Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

ABSTRACT: Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

PROVIDER: PRJNA481781 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10901261.fastq.gz	Fastqsanger.gz
	SRR10901262.fastq.gz	Fastqsanger.gz
	SRR7537870.fastq.gz	Fastqsanger.gz
	SRR7537880.fastq.gz	Fastqsanger.gz
	SRR7537871.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

Project description:We have found that three specific combinations of two transcription factors, comprising Hnf4alpha plus Foxa1, Foxa2 or Foxa3, could convert mouse embryonic fibroblasts (MEFs) into cells that closely resemble hepatocytes in vitro, and DNA binding, N-terminal, and C-terminal domains (DBD, NTD, and CTD, respectively) of Foxa proteins are swappable in the direct reprogramming of the iHep cells. Then we used ChIP-seq to explore the targets of the domain swapped mutant forms of Foxa proteins during conversion event to iHep cells.

2020-08-06 | GSE117332 | GEO

Foxa and Hnf4alpha targets during conversion from mouse embryonic fibroblasts (MEFs) to hepatocyte-like (iHep) cells

Project description:We have found three specific combinations of two transcription factors, comprising Hnf4alpha plus Foxa1, Foxa2 or Foxa3, could convert mouse embryonic fibroblasts (MEFs) into cells that closely resemble hepatocytes in vitro. Then we used ChIP-seq to explore the targets of Foxa and Hnf4alpha during conversion event to iHep cells.

2020-08-06 | GSE90536 | GEO

Foxa and Hnf4alpha targets during conversion from mouse embryonic fibroblasts (MEFs) to hepatocyte-like (iHep) cells and hepatocytes (Hep).

2020-08-06 | GSE90538 | GEO

miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

2011-11-01 | GSE25139 | GEO

miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

Project description:We have analyzed miRNA expression profile in FO and MZ B cells to identified differentially expressed miRNAs between this two subsets that could be potencially involved in the regulation of terminal B cell differentiation Spleens from CD19-Creki/+Dicerfl/+ and CD19-Creki/+Dicerfl/fl mice were collected and after erythrocyte lysis, splenocytes were stained with anti-B220, anti-CD21 and anti-CD23 antibodies. B220+CD21brightCD23+ (MZ) and B220+CD21+CD23bright (FO) B cell populations were sorted and total RNA of purified populations was extracted with TRIzol. miRNA microarray hybridations were performed on Mouse miRNA Microarray platform (Agilent Technologies).

2011-11-01 | E-GEOD-25139 | biostudies-arrayexpress

Foxa-deficiency Restricts Hepatitis B Virus Biosynthesis Through Epigenic Silencing [NanoSting]

Project description:In the HBV transgenic mouse model of chronic infection, the forkhead box protein A/hepatocyte nuclear factor 3 (Foxa/HNF3) family of pioneer transcription factors are required to support postnatal viral demethylation and subsequent HBV transcription and replication. Liver-specific Foxa-deficient mice with hepatic expression of only Foxa3 do not support HBV replication but display biliary epithelial hyperplasia with bridging fibrosis. However, liver-specific Foxa-deficient mice with hepatic expression of only Foxa1 or Foxa2 also successfully restrict viral transcription and replication but display only minimal alterations in liver physiology. These observations suggest that the level of Foxa activity, rather than the combination of specific Foxa genes, is a key determinant of HBV biosynthesis. Together, these findings suggest that targeting Foxa activity could lead to HBV DNA methylation and transcriptional inactivation, resulting in the resolution of chronic HBV infections which are responsible for approximately one million deaths annually worldwide.

2024-07-16 | GSE263120 | GEO

Sequence logic at enhancers governs a dual mechanism of endodermal organ fate induction by FOXA pioneer factors

Project description:FOXA pioneer transcription factors (TFs) associate with primed enhancers in endodermal organ precursors. Using a human stem cell model of pancreas differentiation, we here discover that only a subset of pancreatic enhancers is FOXA-primed, whereas the majority is unprimed and engages FOXA upon lineage induction. Primed enhancers are enriched for signal-dependent TF motifs and harbor abundant and strong FOXA motifs. Unprimed enhancers harbor fewer, more degenerate FOXA motifs, and FOXA recruitment to unprimed but not primed enhancers requires pancreatic TFs. Strengthening FOXA motifs at an unprimed enhancer near NKX6.1 renders FOXA recruitment pancreatic TF-independent, induces priming, and broadens the NKX6.1 expression domain. We make analogous observations about FOXA binding during hepatic and lung development. Our findings suggest a dual role for FOXA in endodermal organ development: First, FOXA facilitate signal-dependent lineage initiation via enhancer priming, and second, FOXA enforce organ cell type-specific gene expression via indirect recruitment by lineage-specific TFs.

2021-10-18 | GSE148368 | GEO

Collapse of the hepatic gene regulatory network in the absence of FoxA factors

Project description:FoxA transcription factors are critical for liver development through their pioneering activity, which initiates a highly complex network thought to become resistant to the loss of any individual hepatic transcription factor via mutual redundancy. To investigate the dispensability of FoxA factors for this regulatory network, we ablated all FoxA genes in the adult liver. Remarkably, loss of FoxA caused a rapid and massive reduction in the expression of key liver genes back to the low levels of the fetal prehepatic endoderm stage, leading to necrosis and lethality within days. Mechanistically, we found FoxA proteins to be required for maintaining chromatin activity, nucleosome positioning and binding by other hepatic transcription factors. Thus, the hepatic gene regulatory network is dependent on the FoxA proteins throughout life.

2020-07-10 | GSE140423 | GEO

Foxa-deficiency Restricts Hepatitis B Virus Biosynthesis Through Epigenic Silencing [Bisulfite-Seq]

2024-07-16 | GSE263033 | GEO

FoxA-dependent demethylation of DNA initiates epigenetic memory of cellular identity

Project description:Tissue-specific DNA methylation patterns are created by transcription factors that recruit methylation and demethylation enzymes to cis-regulatory elements. To date, it is not known whether transcription factors are needed to continuously maintain methylation profiles in development and mature tissues or whether they only establish these marks during organ development. We queried the role of the pioneer factor FoxA in generating hypomethylated DNA at liver enhancers. We discovered a set of FoxA binding sites that undergo regional, FoxA-dependent demethylation during organ development. Conditional ablation of FoxA genes in the adult liver demonstrated that continued FoxA presence was not required to maintain the hypomethylated state, even when massive cell proliferation was induced. This study provides strong evidence for the stable, epigenetic nature of tissue-specific DNA methylation patterns directed by lineage-determining transcription factors during organ development.

2021-04-20 | GSE124384 | 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