Evidence map›Paper›PMID 39585161›Full record

ArticleEpigenomics

CXXC5 stabilizes DNA methylation patterns in mouse embryonic stem cells.

Seung-Gi Jin, Jennifer Johnson, Zhijun Huang, Wei Cui, Thomas Dunwell, Gerd P Pfeifer

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In one paragraph

Article in Epigenomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Seung-Gi JinDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Jennifer JohnsonDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Zhijun HuangDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Wei CuiDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Thomas DunwellGeneFirst, Abingdon Science Park, Oxfordshire, UK.
Gerd P PfeiferDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.ORCID 0000-0002-5080-9604

Funding

DNA hypermethylation in lung tumorsR01CA234595 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI PFEIFER, GERD P · 2019 to 2023
$2.4M
NCI NIH HHS R01 CA234595
6 · The paper itself

Abstract

aimsMammalian genomes encode 12 proteins that contain a CXXC zinc finger domain. Most members of this family are large multi-domain proteins that function in the control of DNA methylation and histone methylation patterns. CXXC5 is a smaller member of the family, along with its closest homologue CXXC4. These two proteins lack known catalytic domains. Here, we have characterized CXXC5 in mouse embryonic stem (ES) cells. MATERIALS &

methodsWe used gene knockouts, RNA sequencing, and DNA methylation analysis by whole-genome bisulfite sequencing. RESULTS &

conclusionsWe show that CXXC5 is a nuclear protein that interacts with 5-methylcytosine oxidases (TET proteins). Removal of CXXC5 from ES cells leads to very few changes in gene expression. CXXC5 extensively colocalizes with TET1 and TET2 at CpG islands. CXXC5 inactivation leads to a substantial reduction of DNA methylation levels that affects all genomic compartments including genic and intergenic regions and CpG island shores. We propose a model in which CXXC5 serves as an anchor for TET proteins at CpG islands. In the absence of CXXC5, the 5-methylcytosine oxidases become dislodged from CpG islands and are enabled to induce genome-scale DNA demethylation. Thus, CXXC5 serves as a stabilizer of DNA methylation patterns.

Indexed as

CpG IslandsDioxygenasesDNA-Binding ProteinsDNA MethylationMouse Embryonic Stem CellsAnimalsMiceProto-Oncogene ProteinsTranscription FactorsDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTET1 protein, mouseTet2 protein, mouseTranscription Factors5-methylcytosineCXXC4CXXC5DNA methylationTET1

Identifiers

PMID39585161
PMCPMC11622772

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.