Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer

ABSTRACT: 5-hydroxymethylcytosine (5-mC) and gene expression profiling of T84 cell differentiation; 5-hmC profiling of colon cancer colonocyte fractions T84 cell differentiation was monitored as cells formed confluent monolayers in tissue culture

ORGANISM(S): Homo sapiens

SUBMITTER: Christopher Mariani

PROVIDER: E-GEOD-69333 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer.

Chapman Christopher G CG Mariani Christopher J CJ Wu Feng F Meckel Katherine K Butun Fatma F Chuang Alice A Madzo Jozef J Bissonnette Marc B MB Kwon John H JH Godley Lucy A LA

Scientific reports 20151203

The formation of differentiated cell types from pluripotent progenitors involves epigenetic regulation of gene expression. DNA hydroxymethylation results from the enzymatic oxidation of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) by the ten-eleven translocation (TET) 5-mC dioxygenase enzymes. Previous work has mapped changes in 5-mC during differentiation of intestinal stem cells. However, whether or not 5-hmC regulates colonocyte differentiation is unknown. Here we show that 5-hm ...[more]

PMID: 26631571

Similar Datasets

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer

Project description:5-hydroxymethylcytosine (5-mC) and gene expression profiling of T84 cell differentiation; 5-hmC profiling of colon cancer colonocyte fractions

2015-12-09 | GSE69333 | GEO

TET-catalyzed 5-hydroxymethylcytosine regulates gene expression in differentiating colonocytes and colon cancer.

Project description: Not available

| S-EPMC4668370 | biostudies-literature

Binding proteins of Hydroxymethylcytosine-modified CpG dyads from mouse brain tissue

Project description:Cytosine (C) modifications within CpG dyads are central regulatory elements of mammalian genomes. In addition to 5-methylcytosine (mC), genomes can also contain high levels of 5-hydroxymethylcytosine (hmC) that is read differently by nuclear proteins than mC. However, hmC can co-exist with C and mC in different combinations in the two strands of CpG dyads, such as hmC/C, hmC/mC, or hmC/hmC, and it is poorly understood, how these combinatorial marks differ in their protein interactomes and regulatory functions. To systematically identify nuclear proteins that bind to distinct hmC-containing CpG dyads, we conducted DNA pulldown experiments using promoter probes harboring defined dyad modifications. In this study, we used nuclear extracts from mouse brain tissue and a DNA probe based on part of the Sp1 promoter sequence. For each dyad configuration, C/C, mC/mC, hmC/mC, hmC/C, and hmC/hmC, five technical replicates were performed.

2025-07-30 | MSV000098682 | MassIVE

Binding proteins of Hydroxymethylcytosine-modified CpG dyads

Project description:Cytosine (C) modifications within CpG dyads are central regulatory elements of mammalian genomes. In addition to 5-methylcytosine (mC), genomes can also contain high levels of 5-hydroxymethylcytosine (hmC) that is read differently by nuclear proteins than mC. However, hmC can co-exist with C and mC in different combinations in the two strands of CpG dyads, and it is poorly understood, how these combinatorial marks differ in their protein interactomes and regulatory functions. To identify nuclear binding proteins, we employed DNA promoter probes with differentially modified CpG dyads in pulldown experiments. The datasets comprise three biological replicates of HEK293T nuclear proteins binding to a VEGFA promoter sequence with differentially modified CpG dyads. Each biological replicate contains five technical replicates per modified CpG dyad, resulting in a total of 15 replicates for C/C, mC/mC and hmC/mC, and 10 replicates for hmC/C and hmC/hmC.

2024-08-15 | MSV000095609 | MassIVE

Tet-assisted bisulfite sequencing of 5-hydroxymethylcytosine.

Project description: Not available

| S-EPMC3641661 | biostudies-literature

Tet-mediated formation of 5-hydroxymethylcytosine in RNA.

Project description: Not available

| S-EPMC4140497 | biostudies-literature

Whole-genome analysis of 5-hydroxymethylcytosine and 5-methylcytosine at base resolution in the human brain

Project description:5-Hydroxymethylcytosine (hmC) is particularly abundant in mammalian brains with yetto be revealed functions. Here, we present genome-wide and single-base-resolutionmaps of hmC and mC in the human brain. We demonstrated that hmCs increasemarkedly from the fetal to the adult stage, and in the adult brain, 13.4% of all CpGs arehighly hydroxymethylated with strong enrichment at genic regions and distal regulatoryelements. Notably, hmC peaks were identified at the 5' splicing sites at the exon-intronboundary, suggesting a mechanistic link between hmC and splicing. We also report asurprising transcription-correlated hmC bias toward the sense strand and an mC biastoward the antisense strand of gene bodies. Furthermore, hmC is negatively correlatedwith H3K27me3-marked repressive genomic regions, and is more enriched in poisedenhancers than active enhancers. Our results provide insights into understanding themultiple potential functions of hmC in the human brain. A cell type specific hydroxymethylome sample of NeuN+ neurons in frontal lobe from the same adult individual, whose TAB-Seq data was deposited in GSE46710

2014-02-22 | E-GEOD-55249 | biostudies-arrayexpress

Epigenetic optical mapping of 5-hydroxymethylcytosine in nanochannel arrays

Project description:We present a long-read, single-molecule mapping technology that generates hybrid genetic/epigenetic profiles of native chromosomal DNA. The genome-wide distribution of 5-hmC in human peripheral blood cells correlates well with 5-hmC DNA immunoprecipitation (hMeDIP) sequencing. However, the long single-molecule read-length of 100 kbp-1 Mbp produces 5-hmC profiles across variable genomic regions that failed to show up in the sequencing data. In addition, optical 5-hmC mapping shows a strong correlation between the 5-hmC density in gene bodies and the corresponding level of gene expression.

2018-06-08 | GSE115454 | GEO

Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [colonocytes]

Project description:Chronic inflammation is epidemiologically linked to the pathogenesis of gastrointestinal diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). However, our understanding of the molecular mechanisms controlling gut inflammation remains insufficient, hindering the development of targeted therapies for IBD and CRC. In this study, we uncovered C15ORF48/miR-147 as a novel negative regulator of gut inflammation, operating through the modulation of epithelial cell metabolism. C15ORF48/miR-147 encodes two molecular products, C15ORF48 protein and miR-147-3p microRNA, which are predominantly expressed in intestinal epithelium. C15ORF48/miR-147 ablation leads to gut dysbiosis and exacerbates chemically-induced colitis in mice. C15ORF48 and miR-147-3p work together to suppress colonocyte metabolism and inflammatory responses, and thus bridging mitochondrial metabolism and inflammation.

2024-07-17 | GSE246492 | GEO

Loss of 5-hydroxymethylcytosine is an epigenetic hallmark of melanoma

Project description:DNA methylation at the 5-position of cytosine (5-mC) is a key epigenetic mark critical for varius biological and pathological processes. 5-mC can be converted to 5-hydroxymethylcytosine (5-hmC) by the Ten-Eleven Translocation (TET) family of DNA hydroxylases. Here we report that "loss of 5-hmC" is an epigenetic hallmark of melanoma with diagonostic and prognostic implications. Genome-wide mapping of 5-hmC in nevi and melanomas for the first time revealed loss of 5-hmC landscape in the melanoma epigenome. Downregulation of Isocitrate Dehydrogenase 2 (IDH2) and TET family enzymes proved to be one of the mechanisms underlying the loss of 5-hmC during melanoma development, and rebuilding the 5-hmC landscape in the melanoma epigenome by reintroducing active TET2 or IDH2 suppressed melanoma growth and increased tumor-free survival. Thus, our study establishes that "loss of 5-hmC" is a new epigenetic hallmark of melanoma and links IDH and TET family enzymes-mediated 5-hmC putative tumor suppressor pathway to the suppression of melanoma progression.

2012-09-18 | GSE38231 | 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