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

R-loop formation at Snord116 mediates topotecan inhibition of Ube3a-antisense and allele-specific chromatin decondensation

5 Aug 2013

Abstract excerpt

Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are oppositely imprinted autism-spectrum disorders with known genetic bases, but complex epigenetic mechanisms underlie their pathogenesis. The PWS/AS locus on 15q11-q13 is regulated by an imprinting control region that is maternally methylated and silenced. The PWS imprinting control region is the promoter for a one megabase paternal transcript encoding the...

Read the complete abstract on PubMed

Topics

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

Share to Epigenetics and DNA Methylation
Share to Genetic Syndromes and Imprinting
Share to Prenatal Screening and Diagnostics

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23918391
DOI: 10.1073/pnas.1305426110

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

R-loop formation at Snord116 mediates topotecan inhibition of Ube3a-antisense and allele-specific chromatin decondensationPMID 23918391Read ↗

Small molecule inhibitors of G9a reactivate the maternal PWS genes in Prader-Willi-Syndrome patient derived neural stem cells and differentiated neuronsSemantic proximity Read ↗

Imprinting regulates mammalian snoRNA-encoding chromatin decondensation and neuronal nucleolar sizeSemantic proximity Read ↗

Mechanism of EHMT2-mediated genomic imprinting associated with Prader-Willi syndromeSemantic proximity Read ↗

Topoisomerase inhibitors unsilence the dormant allele of Ube3a in neurons.Semantic proximity Read ↗

Identifying key underlying regulatory networks and predicting targets of orphan C/D box <i>SNORD116</i> snoRNAs in Prader-Willi syndromeSemantic proximity Read ↗

Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editingSemantic proximity Read ↗

Integration of CTCF Loops, Methylome, and Transcriptome in Differentiating LUHMES as a Model for Imprinting Dynamics of the 15q11-q13 Locus in Human NeuronsSemantic proximity Read ↗

Ube3a unsilencer for the potential treatment of Angelman syndromeSemantic proximity Read ↗

Integration of CTCF loops, methylome, and transcriptome in differentiating LUHMES as a model for imprinting dynamics of the 15q11-q13 locus in human neurons.Semantic proximity Read ↗

Imprinted expression of UBE3A in non-neuronal cells from a Prader–Willi syndrome patient with an atypical deletionSemantic proximity Read ↗

Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editingSemantic proximity Read ↗

Prader-Willi locus <i>Snord116</i> RNA processing requires an active endogenous allele and neuron-specific splicing by <i>Rbfox3/NeuN</i>Semantic proximity Read ↗

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