Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

17 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A toggle-switch between miR-142 and LIF-signaling creates heterogeneity among mouse ES cells.

ABSTRACT: Time course RNA-seq of mouse embryonic stem cells with different expression levels of miR-142 differentiated to endoderm

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Pierre Neveu

PROVIDER: E-MTAB-3234 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

A toggle-switch between miR-142 and LIF-signaling creates heterogeneity among mouse ES cells

Project description:miRNA sequencing in mouse embryonic stem cells according to miR-142 reporter activity

2015-12-31 | E-MTAB-2831 | biostudies-arrayexpress

A toggle-switch between miR-142 and LIF-signaling creates heterogeneity among mouse ES cells

Project description:RNA-seq of mouse embryonic stem cells sorted according to miR-142 activity levels

2015-12-31 | E-MTAB-2830 | biostudies-arrayexpress

Gene expression profiling using RNA and miRNA sequencing of mouse embryonic stem cells during fate acquisition

Project description:RNA-seq of mouse embryonic stem cells differentiated to the three germ layers and an epiblast stem cell-like state; RNA-seq of mouse tissues

2019-12-06 | E-MTAB-4904 | biostudies-arrayexpress

Characterization of the self-organization of primitive streak and neuroectoderm fates

Project description:Characterization of the signaling requirements to determine primitive streak and neuroectoderm fates in mouse embryonic stem cells.

2022-01-20 | E-MTAB-10242 | biostudies-arrayexpress

RNA-seq of wild-type mouse embryonic stem cells (mESC) during spontaneous differentiation

Project description:Transcriptomic analysis of mouse embryonic stem cells (mESC) maintained in the pluripotent state or allowed to differentiate for 3 or 7 days by leukaemia inhibitory factor (LIF) withdrawal.

2023-05-27 | E-MTAB-9261 | biostudies-arrayexpress

RNA-seq of wild-type, Gal-1 knockout, Gal-3 knockout and Gal-1/Gal-3 double knockout mouse embryonic stem cells (mESC) deprived of LIF for 7 days

Project description:Galectin-1 (Gal-1) and Galectin-3 (Gal-3) are conserved carbohydrate-binding proteins that also display RNA-binding activity. We generated mouse embryonic stem cells (mESC) constitutively depleted of Gal-1 and/or Gal-3 using CRISPR-Cas9, and assessed the transcriptomic effects of the individual or concomitant depletion of Gal-1 and Gal-3 in mESCs differentiated by deprivation of the leukaemia inhibitory factor (LIF) for 7 days. Wild-type cells were employed as control.

2023-05-27 | E-MTAB-9262 | biostudies-arrayexpress

Generation of organized anterior foregut epithelia from pluripotent stem cells using small molecules

Project description:Anterior foregut endoderm (AFE) gives rise to many tissue types of interest for therapeutic research including the esophagus, salivary glands, lung, thymus, parathyroid and thyroid. Despite its importance, only few reports describe the generation of AFE from pluripotent stem cells (PSCs) by directed differentiation. Here, we describe a novel protocol to derive a subdomain of AFE, identified by expression of Pax9, from PSCs using small molecules and chemically defined conditions. Generation of a reporter PSC line allows isolation and characterization of Pax9+ AFE cells. When transplanted in vivo, Pax9+ AFE can form several distinct types of complex anterior foregut epithelia including mucosal glands and stratified squamous epithelium. Finally, we show that the directed differentiation protocol can be used to generate AFE from DiGeorge Syndrome patient-specific human induced PSCs, thus creating a platform to produce anterior foregut derivatives for therapy and to enable the study of disorders of the AFE. Total RNA obtained from FACS purified from in vitro dervied mouse definitive endoderm, anterior foregut and ES cells. AFE cells were derived from a 129X1/SvJ background, DE cells from 129X1/SvJ x 129S1/SV-+p+Tyr- cKitlSl-J/+ (R1 ES cells) and non reporter ES cells from a 129P2/OlaHsd background.

2013-04-15 | E-GEOD-42139 | biostudies-arrayexpress

ChIP-seq of H3.3K4A/K36A mutant ESCs 2

Project description:Study to investigate the role of histone residues H3K4 and H3K36 for gene expression, histone localization and neuronal lineage specification by mutation of K4 and K36 in H3.3 to alanine. Histone variant H3.3 differs from the canonical H3.1/H3.2 by only 4 to 5 amino acids, which are necessary for nucleosome assembly independent of DNA replication, and is encoded by two gene copies. Complete loss of the two H3.3 genes (H3f3a and H3f3b) leads to embryonic lethality while single gene knockout yields viable mice. We used CRISPR-Cas9 to delete H3f3a and introduce homozygous point-mutations into H3f3b, thus ensuring that the entire pool of H3.3 protein carries the mutation of interest. We differentiated H3.3ctrl (H3f3a knock-out; H3f3b wild type), H3.3K4A mutant (H3f3a knock-out; H3f3b K4A) and H3.3K36A mutant (H3f3a knock-out; H3f3b K36A) ESCs into glutamatergic neurons. Genomic localization of H3.3 protein was determined by ChIP-Sequencing in ESCs (D0). Distribution patterns of RNA Polymerase II Phosphorylated on Serine 5 (RNA Pol II Ser5P), of histone modification H3K27me3 and chromatin remodeler components Brg1/Smarca4 (Swi/Snf) and Chd4 (NuRD) were measured by ChIP-Sequencing in ESCs (D0) to assess the impact of the H3.3K4A mutation on the epigenetic landscape. Distribution patterns of H3.3 were assessed by ChIP-Sequencing in HEK293T cells after depletion of Brg1/Smarca4 (Swi/Snf) and Chd4 (NuRD).

2020-01-28 | E-MTAB-8614 | biostudies-arrayexpress

ATAC-seq of ESC or in vitro differentiated endoderm cells after epigenetic editing and upon release of the trigger

Project description:Chromatin accessibility was assayed in ESC after epigenetic editing with dCas9::KRAB (or dCas9::GFP as a control) and subsequently in ESC and Endoderm differentiated cells upon release of the trigger. Samples were collected in two biological replicates after 7 days of DOX induction in ESC (epigenetic editing) and after 7 days of DOX washout (release of the trigger) in ESC and Endoderm cells.

2021-11-23 | E-MTAB-10523 | biostudies-arrayexpress

ChIP-seq of H3.3K4A/K36A mutant ESCs and neurons

Project description:Study to investigate the role of histone residues H3K4 and H3K36 for gene expression, histone localization and neuronal lineage specification by mutation of K4 and K36 in H3.3 to alanine. Histone variant H3.3 differs from the canonical H3.1/H3.2 by only 4 to 5 amino acids, which are necessary for nucleosome assembly independent of DNA replication, and is encoded by two gene copies. Complete loss of the two H3.3 genes (H3f3a and H3f3b) leads to embryonic lethality while single gene knockout yields viable mice. We used CRISPR-Cas9 to delete H3f3a and introduce homozygous point-mutations into H3f3b, thus ensuring that the entire pool of H3.3 protein carries the mutation of interest. We differentiated H3.3ctrl (H3f3a knock-out; H3f3b wild type), H3.3K4A mutant (H3f3a knock-out; H3f3b K4A) and H3.3K36A mutant (H3f3a knock-out; H3f3b K36A) ESCs into glutamatergic neurons. Genomic localization of H3.3 protein was determined by ChIP-Sequencing in ESCs (D0). Histone modifications patterns of H3K4me1, H3K4me3 and H3K27ac were measured by ChIP-Sequencing in ESCs (D0) to assess the impact of the H3.3K4A mutation on the epigenetic landscape. Levels of H3K36me3 were measured by ChIP-Sequencing in WT and H3.3K36A mutant ESCs (D0), NPCs (D8) and neurons (D12) to assess the impact of the H3.3K36A mutation on H3K36me3 levels in development.

2020-01-28 | E-MTAB-6822 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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