Restless legs syndrome-associated intronic common variant in Meis1 alters enhancer function in the developing telencephalon.

doi:10.1101/gr.166751.113

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

Community

Back to search

Article

Restless legs syndrome-associated intronic common variant in Meis1 alters enhancer function in the developing telencephalon.

Genome research - 1 Apr 2014

Spieler Derek, Kaffe Maria, Knauf Franziska, Bessa José, Tena Juan J, Giesert Florian, Schormair Barbara, Tilch Erik, Lee Heekyoung, Horsch Marion, Czamara Darina, Karbalai Nazanin, von Toerne Christine, Waldenberger Melanie, Gieger Christian, Lichtner Peter, Claussnitzer Melina, Naumann Ronald, Müller-Myhsok Bertram, Torres Miguel, Garrett Lillian, Rozman Jan, Klingenspor Martin, Gailus-Durner Valérie, Fuchs Helmut, Hrabě de Angelis Martin, Beckers Johannes, Hölter Sabine M, Meitinger Thomas, Hauck Stefanie M, Laumen Helmut, Wurst Wolfgang, Casares Fernando, Gómez-Skarmeta Jose Luis, Winkelmann Juliane

Abstract excerpt

Genome-wide association studies (GWAS) identified the MEIS1 locus for Restless Legs Syndrome (RLS), but causal single nucleotide polymorphisms (SNPs) and their functional relevance remain unknown. This locus contains a large number of highly conserved noncoding regions (HCNRs) potentially functioning as cis-regulatory modules. We analyzed these HCNRs for allele-dependent enhancer activity in zebrafish and mice...

Read the complete abstract on PubMed

Topics

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

Share to Basal Ganglia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Enhancer Elements, Genetic

Share to Homeodomain Proteins

Share to Introns

Share to Myeloid Ecotropic Viral Integration Site 1 Protein

Share to Neoplasm Proteins

Share to Restless Legs Syndrome

Share to Telencephalon

Source

Open in PubMed Open full text

Identifiers

PMID: 24642863
DOI: 10.1101/gr.166751.113
PMCID: PMC3975059

Genes

MEIS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Restless legs syndrome-associated intronic common variant in Meis1 alters enhancer function in the developing telencephalon.PMID 24642863Read ↗

Intronic elements associated with insomnia and restless legs syndrome exhibit cell type-specific epigenetic features contributing to <i>MEIS1</i> regulationSemantic proximity Read ↗

Targeted resequencing and systematic in vivo functional testing identifies rare variants in MEIS1 as significant contributors to restless legs syndrome.Semantic proximity Read ↗

MEIS1 and Restless Legs Syndrome: A Comprehensive ReviewSemantic proximity Read ↗

MEIS1 intronic risk haplotype associated with restless legs syndrome affects its mRNA and protein expression levels.Semantic proximity Read ↗

RLS-associated MEIS transcription factors control distinct processes in human neural stem cellsSemantic proximity Read ↗

Genome-wide association study of restless legs syndrome identifies common variants in three genomic regions.Semantic proximity Read ↗

A direct interaction between two Restless Legs Syndrome predisposing genes: MEIS1 and SKOR1.Semantic proximity Read ↗

Identification of novel risk loci for restless legs syndrome in genome-wide association studies in individuals of European ancestry: a meta-analysis.Semantic proximity Read ↗

Non-coding structural variants identify a commonly affected regulatory region steering<i>FOXG1</i>transcription in early neurodevelopmentSemantic proximity Read ↗

Genetics of restless legs syndrome.Semantic proximity Read ↗

Enhancer-adoption as a mechanism of human developmental disease.Semantic proximity Read ↗

Reducing methylation of histone 3.3 lysine 4 in the medial ganglionic eminence and hypothalamus recapitulates neurodevelopmental disorder phenotypesSemantic proximity Read ↗

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