ArticleNature genetics2014
The noncoding RNA IPW regulates the imprinted DLK1-DIO3 locus in an induced pluripotent stem cell model of Prader-Willi syndrome.
Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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89 citing papers in PubMed, 174 citations in OpenAlex.
- Placental defects revealed by modelling Prader-Willi syndrome in mice.Disease models & mechanisms · 2026Article
- Allele-specific CRISPR perturbation of the imprinted Dlk1-Dio3 domain reveals regulation of BMP-NOTCH-VEGF signaling in embryonic organogenesis.Cell death and differentiation · 2026Article
- Multi-omics characterization of developing forebrain organoids unravels the dynamic molecular events of Rett syndrome pathogenesis.Journal of neurodevelopmental disorders · 2026Article
- The superpowers of imprinting control regions.Genome research · 2026Review
- How Imprinted Genes Shape Nurturing Behaviours and Neural Circuits.Brain, behavior and evolution · 2026Review
- Characterizing the Long Non-Coding RNA Profile of Endometrial Mesenchymal Stem/Stromal Cell-Derived Extracellular Vesicles and Their Anti-Inflammatory Role in Osteoarthritis.International journal of molecular sciences · 2025Article
- Light and sex modifybioRxiv : the preprint server for biology · 2025Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- Transgenerational epigenetic self-memory ofEpigenetics · 2024Article
- Review
- The role of long noncoding RNAs in ocular angiogenesis and vascular oculopathy.Cell & bioscience · 2024Review
- Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- m6A-Mediated Upregulation of Imprinted in Prader-Willi Syndrome Induces Aberrant Apical-Basal Polarization and Oxidative Damage in RPE Cells.Investigative ophthalmology & visual science · 2024Article
- Review
- Syndromic and Monogenic Obesity: New Opportunities Due to Genetic-Based Pharmacological Treatment.Children (Basel, Switzerland) · 2024Review
- Imprinted Long Non-Coding RNAs in Mammalian Development and Disease.International journal of molecular sciences · 2023Review
- Imprinting disorders.Nature reviews. Disease primers · 2023Review
- Novel MKRN3 Missense Mutations Associated With Central Precocious Puberty Reveal Distinct Effects on Ubiquitination.The Journal of clinical endocrinology and metabolism · 2023Article
- Maintenance of methylation profile in imprinting control regions in human induced pluripotent stem cells.Clinical epigenetics · 2022Article
- Atypical 15q11.2-q13 Deletions and the Prader-Willi Phenotype.Journal of clinical medicine · 2022Article
29 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Parental imprinting is a form of epigenetic regulation that results in parent-of-origin differential gene expression. To study Prader-Willi syndrome (PWS), a developmental imprinting disorder, we generated case-derived induced pluripotent stem cells (iPSCs) harboring distinct aberrations in the affected region on chromosome 15. In studying PWS-iPSCs and human parthenogenetic iPSCs, we unexpectedly found substantial upregulation of virtually all maternally expressed genes (MEGs) in the imprinted DLK1-DIO3 locus on chromosome 14. Subsequently, we determined that IPW, a long noncoding RNA in the critical region of the PWS locus, is a regulator of the DLK1-DIO3 region, as its overexpression in PWS and parthenogenetic iPSCs resulted in downregulation of MEGs in this locus. We further show that gene expression changes in the DLK1-DIO3 region coincide with chromatin modifications rather than DNA methylation levels. Our results suggest that a subset of PWS phenotypes may arise from dysregulation of an imprinted locus distinct from the PWS region.
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