Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at the single-cell level of Neurog3 derived tomato cells from Neurog3Cre and Neurog3Cre-FoxO1 f/f (NFKO) of the small intestine

ABSTRACT: Gene expression profile at the single-cell level of Neurog3 derived tomato cells from Neurog3Cre and Neurog3Cre-FoxO1 f/f (NFKO) of the small intestine

PROVIDER: PRJNA832977 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profile at the single-cell level of Neurog3 derived tomato cells from Neurog3Cre and Neurog3Cre-FoxO1 f/f (NFKO) of the small intestine

Project description:To discover cells with mixed enteroendocrine/Paneth/goblet features arising from Neurog3+ progenitors in WT and NFKO mice, we used single-cell RNA sequencing (scRNA-seq) to analyze the diversity of Neurog3 derived cells in the small intestine.

2022-11-06 | GSE201776 | GEO

Gene expression of Neurog3 derived small intestine cells from Neurog3Cre-FoxO1 f/f (NFKO) mice

Project description:To investigate the characteristics of CD24 subdivied Neurog3-derived (Tomato+) cells: CD24neg/Ngn3Tomato+, CD24+/Ngn3Tomato+ and NgnTomato3neg

2022-11-06 | GSE201832 | GEO

Gene expression of Neurog3 derived small intestine cells from Neurog3Cre-FoxO1 f/f (NFKO) mice

Project description:Gene expression of Neurog3 derived small intestine cells from Neurog3Cre-FoxO1 f/f (NFKO) mice

| PRJNA833144 | ENA

Neurog3 gene dosage effect on the differentiaiton of intestinal enteroendocrine progenitors

Project description:Analysis of FACS-sorted intestinal Neurog3+/+ and Neurog3+/- cells from Neurog3 fluorencent reporter mice carrying two-(+/+) or one- (+/-) Neurog3 alleles. In the intestine, Neurog3 is an enteroendocrine (EE) lineage determinating transcription factor that transiently expressed in early EEC progenitors. By comparison the molecular profiles of Neurog3+/+ and Neurog3+/- cells, we hypothesized that Neurog3 gene dosage regulates the allocation of EE progenitor fates towards EEC vs. goblet cells.

2020-08-13 | GSE149203 | GEO

Genome wide profiling of NEUROG3 occupancy in human pancreatic endocrine progenitors [CUT&RUN]

Project description:Despite this critical role in islet cell development, the precise function and downstream genetic programs regulated directedly by NEUROG3 remain elusive. We therefore mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (iPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets. To this aim, we generated a novel hiPSC line (NEUROG3-HA-P2A-Venus), where NEUROG3 is HA-tagged and fused to a self-cleaving fluorescent VENUS reporter. We used the CUT&RUN technique, an alternative method to CHIP-seq allowing transcription factor profiling from a low cell number, to map NEUROG3 occupancy and epigenetic marks in pancreatic endocrine progenitors (PEP) differentiated from this hiPSC line. To optimize the stringency and relevance of NEUROG3 binding sites, we focused our analysis on regions identified both with HA and NEUROG3 antibodies and integrated NEUROG3 occupancy data with chromatin status and gene expression in PEPs and their NEUROG3-dependence. Mapping of NEUROG3 genome occupancy in PEPs uncovers an unexpectedly broad, direct control of the endocrine gene regulatory network (GRN) and raises novel hypotheses on how this master regulator controls islet and beta cell differentiation.

2021-08-04 | GSE171963 | GEO

Genes differentially expressed between NEUROG3-Venus positive and negative hiPSC line differentiated to pancreatic endocrine progenitors [RNA-Seq]

2021-08-04 | GSE179261 | GEO

TDAG51 is a novel coactivator of FoxO1

Project description:Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important in innate immunity. Here, we show that T cell death-associated gene 51 (TDAG51/PHLDA1) is a novel coactivator of the transcription factor FoxO1, regulating inflammatory mediator production in the lipopolysaccharide (LPS)-induced inflammatory response. TDAG51 induction by LPS stimulation was mediated by the TLR2/4 signaling pathway in bone marrow-derived macrophages (BMMs). LPS-induced inflammatory mediator production was significantly decreased in TDAG51-deficient BMMs. In TDAG51-deficient mice, LPS- or pathogenic Escherichia coli infection-induced lethal shock was reduced by decreasing serum proinflammatory cytokine levels. The recruitment of 14-3-3 to FoxO1 was competitively inhibited by the TDAG51-FoxO1 interaction, leading to blockade of FoxO1 cytoplasmic translocation and thereby strengthening FoxO1 nuclear accumulation. TDAG51/FoxO1 double-deficient BMMs showed significantly reduced inflammatory mediator production compared with TDAG51- or FoxO1-deficient BMMs. TDAG51/FoxO1 double deficiency protected mice against LPS- or pathogenic E. coli infection-induced lethal shock by weakening the systemic inflammatory response. Thus, these results indicate that TDAG51 acts as a coactivator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response.

2023-06-24 | PXD039815 | Pride

Gene expression profile at single cell level of NKX6.1- and -NEUROG3 expressing cells and their progeny derived from human induced pluripotent stem cells

Project description:We examined by single cell RNA sequencing the heterogeneity and progeny of NKX6.1 and/or NEUROG3 expressing cells produced in vitro by the differentiation of hiPSC cells

2023-08-09 | GSE202092 | GEO

RNA-seq of Human Embryonic Stem Cell derived pancreas progenitor differentiation, Day 13 of wildtype, HES1-/-, NEUROG3-/- and HES1-/-NEUROG3-/- genotypes

Project description:To better understand the mechanism by which HES1 regulates pancreas development we took advantage of recent developments in directed differentiation of human embryonic stem cells (hESCs) to the pancreatic endocrine lineage via a series of progenitor stages (Figure 1 and (Rezania et al., 2014). Using the iCRISPR platform (González et al., 2014), we introduced indels in the HES1 and NEUROG3 genes, either singly or in combination in iCRISPR H1 cells. Using previously described gRNAs (Zhu et al., 2016) to target exon2 of the NEUROG3 gene and exon2 of the HES1 gene we detected by Sanger and RNA-sequencing a 2 bp insertion and a T insertion, respectively, resulting in premature STOP codons in two/multiple clonal cell lines carrying the introduced mutation and the loss of NEUROG3 by immunostaining We then subjected two or more clonal lines of H1-iCRISPR (wildtype), HES1−/−, NEUROG3−/− and HES1−/−NEUROG3−/− (abbreviated H1N3-dKO or H1−/−N3−/−) to differentiation to β-like cells using a modified version of the protocol from Rezania et al. (2014). Marker analysis showed that all cell lines maintained pluripotency (OCT4+) as hESC and were able to differentiate to FOXA2+ and SOX17+ co-positive definitive endoderm (DE, Day 3), PDX1+ cells at the posterior foregut stage (PF, Day 7), to bipotent progenitors marked by PDX1+ and NKX6-1+ at the Pancreatic Endoderm stage (PE, Day 10), and the Endocrine Precursor stage (EP, Day 13)

2020-09-30 | E-MTAB-7185 | biostudies-arrayexpress

Neurog3-independant role of Notch signaling in pancreas explants. Microarray of pancreata of Wildtype or Neurog3tTA/tTA (Neurog3-Null) background at E12.5, explanted for 3d + treatment 24h with DAPT/vehicle.

Project description:Since loss of Hes1 and Notch signalling drives progenitors to the endocrine lineage, we set up a pancreas explant system with crosses of heterozygous Neurog3tTA/+, a knock-in allele which makes the homozygote Neurog3tTA/tTA embryos deficient in Neurog3 (hereafter Neurog3-null). Hereby endocrine differentiation is impeded and we can study the Neurog3-independent role of Notch signalling by DAPT inhibition of γ-secretase. E12.5 wildtype and Neurog3-null pancreata were explanted on fibronectin, grown for 3 days, and then treated with vehicle control (0.1% DMSO) or DAPT for 24h. RNA was isolated and subjected to Agilent microarray analysis

2022-02-27 | E-MTAB-6898 | 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