defects in CdLS.

2023-05-07 | GSE151589 | GEO

Peptide mapping of SRSF7_RS-GFP isoforms in murine P19 cells

Project description:Here we mapped peptides of mouse SRSF7_RS-GFP purified from P19 cells.

2020-05-27 | PXD016871 | Pride

Gene expression changes in limb buds of Nipbl-haploinsufficient mice

Project description:Multiple genes are dysregulated in hindlimb buds of Nipbl-deficient embryos. In all, more than 1000 limb bud genes were found to be significantly altered in expression by microarray analysis of E10.5 mouse hindlimb buds. Small changes in expression (mostly decreases) were observed for genes involved in FGF, BMP, and SHH pathways, as well as numerous genes involved in the Wnt/planar cell polarity signaling pathway. Genes involved in the Mediator complex, Cohesin function, and Hox gene expression and functions were also dysregulated in Nipbl deficient limb buds. Microarray analysis using RNA extracted from E10.5 hindlimb limb buds harvested from stage-matched Nipbl+/- (n=12) and wildtype (n=12)

2014-08-30 | E-GEOD-60932 | biostudies-arrayexpress

Transcriptome analysis of mouse embryonic fibroblasts of NIPBL-haploinsufficient mice

Project description:Cohesinopathies are characterized by mutations in the cohesin complex. Mutations in NIPBL, a cohesin loader, result in Cornelia de Lange syndrome (CdLS). CdLS is a congenital genetic disorder distinguished by craniofacial dysmorphism, abnormal upper limb development, delayed growth, severe cognitive retardation, and multiple organ malformations.It has been suggested that CdLS is caused by defects in the cohesin network that alter gene expression and genome organization. However, the precise molecular etiology of CdLS is largely unclear. To gain insights, we sequenced mRNAs isolated from mouse embryonic fibroblasts of both WT and NIPBL-haploinsufficient mice and compared their transcriptomes.

2015-10-01 | GSE64706 | GEO

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