Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of the combined effect of PDX1 and dominant-negative REST (DN-REST) on primary pancreatic exocrine cells

ABSTRACT: Gene expression of the combined effect of PDX1 and dominant-negative REST (DN-REST) on primary pancreatic exocrine cells

PROVIDER: PRJNA528080 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8753430.fastq.gz	Fastqsanger.gz
	SRR8753440.fastq.gz	Fastqsanger.gz
	SRR8753431.fastq.gz	Fastqsanger.gz
	SRR8753441.fastq.gz	Fastqsanger.gz
	SRR8753432.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Gene expression of the combined effect of PDX1 and dominant-negative REST (DN-REST) on primary pancreatic exocrine cells

Project description:Bulk MARS-seq analysis of gene expression in exocrine cells infected with Ad-PDX1, Ad-DN-REST or both. DN-REST activated endocrine genes, many of which exhibited a synergistic effect in coexpression with PDX1. PDX1 alone activated exocrine genes.

2020-03-25 | GSE128546 | GEO

PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance

Project description:Aberrant activation of embryonic signaling pathways is frequent in pancreatic ductal adenocarcinoma (PDA) making developmental regulators therapeutically attractive. Here, we demonstrate diverse functions for PDX1, a transcription factor indispensable for pancreas development, in the progression from normal exocrine cells to metastatic PDA. We identify a critical role for PDX1 in maintaining acinar cell identity, thus resisting the formation of PanIN-derived PDA. Upon neoplastic transformation, the role of PDX1 changes from tumor suppressive to oncogenic. Interestingly, subsets of malignant cells lose PDX1 expression while undergoing EMT and PDX1 loss is associated with poor outcome. This stage-specific functionality arises from profound shifts in PDX1 chromatin occupancy from acinar cells to PDA. In summary, we report distinct roles of PDX1 at different stages of PDA, suggesting that therapeutic approaches against this potential target need to account for its changing functions at different stages of carcinogenesis. These findings provide insight into the complexity of PDA pathogenesis and advocate a rigorous investigation of therapeutically tractable targets at distinct phases of PDA development and progression.

2017-11-20 | GSE90775 | GEO

PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance [RNA-seq]

2017-11-27 | GSE91052 | GEO

PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance [ChIP-seq batch3]

2017-11-27 | GSE91055 | GEO

PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance [ChIP-seq batch2]

2017-11-27 | GSE91054 | GEO

PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance [ChIP-seq batch1]

2017-11-27 | GSE91053 | GEO

Gene expression of Cell populations sorted from exocrine cells reprogrammed to beta-like cells

Project description:Bulk MARS-seq analysis of gene expression in reprogrammed exocrine cells exhibit many similarities to native beta cells. Reprogrammed cells are enriched for expression of genes that are direct targets of the transcriptional repressor REST.

2020-03-25 | GSE128545 | GEO

CFTR Represses a PDX1 Axis to Govern Pancreatic Ductal Cell Fate [scRNA-seq]

Project description:Inflammation, acinar cell destruction, and ductal cell hyperplasia drive pancreatic remodeling in newborns with cystic fibrosis (CF) lacking a functional CFTR channel. In neonatal CF ferrets, these changes are associated with a transient phase of glucose intolerance that involves islet destruction and subsequent regeneration near hyperplastic ducts. Little is known about the phenotypic changes in CF ductal epithelium and its potential impact on islet function. Using bulk RNA-seq, scRNA-seq, and ATAC-seq on CF ferret models, we demonstrate that ductal CFTR protein constrains PDX1 expression by maintaining PTEN and GSK3b activation. In the absence of CFTR protein, centroacinar cells (or terminal ductal cells) adopted a bi-potent progenitor-like state associated with enhanced WNT/b-Catenin, TGFb and AKT signaling. Notably, using in vitro and in vivo hypomorphic models of mutant CFTR expression, we show that the level of CFTR protein, not its channel function, regulates PDX1 expression. Thus, this study has discovered a cell-autonomous CFTR-dependent mechanism by which CFTR mutations that produced little to no protein could impact pancreatic exocrine/endocrine remodeling in people with CF.

2024-09-18 | GSE264022 | GEO

Identification of Sox9/Pdx1-coregulated Genes During Pancreas Organogenesis

Project description:Sox9/Pdx1 co-regulated target genes were identified by comparing gene expression in Sox9/Pdx1-double heterozygates versus Sox9- or Pdx1- heterozygates pancreata using microarray analysis.

2015-08-07 | GSE62023 | GEO

Transcription profiling of the islets from Pdx1+/- mice compared to islets isolated from Pdx1 +/+ littermates

Project description:The aim of this experiment was to use global gene expression profiling to identify genes that are differentially expressed in the islets from Pdx1+/- mice compared to islets isolated from Pdx1 +/+ littermates. The Pdx1 null mutation consists of a nuclear targeted _-galactosidase cassette fused in-frame with the N terminus of PDX-1.

2009-12-02 | E-MTAB-127 | 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