Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Gene expression and DNA methylation of lung tumors in Dnmt3a deficient vs. WT mice

PROVIDER: PRJNA147783 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR350282.fastq.gz	Fastqsanger.gz
	SRR350283.fastq.gz	Fastqsanger.gz
	SRR350284.fastq.gz	Fastqsanger.gz
	SRR350285.fastq.gz	Fastqsanger.gz
	SRR350286.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Gene expression and DNA methylation of lung tumors in Dnmt3a deficient vs. WT mice

Project description:This SuperSeries is composed of the following subset Series: GSE32415: Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT GSE32484: DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors Refer to individual Series

2011-10-25 | E-GEOD-32487 | biostudies-arrayexpress

Mus musculus

Project description:DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors

| PRJNA154447 | ENA

DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors

Project description:To examine whether Dnmt3a deficiency resulted in genomic methylation changes we performed an unbiased methylome analysis. Methylated DNA isolated from three Dnmt3a deficient and two WT tumors was immunoprecipitated and subjected to high throughput sequencing (MeDIP-Seq). We observed that genes that were less expressed in Dnmt3a deficient tumors tended to have lower methylation levels in gene bodies.

2011-10-26 | GSE32484 | GEO

DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors

2011-10-25 | E-GEOD-32484 | biostudies-arrayexpress

Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT

Project description:Transcriptional profiling of mouse lung tumors comparing Dnmt3a KO/K-ras G12D mutant with Dnmt3a WT/K-ras G12D mutant. The goal is to search for the difference of mRNA abundance between Dnmt3a KO and WT tumors. Two-condition experiment, KO vs. WT tissure. Biological replicates: 12.

2011-10-25 | E-GEOD-32415 | biostudies-arrayexpress

Dnmt3a protects active chromosome domains against cancer-associated hypomethylation

Project description:The results of the study uncover conserved features of cancer methylomes and provide a mechanistic explanation for the tumor-promoting effects of Dnmt3a mutations. Whole genome methylation analysis of Mus musculus. Five samples were analyzed, one control sample containing normal healthy lung tissue, two samples containing big (WTB) or small (WTS) Dnmt3a WT tumors, two samples containing big (KOB) or small (KOS) Dnmt3a knock-out tumors

2013-01-22 | E-GEOD-38651 | biostudies-arrayexpress

Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT

2011-10-26 | GSE32415 | GEO

Mus musculus

Project description:Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT

| PRJNA154519 | ENA

FAK is required for suppressing aberrant nuclear mechanotransduction and DNA methylation to prevent vascular injury

Project description:Mechanical forces generated through adhesive interaction of endothelial cells (EC) influence nuclear envelope and thereby gene transcription. Alteration in EC mechanical forces may trigger aberrant gene transcription leading to lethal vascular diseases including acute lung injury (ALI). The intrinsic pathways that instruct EC nuclear-mechanotransduction and thereby maintains vascular homeostasis remain elusive. We have identified focal adhesion kinase (FAK)-mediated mechanotransduction at the nuclear envelope in instructing transcription of EC-barrier protective genes. We show that loss of EC-FAK increases intracellular tension, which in turn activates nuclear envelop protein emerin, and DNA methyltransferase 3a (DNMT3a). Methylation of transcription factor KLF2 promoter by DNMT3a impaired KLF2 synthesis and transcription of the crucial barrier-maintaining gene, S1PR1. Restoring KLF2 or S1PR1 expression or impairing emerin or DNMT3a activity rescued vascular homeostasis in lungs with FAK-deficient or WT-damaged endothelium. Thus, FAK protects against tension-induced aberrant DNA methylation in EC and is a promising target to prevent ALI.

2022-07-11 | GSE207789 | GEO

KMT2C Loss Promotes Small Cell Lung Cancer Metastasis through DNMT3A-mediated Epigenetic Reprogramming

Project description:Small cell lung cancer (SCLC) is notorious for its early and frequent metastases, which contribute to it as a recalcitrant malignancy. To understand the molecular mechanisms underlying SCLC metastasis, we generated SCLC mouse models with orthotopically transplanted genome-edited lung organoids and performed multi-omics analyses. We found that loss of KMT2C, an H3K4 methyltransferase frequently mutated in extensive stage SCLC, promoted multiple-organ metastases in mice. Metastatic and KMT2C deficient SCLC displayed both histone and DNA hypomethylation. Mechanistically, KMT2C directly regulated the expression of DNMT3A, a de novo DNA methyltransferase, through histone methylation. Forced DNMT3A expression restrained metastasis of KMT2C deficient SCLC through repressing metastasis promoting MEIS/HOX genes. Further, S-(5’-Adenosyl)-L-methionine, the common cofactor of histone and DNA methyltransferases, inhibited SCLC metastasis. Thus, our study revealed a concerted epigenetic reprogramming of KMT2C and DNMT3A-mediated histone and DNA hypomethylation underlying SCLC metastasis, which suggested a new epigenetic therapeutic vulnerability.

2022-02-23 | GSE161570 | 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