Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of Arid3a in proliferation and differentiation of intestinal epithelial cells [RNA-seq]

ABSTRACT: Role of Arid3a in proliferation and differentiation of intestinal epithelial cells [RNA-seq]

PROVIDER: PRJNA1015667 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26044700.fastq.gz	Fastqsanger.gz
	SRR26044701.fastq.gz	Fastqsanger.gz
	SRR26044702.fastq.gz	Fastqsanger.gz
	SRR26044663.fastq.gz	Fastqsanger.gz
	SRR26044664.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Role of Arid3a in proliferation and differentiation of intestinal epithelial cells

Project description:Role of Arid3a in proliferation and differentiation of intestinal epithelial cells

| PRJNA875951 | ENA

Role of Arid3a in proliferation and differentiation of intestinal epithelial cells

Project description:To investigate the role of Arid3a in the intestinal epithelium, we generated an inducible conditional knockout model (VillinCreERT2;Arid3afl/fl -Arid3a cKO) and we compared the gene expression analysis to WT animals (ViliinCreERT2). Animals were injected intraperitoneally with tamoxifen to induce gene deletion.

2024-07-31 | GSE212560 | GEO

Role of Arid3a in proliferation and differentiation of intestinal epithelial cells [RNA-seq]

2024-07-31 | GSE242983 | GEO

ARID3A coordinates the proliferation-differentiation switch of transit-amplifying cells in the intestine

Project description:Intestinal stem cells (ISCs) at the crypt base divide and give rise to progenitor cells that have the capacity to proliferate and differentiate into various mature epithelial cell types in the transit-amplifying (TA) zone. Here, we identified the transcription factor ARID3A as a novel regulator of intestinal epithelial cell proliferation and differentiation at the TA compartment. We show that ARID3A forms an expression gradient from villus tip to the early progenitors at the crypts mediated by TGF-β and WNT signalling. Intestinal epithelial-specific deletion of Arid3a reduces proliferation of TA cells. Bulk and single cell transcriptomic analysis shows increased enterocyte differentiation and reduced secretory cells in the Arid3a cKO intestine. Interestingly, upper-villus gene signatures of both enterocytes and secretory cells are enriched in the mutant intestine. We find that the enhanced enterocyte differentiation in the Arid3a cKO intestine is caused by increased binding of HNF1 and HNF4. Finally, we show that loss of Arid3a impairs irradiation-induced regenerative process by altering the dynamics of proliferation and apoptosis. Our findings imply that ARID3A may play a gatekeeping role in the TA compartment to maintain the “just-right” proliferation-to-differentiation ratio for tissue homeostasis and plasticity

2024-07-31 | GSE243155 | GEO

Arid3a is required for mammalian placenta development

Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina

2016-07-01 | E-GEOD-79638 | biostudies-arrayexpress

CMK LC-MS/MS after CoIP of ARID3A

Project description:In order to determine proteins interacting with ARID3A in the ML-DS cell line CMK, we performed CoIP of endogenous ARID3A followed by LC-MS/MS

2023-03-11 | PXD025027 | Pride

ARID3A coordinates the proliferation-differentiation switch of transit-amplifying cells in the intestine

Project description:ARID3A coordinates the proliferation-differentiation switch of transit-amplifying cells in the intestine

| PRJNA1016446 | ENA

Arid3a is required for mammalian placenta development

2016-07-01 | GSE79638 | GEO

Role of mitochondria in intestinal epithelial cells

Project description:Role of mitochondria in intestinal epithelial cells

| PRJNA857089 | ENA

Role of lysophosphatidic acid in proliferation and differentiation of intestinal epithelial cells.

Project description:Intestinal epithelial cells (IECs) are regenerated continuously from intestinal stem cells (ISCs) near the base of intestinal crypts in order to maintain homeostasis and structural integrity of intestinal epithelium. Epidermal growth factor (EGF) is thought to be important to drive the proliferation and differentiation of IECs from ISCs, it remains unknown whether other growth factors or lipid mediators are also important for such regulation, however. Here we show that lysophosphatidic acid (LPA), instead of EGF, robustly promoted the development of intestinal organoids prepared from the mouse small intestine. Indeed, LPA exhibited the proliferative activity of IECs as well as induction of differentiation of IECs into goblet cells, Paneth cells, and enteroendocrine cells in intestinal organoids. Inhibitors for LPA receptor 1 markedly suppressed the LPA-promoted development of intestinal organoids. LPA also promoted the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 in intestinal organoids, whereas inhibition of mitogen-activated protein kinase/ERK kinase (MEK) 1/2 significantly suppressed the development of, as well as the proliferative activity and differentiation of, intestinal organoids in response to LPA. Our results thus suggest that LPA is a key factor that drives the proliferation and differentiation of IECs.

| S-EPMC6481811 | biostudies-literature

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