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

Ube3a-ATS is an atypical RNA polymerase II transcript that represses the paternal expression of Ube3a

5 Apr 2012

Abstract excerpt

The Angelman syndrome gene, UBE3A, is subject to genomic imprinting controlled by mechanisms that are only partially understood. Its antisense transcript, UBE3A-ATS, is also imprinted and hypothesized to suppress UBE3A in cis. In this research, we showed that the mouse antisense ortholog, Ube3a-ATS, was transcribed by RNA polymerase (RNAP) II. However, unlike typical protein-coding transcripts, Ube3a-ATS was not...

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: 22493002
DOI: 10.1093/hmg/dds130

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Ube3a-ATS is an atypical RNA polymerase II transcript that represses the paternal expression of Ube3aPMID 22493002Read ↗

Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse ModelSemantic proximity Read ↗

Antisense oligonucleotides targeting <i>UBE3A-ATS</i> restore expression of <i>UBE3A</i> by relieving transcriptional interferenceSemantic proximity Read ↗

Maternal disruption of Ube3a leads to increased expression of Ube3a-ATS in trans.Semantic proximity Read ↗

Towards a therapy for Angelman syndrome by targeting a long non-coding RNA.Semantic proximity Read ↗

CRISPR/Cas9 directed to the Ube3a antisense transcript improves Angelman syndrome phenotype in miceSemantic proximity Read ↗

Regulation of the large (approximately 1000 kb) imprinted murine Ube3a antisense transcript by alternative exons upstream of Snurf/Snrpn.Semantic proximity Read ↗

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

Cas9 gene therapy for Angelman syndrome traps Ube3a-ATS long non-coding RNA.Semantic proximity Read ↗

Angelman syndrome-derived neurons display late onset of paternal UBE3A silencingSemantic proximity Read ↗

Development of an ASO therapy for Angelman syndrome by targeting an evolutionarily conserved region at the start of the <i>UBE3A-AS</i> transcriptSemantic proximity Read ↗

BIOLOGICAL SCIENCES: GeneticsSemantic proximity Read ↗

The Prader-Willi syndrome imprinting center activates the paternally expressed murine Ube3a antisense transcript but represses paternal Ube3a.Semantic proximity Read ↗

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