Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sox-Oct motifs contribute to maintenance of the unmethylated H19 ICR in YAC transgenic mice.

Human molecular genetics - 15 Nov 2013

Sakaguchi Ryuuta, Okamura Eiichi, Matsuzaki Hitomi, Fukamizu Akiyoshi, Tanimoto Keiji

Abstract excerpt

Abnormal methylation at the maternally inherited H19 imprinted control region (H19 ICR) is one of the causative alterations leading to pathogenesis of Beckwith-Wiedemann syndrome (BWS). Recently, it was shown in human BWS patients, as well as mouse cell culture experiments, that Sox-Oct motifs (SOM) in the H19 ICR might play a role in protecting the maternal ICR from de novo DNA methylation. By grafting a mouse...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Beckwith-Wiedemann Syndrome
Share to beta-Globins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to CCCTC-Binding Factor

Share to Chromosomes, Artificial, Yeast

Share to Genomic Imprinting

Share to Insulin-Like Growth Factor II

Share to Locus Control Region

Share to Mice, Inbred ICR

Source

Identifiers

PMID: 23821645
DOI: 10.1093/hmg/ddt311

Genes

CTCF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sox-Oct motifs contribute to maintenance of the unmethylated H19 ICR in YAC transgenic mice.PMID 23821645Read ↗

Oct4/Sox2 binding sites contribute to maintaining hypomethylation of the maternal igf2/h19 imprinting control region.Semantic proximity Read ↗

Synthetic DNA fragments bearing ICR cis elements become differentially methylated and recapitulate genomic imprinting in transgenic miceSemantic proximity Read ↗

Identification of the sequences responsible for maternal <i>H19</i> -ICR hypermethylation with Beckwith-Wiedemann syndrome-like overgrowth in miceSemantic proximity Read ↗

Identification of responsible sequences which mutations cause maternal H19-ICR hypermethylation with Beckwith-Wiedemann syndrome-like overgrowth.Semantic proximity Read ↗

The H19 Imprinting Control Region Mediates Preimplantation Imprinted Methylation of Nearby Sequences in Yeast Artificial Chromosome Transgenic MiceSemantic proximity Read ↗

Oct motif variants in Beckwith-Wiedemann syndrome patients disrupt maintenance of the hypomethylated state of the H19/IGF2 imprinting control region.Semantic proximity Read ↗

CTCF binding is not the epigenetic mark that establishes post-fertilization methylation imprinting in the transgenic H19 ICR.Semantic proximity Read ↗

A Randomly Integrated Transgenic <i>H19</i> Imprinting Control Region Acquires Methylation Imprinting Independently of Its Establishment in Germ CellsSemantic proximity Read ↗

CTCF elements direct allele-specific undermethylation at the imprinted H19 locus.Semantic proximity Read ↗

Imprinting of Igf2 and H19 from a 130 kb YAC transgene.Semantic proximity Read ↗

The transgenic IG-DMR sequence of the mouse Dlk1-Dio3 domain acquired imprinted DNA methylation during the post-fertilization periodSemantic proximity Read ↗

CTCF binding sites promote transcription initiation and prevent DNA methylation on the maternal allele at the imprinted H19/Igf2 locus.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.