ArticleNeurogenetics2010
Atp10a, a gene adjacent to the PWS/AS gene cluster, is not imprinted in mouse and is insensitive to the PWS-IC.
Article in Neurogenetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Recommendations for the investigation of animal models of Prader-Willi syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Guideline
- Mechanisms underlying the EEG biomarker in Dup15q syndrome.Molecular autism · 2019Trial
- Neonatal social communication and single genes predict the variability of post-pubertal social behavior in a mouse model of paternal 15q11-13 duplication.Research square · 2026Article
- Species-Specific Parent-Of-Origin Expression of Adam23 in the Mammalian Brain.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Deficiency of the lipid flippase ATP10A causes diet-induced dyslipidemia in female mice.Scientific reports · 2024Article
- Article
- ZFP57 dictates allelic expression switch of target imprinted genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Effects of Dietary Interventions on DNA Methylation: Implications for Obesity Management.International journal of molecular sciences · 2020Review
- Spastic Diplegia in a Haitian Girl with Angelman Syndrome.Journal of pediatric genetics · 2020Article
- Circadian biology and sleep in monogenic neurological disorders and its potential application in drug discovery.Current opinion in behavioral sciences · 2019Article
- Genome-wide association studies of fertility and calving traits in Brown Swiss cattle using imputed whole-genome sequences.BMC genomics · 2017Article
- Long noncoding RNAs in imprinting and X chromosome inactivation.Biomolecules · 2014Review
- The interstitial duplication 15q11.2-q13 syndrome includes autism, mild facial anomalies and a characteristic EEG signature.Autism research : official journal of the International Society for Autism Research · 2013Article
- Smchd1 regulates a subset of autosomal genes subject to monoallelic expression in addition to being critical for X inactivation.Epigenetics & chromatin · 2013Article
- Ube3a-ATS is an atypical RNA polymerase II transcript that represses the paternal expression of Ube3a.Human molecular genetics · 2012Article
- Spread of X-chromosome inactivation into chromosome 15 is associated with Prader-Willi syndrome phenotype in a boy with a t(X;15)(p21.1;q11.2) translocation.Human genetics · 2012Article
- Increased copy number for methylated maternal 15q duplications leads to changes in gene and protein expression in human cortical samples.Molecular autism · 2011Article
- The neurobiology of mouse models syntenic to human chromosome 15q.Journal of neurodevelopmental disorders · 2011Article
- Maternally derived microduplications at 15q11-q13: implication of imprinted genes in psychotic illness.The American journal of psychiatry · 2011Article
- Neuronal chromatin dynamics of imprinting in development and disease.Journal of cellular biochemistry · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations affecting a cluster of coordinately regulated imprinted genes located at 15q11-q13 underlie both Prader-Willi syndrome (PWS) and Angelman syndrome (AS). Disruption of the predominately maternally expressed UBE3A locus is sufficient to meet diagnostic criteria for AS. However, AS patients with a deletion of the entire PWS/AS locus often have more severe traits than patients with point mutations in UBE3A suggesting that other genes contribute to the syndrome. ATP10A resides 200 kb telomeric to UBE3A and is of uncertain imprinted status. An initial report indicated bialleleic expression of the murine Atp10a in all tissues, but a subsequent report suggests that Atp10a is predominantly maternally expressed in the hippocampus and olfactory bulb. To resolve this discrepancy, we investigated Atp10a allelic expression in the brain, DNA methylation status, and sensitivity to mutations of the PWS imprinting center, an element required for imprinted gene expression in the region. We report that Atp10a is biallelically expressed in both the newborn and adult brain, and Atp10a allelic expression is insensitive to deletion or mutation of the PWS imprinting center. The CpG island associated with Atp10a is hypomethylated, a result consistent with the notion that Atp10a is not an imprinted gene.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.