Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling in adult onset ADPKD mouse model based on Pkd2 inactivation

ABSTRACT: Transcriptional profiling in adult onset ADPKD mouse model based on Pkd2 inactivation

PROVIDER: PRJNA629819 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11680775.fastq.gz	Fastqsanger.gz
	SRR11680776.fastq.gz	Fastqsanger.gz
	SRR11680777.fastq.gz	Fastqsanger.gz
	SRR11680778.fastq.gz	Fastqsanger.gz
	SRR11680779.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Transcriptional profiling in adult onset ADPKD mouse model based on Pkd2 inactivation

Project description:We performed unbiased transcriptional profiling in an adult-onset Pkd2 mouse model at an early stage before cysts formed using as controls wild type and PC2+cilia double knockout mice which are protected from ADPKD. By a tripartite comparison, we identified differetially expressed genes which have significant different expression in Pkd2-only knockout with same direction of change from both wild type and Pkd2+Cilia double knockout.

2020-12-31 | GSE149739 | GEO

Genotyping of PKD2 Arg803* in Taiwan ADPKD Cohort

Project description:PKD2 Arg803* is the most common mutation in Taiwan ADPKD Cohort. Genotyping of 96 PKD2 Arg803* individuals was performed in Axiom Genome-Wide TWB 2.0 Array Plate to study the existence of founder mutation in Taiwan

2022-06-07 | E-MTAB-11846 | biostudies-arrayexpress

Identification of ADPKD-related Genes and Pathways in the Cells Overexpressing PKD2

Project description:Based on the dosage effect hypothesis, renal cysts could arise in transgenic murine models overexpressing either PKD1 or PKD2, which are causal genes responsible for autosomal dominant polycystic kidney disease (ADPKD). To prove whether PKD genes overexpression is a universal mechanism driving cystogenesis or is merely restricted to rodents, other animal models are required. Previously, we failed to observe any renal cysts in a PKD2 overexpression transgenic pig model partially due to epigenetic silencing of transgene. Thus, to explore the feasibility of pig models and identification potential affected genes/pathways related to ADPKD, LLC-PK1 cells with high PKD2 expression were generated. RNA-seq was performed and MYC, IER3, ADM were found to be commonly upregulated genes in different PKD2 overexpression cell models. MYC is a well-characterized factor contributing to cystogenesis, and ADM is a biomarker for chronic kidney disease. Thus, theses genes might be indicators of disease progression. Additionally, some ADPKD associated pathways, e.g., MAPK, were also enriched in the cells. Besides, GO analysis demonstrated proliferation, apoptosis, cell cycle regulation, which are hall marks of ADPKD were disturbed. Therefore, our experiment not only identified some biomarkers or indictors regarding ADPKD, but also demonstrated high PKD2 expression would like to drive cystogenesis in future porcine models.

2019-12-04 | GSE141355 | GEO

Next Generation Sequencing of PKD2 mutant mice

Project description:Purpose: Determine the differential gene expression pattern between wildtype, Pkd2-KO and Pkd2-miR-214 KO mice Methods: kidney mRNA profiles of Pkd2-KO and Pkd2-mir-214-KO mice was sequenced with N of 3 in each group Results: 972 differentially expressed transcripts were identified between Pkd2-KO kidneys and Pkd2-miR-214-KO kidneys Conclusion: Deletion of miR-214 promotes interstitial inflammation in mouse models of ADPKD

2019-09-25 | GSE137945 | GEO

Gene expression profiling in human ADPKD cell lines

Project description:Changes in gene expression levels were identified by microarray. Samples were human kidney epithelial cell lines derived from patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) and unaffected controls. Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most common inherited kidney disease, is due to mutations in PKD1 (85%) or PKD2 (15%) but has a highly variable phenotypic disease expression. We conducted parallel microarray profiling in normal and diseased human PKD1 cystic kidney cells to identify altered signatures of microRNA and mRNA target genes potentially implicated in disease expression.

2017-07-05 | E-MTAB-4188 | biostudies-arrayexpress

Identification of ADPKD-related Genes and Pathways in the Cells Overexpressing PKD2

Project description:Identification of ADPKD-related Genes and Pathways in the Cells Overexpressing PKD2

| PRJNA593205 | ENA

MicroRNA expression profiling in human ADPKD cell lines

Project description:Changes in microRNA expression levels were identified by microarray. Samples were human kidney epithelial cell lines derived from patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) and unaffected controls. Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most common inherited kidney disease, is due to mutations in PKD1 (85%) or PKD2 (15%) but has a highly variable phenotypic disease expression. We conducted parallel microarray profiling in normal and diseased human PKD1 cystic kidney cells to identify altered signatures of microRNA and mRNA target genes potentially implicated in disease expression. This dataset contains the results of the microRNA analysis.

2017-07-05 | E-MTAB-4189 | biostudies-arrayexpress

GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

Project description:We report a profile of 35 genes that are differentially expressed in Pkd2- tubuloids compared to controls.

2020-06-08 | GSE151950 | GEO

GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

Project description:GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

| PRJNA637874 | ENA

Pkd2-dependent transcriptome profile in a newly estabilshed mouse Pkd2 knockout cell line

Project description:Purpose: The goal of this study is to explore early changes of gene expression in the new mouse kidney Pkd2 knockout cell model. To identify compreshensive expressional changes of genes by Pkd2 knockout, transcriptomic changes by Pkd2 knockout induced by doxycycline treatment for 6 days at two different passages were profiled and analyzed. Methods: Total RNAs were isolated from cells treated with or without doxycycline for 6 days. Four replicates of each group were generated. cDNA libraries were prepared and sequenced on Illumina HiSeq4000 platform and then sequence reads were qualified and quantified. Differential expression analysis were performed using edgeR. Results: mRNA profiles of the new mouse kidney Pkd2 knockout cell model treated with doxycycline for 6 days were generated using an optimized RNA-Seq workflow. Transcript level quantification using the STAR quant mode was performed to calculate transcript abundance in each sample. Then differential expression analysis identified the differentially expressed genes at different passages of cell culture. Conclusions: This study revealed early transcriptomic changes dependent on Pkd2 in a new in vitro Pkd2 knockout cell model of the mouse kidney.

2023-09-13 | GSE171574 | 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