Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

ABSTRACT: RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

PROVIDER: PRJNA714239 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13959113.fastq.gz	Fastqsanger.gz
	SRR13959114.fastq.gz	Fastqsanger.gz
	SRR13959115.fastq.gz	Fastqsanger.gz
	SRR13959116.fastq.gz	Fastqsanger.gz
	SRR13959117.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 19

Similar Datasets

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in VHL deficient mice.

Project description:RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in VHL deficient mice.

| PRJNA883184 | ENA

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in VHL deficient mice.

Project description:To explore the possible role of SETD2 in renal fibrosis formation, we generated VHL-KO and VHL-KO; SETD2-KO mice with a transgenic Ksp1.3/Cre mouse line. To get an insight into the mechanism of how SETD2 deletion promotes renal fibrogenesis in the absence of VHL, we performed RNA-seq using the renal tubules isolated from VHL-KO and VHL -KO; SETD2-KO mice

2022-10-19 | GSE213922 | GEO

RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

Project description:To explore a possible role of SETD2 in kidney development and tumorigenesis in vivo, we generated Setd2-floxed mice and deleted the Setd2 gene in tubular epithelial cells using a transgenic Ksp1.3/Cre mouse line. Then, we established our own c-MYC-transgene mouse line by overexpressing the human c-MYC under the control of the Ksp promoter to generate kidney disease mouse model. To get an insight into the mechanism of how SETD2 ablation promotes ccRCC formation in a c-MYC-generated PKD model, we performed RNA-seq using the renal tubules isolated from Wild Type, Setd2-KO, MYC-OE and MYC-OE; Setd2-KO mice.

2021-03-14 | GSE168849 | GEO

Proteomics analysis on SETD2 loss induced ccRCC formation

Project description:Patients with polycystic kidney disease (PKD) encounter a high risk of clear cell renal cell carcinoma (ccRCC), a malignant tumor with dysregulated lipid metabolism. SET domain–containing 2 (SETD2) has been identified as an important tumor suppressor gene in ccRCC. However, the role of SETD2 in tumorigenesis during the transition from PKD to ccRCC remains largely unexplored. Herein, we performed metabolomics, lipidomics, transcriptomics and proteomics with SETD2 loss induced PKD-ccRCC transition mouse model. To characterize biological responses triggered by SETD2 deletion during PKD-ccRCC transition at the protein level, we conducted global proteomics studies.

2023-10-31 | PXD038966 | Pride

Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]

Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.

2014-10-14 | E-GEOD-54932 | biostudies-arrayexpress

Transcriptomes of H1650 cells with and without SETD2 depletion

Project description:RNA sequencing of H1650 cells with and without SETD2 depletion to identify SETD2-regulated genes

2020-05-19 | GSE150809 | GEO

Transcriptomes of H1650 cells with and without SETD2 depletion

Project description:Transcriptomes of H1650 cells with and without SETD2 depletion

| PRJNA633667 | ENA

RNA-sequencing of renal cells from Setd2-wildtype PKD and Setd2-knlckout ccRCC mice.

Project description:To explore potential role of SETD2 in PKD-ccRCC transition in vivo, we generated a PKD mouse model by overexpressing oncogene c-MYC under the control of the Ksp promoter (KM mice), and knockout Setd2 gene using the same Ksp promoter in this PKD mice (KMs mice) to establish a ccRCC mouse model. To further characterize biological responses trigered by SETD2 deletion during PKD-ccRCC transition at the mRNA level, we next conducted global transcriptomics studies.

2022-12-26 | GSE221136 | GEO

Setd2 knockdown.

Project description:Setd2 knockdown leads to subtle but significant changes in gene expression and alternative splicing.

2020-06-18 | GSE147077 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

Project description:H3K36me3 catalyzed by histone methyltransferase SETD2 is one of the most conserved epigenetic marks from yeast to mammals. SETD2 is frequently mutated in multiple cancers and acts as a tumor suppressor. Here, utilizing a liver-specific deletion of Setd2 mice model, we found that Setd2 depletion is sufficient to trigger hepatocarcinoma (HCC) spontaneously. Meanwhile, in a DEN-induced HCC model, Setd2 depletion significantly promoted tumor number and size. The mechanistic study showed that Setd2 suppresses HCC not only through modulating DNA damage response, but also regulating lipid metabolism in liver. Setd2 deficiency down-regulated the expression of cholesterol efflux genes and caused lipid accumulation. ChIP-Seq analysis further revealed that Setd2 deletion induced AP-1 activation in liver, which was probably trigged by accumulated cholesterol. AP-1 is a well-known oncogene in HCC and inhibits p53 in Setd2-deficient cells. Taken together, we found the role of an important epigenetic gene in regulating cholesterol homeostasis and HCC, and revealed the underlying mechanisms.

2021-09-01 | GSE136743 | 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