Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq data from ES and differentiated cells in Chd8 WT vs Chd8 KD and Chd8 KO cells

ABSTRACT: RNAseq data from ES and differentiated cells in Chd8 WT vs Chd8 KD and Chd8 KO cells

PROVIDER: PRJNA702132 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13723000_1.fastq.gz	Fastqsanger.gz
	SRR13723000_2.fastq.gz	Fastqsanger.gz
	SRR13723001_1.fastq.gz	Fastqsanger.gz
	SRR13723001_2.fastq.gz	Fastqsanger.gz
	SRR13723002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 78

Similar Datasets

RNAseq data from ES and differentiated cells in Chd8 WT vs Chd8 KD and Chd8 KO cells

Project description:In this study, we compare the transcriptomic difference between WT and Chd8 depleted ES aand differentiating ES cells. We report significant differences between Chd8 WT and KD/KO cell lines.

2021-04-27 | GSE166858 | GEO

Role of Chd8 in Xist regulation

Project description:In this project, we have studied the role of Chd8 in Xist regulation and XCI initiation by means of Chd8 Knock-Downs (KD) and Knock-Out (KO).

2021-09-10 | PXD024155 | Pride

Gene expression profile in Yaf2 KD and/or RYBP KO ES cells.

Project description:Gene expression change by Yaf2 KD in wild type or RYBP KO ES cells.

2012-04-04 | GSE32288 | GEO

Gene expression profile in Yaf2 KD and/or RYBP KO ES cells.

Project description:Gene expression change by Yaf2 KD in wild type or RYBP KO ES cells. Total RNAs were extracted from the respective ES cells, and were subjected to microarray analysis using Affymetrix GeneChip Mouse Genome 430A 2.0 arrays

2012-04-03 | E-GEOD-32288 | biostudies-arrayexpress

Bulk RNA-seq of cerebral organoids investigating the role of CHD8 in cortical development

Project description:We used cerebral organoids generated from wildtype and CHD8 +/- human ES cells to study the effects of CHD8, one of the top ASD risk genes, on early cortical development. CHD8 +/- hESC were generated using the CRISPR/Cas9 system to create a deletion within the helicase domain. Cerebral organoids were generated according to the protocol from Lancaster et al 2013 with minor modifications.

2022-02-01 | E-MTAB-9933 | biostudies-arrayexpress

shRNAi profiling of huuman CHD8 depleted cells

Project description:CHD8 is a putative chromatin remodeling ATPase of the SNF2 family. We found that depletion of CHD8 impairs cell proliferation. In order to identify CHD8 target genes, we performed a transcriptomic analysis of CHD8-depleted cells. CHD8 was knockdown by doxycyclin-dependent expression of a shRNA that target the CHD8 mRNA. Experiment Overall Design: C33KD2 is a stable cell line where expression of a shRNA, that targets the CHD8 mRNA, is dependent on doxycycline. Addition of doxyclycin provokes a significant reduction in the level of CHD8 protein. Total RNA samples coming from C33KD2 cells cultured for 48 hours either with or without 2 µg/ml doxycycline were used to generate complementary RNA labelled with Cy5 with the Agilent Low RNA Input Fluorescent Linear Amplification Kit (Agilent Technologies). The reference sample was Stratagene human universal reference and was amplified at the same time as the sample RNA using the same method. Reference samples were labeled using Cy3.

2009-05-14 | E-GEOD-11422 | biostudies-arrayexpress

CHD8 and ELK1 cooperativity regulate cellular sensitivity to MAPK/ERK pathway

Project description:The chromodomain helicase DNA binding protein CHD8 is among the most frequently found de-novo mutations in autism. Unlike other autism-risk genes, CHD8 mutations appear to be fully penetrant. Despite this prominent disease involvement, relatively little is known about its molecular function. Based on sequence homology, CHD8 is believed to be a chromatin regulator but mechanisms for its genomic targeting and its function on chromatin are unclear. Here, we developed a human cell model carrying conditional CHD8 loss-of-function alleles. Remarkably, while undifferentiated human embryonic stem (ES) cells required CHD8 for survival, postmitotic neurons survived following CHD8 depletion. Chromatin accessibility revealed that CHD8 is a highly potent and general chromatin activator, enhancing transcription of its direct target genes. We also found that CHD8 genomic binding in human neurons was significantly enriched at ELK1 DNA binding motifs as previously found in other cell types. Given its prominent role as effector molecule of the MAPK/ERK pathway, we decided to further explore its relationship with CHD8. ELK1 motif-containing CHD8 binding sites showed a higher degree of chromatin opening function of CHD8 than other CHD8 binding sites. Moreover, ELK1 was required for CHD8 binding to Elk1-containing sites, but not other sites. Finally, the anti-apoptotic function of CHD8 in human ES cells could be rescued by depletion of ELK1 and the enhancement of neurogenesis by ELK1 was dependent on presence of CHD8. In summary, our results establish a clear role of CHD8 for chromatin opening and transcriptional activation and a molecular and functional interdependence of CHD8 and ELK1. These data imply the involvement of the MAPK/ERK pathway effector ELK1 in the pathogenesis of autism caused by CHD8 mutations.

2019-11-27 | GSE141085 | GEO

Expression data from undifferentiated and differentiated mouse female ES cells PGK12.1

2013-02-15 | GSE44251 | GEO

Expression data from undifferentiated and differentiated human ES cells

Project description:GCNF controls the level of Oct4 expression during ES cell differentiation and early mouse embryonic development. GCNF was overexpressed in H9 human ES cells using Tet-On Inducible system. mRNA microarray analysis demonstrated that overexpression of GCNF globally regulates gene expression in undifferentiated and differentiated hES cells. Within altered genes, GCNF down-regulated 36% of the genes, and up-regulated 64% of the genes in undifferentiated hES cells. In addition, GCNF also showed a regulatory gene pattern that is different from RA treatment during hES cell differentiation.

2016-12-23 | GSE76282 | GEO

Expression data from undifferentiated and differentiated mouse female ES cells PGK12.1

Project description:Affymetrix 430 2.0 mouse arrays were used for expression analyses in undifferentiated and differentiated PGK12.1 ES cells. We found that the X:autosome expression ratios calculated from the mean expression values of X-linked and autosomal genes from microarrays was ~1.4 in undifferentiated female ES cells and then decreased to 1.2 in PGK12.1 cells after 15-day embryoid body differentiation. Thus, a substantial level of X upregulation is already evident in these ES cells prior to differentiation. Our findings based on Affymetrix expression arrays are consistent with microarray analysis from other labs and our RNA-seq analysis of mouse female PGK12.1 ES cells. Mouse female ES cells PGK12.1 were differentiated by the EB (embryoid body) differentiation protocol. The presence of two active X chromosomes in undifferentiated female ES cells and one active X in 15-day differentiated cells was verified by Xist RNA FISH. Total RNA was prepared from undifferentiated and 15-day differentiated PGK12.1 and was used for expression array analyses to examine exprssion of the X chromosome during differentiation.

2013-02-15 | E-GEOD-44251 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data