Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression differences between wild-type and Vhl mutant mice in kidney stones process

ABSTRACT: Gene expression differences between wild-type and Vhl mutant mice in kidney stones process

PROVIDER: PRJNA863292 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20697546_1.fastq.gz	Fastqsanger.gz
	SRR20697546_2.fastq.gz	Fastqsanger.gz
	SRR20697547_1.fastq.gz	Fastqsanger.gz
	SRR20697547_2.fastq.gz	Fastqsanger.gz
	SRR20697548_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Gene expression differences between wild-type and Vhl mutant mice in kidney stones process

Project description:To investigate the transcriptome differences between wild-type and Vhl mutant mice in kidney stones process, we established CaOx-induced nephrolithiasis mouse model and performed RNA-sequencing.

2023-10-31 | GSE209996 | GEO

Human Matrix Kidney Stones Proteome

Project description:Protein composition of human kidney matrix stones by nano-LC-MS/MS.

2023-10-24 | PXD033298 | Pride

Gene expression differences in mouse kidneys after CaOx-induced nephrolithiasis

Project description:To investigate the transcriptome differences in kidney stones process, we established CaOx-induced nephrolithiasis mouse model and performed RNA-sequencing.

2023-10-31 | GSE208528 | GEO

Urinary Microbiome From Patients With Kidney Stones

Project description:Urinary Microbiome From Patients With Kidney Stones Raw Sequence Reads

| PRJNA516685 | ENA

Microarray characterization of Vhl; Vhl, Hif1a; Vhl, Hif2a and Vhl, Hif1a, Hif2a deficient primary kidney cells

2016-01-08 | GSE75745 | GEO

RNAseq transcriptome analysis of THP-1 macrophages activated by VHL-deficient kidney tubule cells

Project description:Clear-cell renal cell carcinoma (ccRCC) is the most prevalent subtype of renal cell carcinoma (up-to 70% of all RCC types). There is a very close causal correlation between ccRCC and inactivation of the tumor suppressor gene von Hippel-Lindau (VHL) located on chromosome 3p25‐26. Up to 80% of sporadic ccRCC carry genomic mutations or epigenetic inactivation of VHL and nearly 100% familial ccRCC (in VHL disease) contain VHL deficiency. Accumulating evidence has indicated that ccRCC arises at the site of chronic inflammation and this solid tumor contains a substantial number of infiltrated immune cells. This indicates that ccRCC may be induced by the interaction between kidney tubule cells carrying inactivated VHL gene and the inflammatory microenvironment. In this study we characterized the interaction between VHL-deficient kidney tubule cells and macrophages with relevance to ccRCC formation, and found that human macrophages induced by VHL-deficient kidney tubule cells exhibit distinct gene expression program containing the signatures of tumor-associated macrophages that can promote ccRCC progression.

2022-03-12 | GSE183976 | GEO

Vhl and Pbrm1 double deletion effect on kidney

Project description:Vhl and Pbrm1 double deletion effect on kidney

| PRJNA326726 | ENA

Microarray characterization of Vhl; Vhl, Hif1a; Vhl, Hif2a and Vhl, Hif1a, Hif2a deficient primary kidney cells

Project description:To unravel the potential cooperative roles of oxygen-regulated signaling pathways; von Hippel-Lindau (VHL) tumor suppressor protein and hypoxia-inducible factor (HIF) transcription factors, we have generated mutant mice with; Vhlh, Vhlh/Hif1Î±, Vhlh/Hif2Î± and Vhlh/Hif1Î±/Hif2Î± gene alleles floxed. Subsequently primary kidney cells were isolated, cultured and infected with Adenoviruses bearing either Cre/GFP or GFP expression only. Agilent cDNA microarrays were utilized to compare the gene expression profiles of the kidney epithelial cells from aforementioned cell cultures to gain insight about the molecules and signaling pathways that drive aberrant cellular proliferation in clear cell renal cell carcinoma (ccRCC). 24 independent biological samples from 4 genetic experimental conditions were hybridized in two- color format on 13 Mouse GE 4x44K v2 Microarray Kit (Design ID 026655) arrays. Eventual dye specific hybridization effects were controlled with dye swap on biological replicates. For an each experimental condition 3 arrays were use, except of one where 4 arrays were used (one sample combination in repetition with a dye swap). For the final analysis the gene expression levels were dye effect corrected and values for biological replicates were averaged to obtain a matrix with gene expression levels for 4 independent biological (1. Vhlh-/-, 2. Vhlh-/-/Hif1Î±-/-, 3. Vhlh-/-/Hif2Î±-/- and 4. Vhlh-/-/Hif1Î±-/-/Hif2Î±-/-) conditions.

2016-01-08 | E-GEOD-75745 | biostudies-arrayexpress

2-hydroxyglutarate drives whole-genome hypermethylation in kidney cancer cells with inactivated VHL

Project description:Hypermethylation of tumor suppressors and other aberrations of DNA methylation in tumors play a significant role in cancer progression. DNA methylation can be affected by various environmental conditions including hypoxia. The response to hypoxia is mainly achieved through activation of the transcription program associated with HIF1a transcription factor. VHL inactivation by genetic or epigenetic events, which also induces aberrant activation of HIF1a, is the most common driver event for renal cancer. With whole-genome bisulfite sequencing and LC-MS, we demonstrated that VHL inactivation induced global genome hypermethylation in human kidney cancer cells under normoxic conditions. This effect was reverted by exogenous expression of wild-type VHL. We show that global genome hypermethylation in VHL mutants can be explained by the accumulation of 2-hydroxyglutarate -- a metabolite that inhibits DNA demethylation by Tet enzymes.

2021-06-01 | GSE151787 | GEO

Transcriptome changes of whole kidney from conditional Vhl gene knockout in sub-populations of mouse kidney tubule cells

Project description:We are studying a tumor suppressor gene, von Hippel-Lindau (VHL). In humans, VHL mutations cause renal cell carcinoma of the clear cell type (ccRCC). We have generated a knockout mouse strain in which mouse Vhl is conditionally deleted in the kidney epithelium (that is, a subset of tubules including collecting ducts and ascending loop of Henle). Instead of ccRCC, these mice developed severe inflammation and fibrosis, accompanied by hyperplasia and the appearance of transformed clear cells. These phenotypes therefore support the notion that inflammation is the tissue precondition of cancer. Our hypothesis is that VHL loss-of-function-induced inflammation contribute to the initiation of carcinogenesis, through a mechanism that we want to determine. The aim of the microarray is to identify genes involved in the overgrowth of the epithelium, as well as in inflammation and fibrosis that may be important for ccRCC initiation.

2018-06-28 | GSE116326 | 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