Article

Paternally expressed imprinted <i>Snord116</i> and <i>Peg3</i> regulate hypothalamic orexin neurons

2019-10-28

Abstract excerpt

Imprinted genes are highly expressed in the hypothalamus; however, whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at chromosome 15q11-q13, is characterised by hypothalamic insufficiency. Here, we investigate the role of the paternally expr...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: aa2e26d9-fbb7-5c56-8877-419d21a12cea
DOI: 10.1101/820738

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Paternally expressed imprinted <i>Snord116</i> and <i>Peg3</i> regulate hypothalamic orexin neuronsDOI 10.1101/820738Read

Loss of SNORD115 mitigates SNORD116-driven sleep abnormalities in mouse models of Prader-Willi syndromeSemantic proximity Read

The paternally imprinted gene <i>Snord116</i> regulates cortical neuronal activitySemantic proximity Read

Loss of the imprinted, non-coding Snord116 gene cluster in the interval deleted in the Prader Willi syndrome results in murine neuronal and endocrine pancreatic developmental phenotypes.Semantic proximity Read

Light and sex modify <i>Snord116</i> genotype effects on metabolism, behavior, and imprinted gene networks following circadian entrainmentSemantic proximity Read

What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?Semantic proximity Read

Deletion of the Snord116/SNORD116 Alters Sleep in Mice and Patients with Prader-Willi Syndrome.Semantic proximity Read

Evolutionary and biological insights into the paternally expressed Snord116-Ipw-Snord115 gene array at the imprinted Prader-Willi syndrome domainSemantic proximity Read

The imprinted gene Magel2 regulates normal circadian output.Semantic proximity Read

Subcellular partitioning of <i>Nhlh2</i> mRNA reveals how <i>SNORD116</i> loss contributes to Prader-Willi SyndromeSemantic 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

Hypothalamic loss of Snord116 recapitulates the hyperphagia of Prader-Willi syndrome.Semantic 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