Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells to Posterior Neural Progenitors

ABSTRACT: GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells to Posterior Neural Progenitors

PROVIDER: PRJNA431403 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6506800.fastq.gz	Fastqsanger.gz
	SRR6506810_1.fastq.gz	Fastqsanger.gz
	SRR6506810_2.fastq.gz	Fastqsanger.gz
	SRR6506820_1.fastq.gz	Fastqsanger.gz
	SRR6506820_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 52

Similar Datasets

GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells to Posterior Neural Progenitors

Project description:Anterior-posterior (A-P) specification of the neural tube involves initial acquisition of anterior fate followed by the induction of posterior characteristics in the primitive anterior neuroectoderm. Several morphogens have been implicated in the regulation of A-P neural patterning; however, our understanding of factors regulating these morphogens remains incomplete. Here we show that the Krüppel-like zinc finger transcription factor GLI-Similar 3 (GLIS3) directs differentiation of human embryonic stem cells into posterior neural progenitor cells in lieu of the default anterior pathway. Transcriptomic analyses reveal that this switch in cell fate is due to rapid activation of an autocrine WNT signaling pathway. Mechanistically, through genome-wide RNA-Seq, ChIP-Seq and functional analyses, we show that GLIS3 binds to and directly regulates the transcription of several WNT genes, including the strong posteriorizing factor WNT3A. Inhibition of WNT signaling is sufficient to abrogate GLIS3-induced posterior specification. Altogether, our findings suggest a critical role for GLIS3 in A-P specification through the direct transcriptional activation of WNT genes.

2018-11-21 | GSE109562 | GEO

GLIS3 Transcriptionally Activates WNT Genes to Promote Differentiation of Human Embryonic Stem Cells into Posterior Neural Progenitors.

Project description:Anterior-posterior (A-P) specification of the neural tube involves initial acquisition of anterior fate followed by the induction of posterior characteristics in the primitive anterior neuroectoderm. Several morphogens have been implicated in the regulation of A-P neural patterning; however, our understanding of the upstream regulators of these morphogens remains incomplete. Here, we show that the Krüppel-like zinc finger transcription factor GLI-Similar 3 (GLIS3) can direct differentiation of human embryonic stem cells (hESCs) into posterior neural progenitor cells in lieu of the default anterior pathway. Transcriptomic analyses reveal that this switch in cell fate is due to rapid activation of Wingless/Integrated (WNT) signaling pathway. Mechanistically, through genome-wide RNA-Seq, ChIP-Seq, and functional analyses, we show that GLIS3 binds to and directly regulates the transcription of several WNT genes, including the strong posteriorizing factor WNT3A, and that inhibition of WNT signaling is sufficient to abrogate GLIS3-induced posterior specification. Our findings suggest a potential role for GLIS3 in the regulation of A-P specification through direct transcriptional activation of WNT genes. Stem Cells 2018 Stem Cells 2019;37:202-215.

| S-EPMC6368876 | biostudies-literature

GLIS3

Project description:GLIS3

| PRJNA1002242 | ENA

A Glis3-CD133-Wnt signaling axis regulating the self-renewal of adult murine pancreatic progenitor-like cells in colonies/organoids

Project description:Adult pancreatic progenitor cells are a potential source of renewable insulin producing cells that can be used in regenerative medicine and cell replacement therapy for type-1 diabetes. We sought to understand the mechanisms by which adult pancreatic progenitor cells undergo self-renewal. The effects of knockdown of Glis3, CD133 (Prominin-1) and beta-catenin were investigated and we found that Glis3 and CD133 are capable of regulating self-renewal through Wnt gene expression.

2019-06-30 | GSE124944 | GEO

Regulation of gene expression by GLIS3 during neonatal kidney development

Project description:Loss of transcription factor GLIS3 function in humans and mice leads to the development of neonatal polycystic kidney disease (PKD). To investigate how loss of GLIS3 function in kidney affects postnatal kidney development and PKD, we analyzed the gene expression profiles of kidneys from WT and Glis3-null mice at P7, P14, and P28 by RNA-Seq analysis using Glis3 global KO model Glis3-mCherry and kidney specific knockout model Glis3-PAX8Cre.

2023-12-31 | GSE240071 | GEO

Glis3: The role in osteoblast differentiation and adipocyte differentiation

Project description:The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Keywords: Glis3, osteoblast differentiation, adipocyte differentiation, FGF18, BMP2

2007-05-22 | GSE5379 | GEO

Glis3 plays a crucial role in thyroid hormone production

Project description:The serum hormone levels including T3 and T4 were dramatically decreased in Glis3-null mice due to reduced production of thyroid hormones in thyroid. Gene expression profile and EdU incorporation analysis between WT and Glis3-null mice showed that the cell proliferation was greatly reduced in Glis3-null thyroid. Goitergenic diet (low iodine diet; LID) dramatically enhanced serum TSH levels in both WT and Glis3-null mice, however thyroid goiter was observed in WT mice but not in Glis3-null mice. A subset of genes associated with thyroid hormone production including Pendrin (Slc26a4), Nis (Na+/I– symporter, Slc5a5), Duoxa2 (dualoxidase A2), Tpo (thyroperoxidase), and Dio1 (Deiodinase1) was significantly induced in WT but not in Glis3-null mice by LID feeding.

2017-11-06 | GSE86841 | GEO

Examination of Glis3 binding and affects on gene expression in mouse pancreas

Project description:RNA sequencing of mouse islets from mice containing a pancreas-specific deletion of Glis3, and control littermates. Also, ChIP-seq analysis of Glis3 binding using a Glis3-eGFP mouse (endogenous Glis3 fused to enhanced GFP) and GFP antibody.

2020-12-01 | GSE122120 | GEO

Identification of GLIS3 and HNF1b target genes in kidney

Project description:Comparison of cistromes from GLIS3 and HNF1b ChIP-Seq analysis using mouse kidney was performed to examine whether there was a significant overlap in target genes between GLIS3 and HNF1b.

2023-12-31 | GSE240072 | GEO

Discovery of a Drug Candidate for GLIS3-Associated Diabetes

Project description:Through development and use of a minimal component protocol for derivation of late stage pancreatic progenitors and beta-like cells, we compared WT and GLIS3-/- pancreatic cells at different stages and discovered that GLIS3-/- cells show an ectopic activation of TGF-beta signaling.

2018-05-05 | GSE114051 | GEO

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