Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of GLIS3 and HNF1b target genes in kidney

ABSTRACT: Identification of GLIS3 and HNF1b target genes in kidney

PROVIDER: PRJNA1002246 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25520059.fastq.gz	Fastqsanger.gz
	SRR25520060.fastq.gz	Fastqsanger.gz
	SRR25520061.fastq.gz	Fastqsanger.gz
	SRR25520062.fastq.gz	Fastqsanger.gz
	SRR25520063.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

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

Regulation of GLIS3 in 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.

2024-12-18 | GSE240532 | GEO

Regulation of gene expression by GLIS3 during neonatal kidney development

2023-12-31 | GSE240071 | GEO

Human pluripotent stem cell-derived kidney organoids reveal tubular epithelial pathobiology of heterozygous HNF1B-associated dysplastic kidney malformations K

Project description:Hepatocyte nuclear factor 1B (HNF1B) encodes a transcription factor expressed in developing human kidney epithelia. Heterozygous HNF1B mutations are the commonest monogenic cause of dysplastic kidney malformations (DKMs). To understand their pathobiology, we generated heterozygous HNF1B mutant kidney organoids from CRISPR-Cas9 gene-edited human ESCs and iPSCs reprogrammed from a family with HNF1B-asscociated DKMs. Mutant organoids contained enlarged malformed tubules and displayed deregulated cell turnover. This submission contains kidney tissue samples.

2024-04-29 | E-MTAB-12822 | biostudies-arrayexpress

Human pluripotent stem cell-derived kidney organoids reveal tubular epithelial pathobiology of heterozygous HNF1B-associated dysplastic kidney malformations CL

2024-04-29 | E-MTAB-12824 | biostudies-arrayexpress

GLIS3

Project description:GLIS3

| PRJNA1002242 | ENA

Identification of Tfcp2l1 target genes in the mouse kidney

Project description:Identification of Tfcp2l1 target genes in the mouse kidney

| PRJNA347368 | ENA

Gene expression array between wild-type and mutant Hnf1b cells

Project description:The complete specrtum of genes that are subject to regulation by Hnf1b in mouse kidney cells is not known. We used microarray to determine genes that are significenlty deregulated in repsonse to altered HNF1b activity.

2015-08-17 | GSE72033 | GEO

Regulation of gene expression by GLIS3 during neonatal kidney development

Project description:Regulation of gene expression by GLIS3 during neonatal kidney development

| PRJNA1002245 | ENA

Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B

Project description:HNF1B (Hepatocyte Nuclear Factor 1-Beta) is a POU-homeobox transcription factor expressed in kidney and frequently mutated in patients suffering from Congenital Anomalies of the Kidney and the Urinary Tract (CAKUT). HNF1B is a bookmarking factor, able to bind mitotic chromatin and necessary for the post-mitotic reactivation of gene expression. In order to characterize the molecular functions of HNF1B as a bookmarking factor, we performed ChIPseq on asynchronous and mitotic renal cells. We developed a novel ChIP method with a non-aqueous crosslinking (NAQC) to circumvent the well-known artefactual effects of formaldehyde crosslinking of mitotic chromosomes. NAQC-ChIP allowed the retention of the mitotic signal that was lost with a regular ChIP. With this novel methodology, we show that the vast majority HNF1B binding sites detected in asynchronous cells are also bound in mitosis.

2024-12-01 | GSE269260 | 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