Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

ABSTRACT: De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

PROVIDER: PRJNA573110 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10156761_1.fastq.gz	Fastqsanger.gz
	SRR10156761_2.fastq.gz	Fastqsanger.gz
	SRR10156762_1.fastq.gz	Fastqsanger.gz
	SRR10156762_2.fastq.gz	Fastqsanger.gz
	SRR10156763_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

Project description:The aberrant gain of DNA methylation at CpG islands (CGIs) is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CGIs are targeted by de novo DNA methyltransferases (DNMTs) in a sequence-specific manner but this has not been tested. Using ectopically integrated CGIs, we find that aberrantly methylated CGIs are subject to low levels of de novo DNMT activity in colorectal cancer cells. By delineating DNMT targets, we find that instead de novo DNMT activity is targeted primarily to CGIs marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CGIs are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNMT activity at CGIs in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.

2020-11-24 | GSE137812 | GEO

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (H3K36me3 ChIP-Rx_seq)

2020-11-24 | GSE158404 | GEO

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

2020-11-24 | GSE158405 | GEO

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (H3K36me3 ChIP-Rx_seq)

Project description:De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (H3K36me3 ChIP-Rx_seq)

| PRJNA665179 | ENA

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island

Project description:De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island

| PRJNA665164 | ENA

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-24 | GSE158406 | GEO

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands.

Project description:The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.

| S-EPMC7846778 | biostudies-literature

De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

Project description:De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

| PRJNA665180 | ENA

H3K36me3 profiling in mTEClo

Project description:AIRE-sensitive genes are marked with low levels of H3K36me3 in mTEClo

2022-01-07 | GSE176371 | GEO

Targeted Profiling of Epitranscriptomic Reader, Writer and Eraser Proteins Regulated by H3K36me3

Project description:Trimethylation of lysine 36 on histone H3 (H3K36me3), an epigenetic mark associated with actively transcribed genes, plays an important role in multiple cellular processes, including transcription elongation, DNA methylation, DNA repair, and RNA m6A methylation, etc. Aberrant expression and mutations of the main methyltransferase for H3K36me3, i.e., SET domain-containing 2 (SETD2), were shown to be associated with various cancers. Here, we performed targeted profiling of 154 epitranscriptomic RWE proteins using a scheduled liquid chromatography-parallel-reaction monitoring (LC-PRM) method coupled with the use of stable isotope-labeled (SIL) peptides as internal standards to investigate how H3K36me3 modulates the chromatin occupancies of epitranscriptomic reader, writer, and eraser (RWE) proteins. Our results showed consistent changes in chromatin occupancies of RWE proteins upon losses of H3K36me3 and H4K16ac, and a role of H3K36me3 in recruiting METTL3 to chromatin upon DNA double strand break induction. In addition, protein-protein interaction network and Kaplan-Meier survival analyses revealed the importance of METTL14 and TRMT11 in kidney cancer. Taken together, our work revealed cross-talks between H3K36me3 and epitranscriptomic RWE proteins and uncovered potential roles of these RWE proteins in H3K36me3-mediated biological processes.

2023-05-25 | PXD041343 | Pride

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