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

https://doi.org/10.1101/640938
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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1002/1096-8628(200022)97:2<136::aid-ajmg5>3.0.co;2-vopenalex-snapshot
Prader-Willi and Angelman syndromes: Sister imprinted disorders
inferredcites →https://doi.org/10.1002/ajmg.a.31765openalex-snapshot
DNA demethylation reactivation of imprinted genes in cell lines from patients with Prader‐Willi syndrome and a mouse model
inferredcites →https://doi.org/10.1002/ajmg.a.36653openalex-snapshot
A double‐blind randomized controlled trial of oxytocin nasal spray in Prader Willi syndrome
inferredcites →https://doi.org/10.1002/ajmg.a.38160openalex-snapshot
Oxytocin treatment in children with Prader–Willi syndrome: A double‐blind, placebo‐controlled, crossover study
inferredcites →https://doi.org/10.1007/s10048-009-0209-xopenalex-snapshot
Prader–Willi syndrome, Snord115, and Htr2c editing
inferredcites →https://doi.org/10.1007/s40618-015-0312-9openalex-snapshot
Prader-Willi syndrome: a review of clinical, genetic, and endocrine findings
inferredcites →https://doi.org/10.1016/j.cell.2018.09.010openalex-snapshot
Stem Cells, Genome Editing, and the Path to Translational Medicine
inferredcites →https://doi.org/10.1016/j.celrep.2016.03.007openalex-snapshot
G9a/GLP Complex Maintains Imprinted DNA Methylation in Embryonic Stem Cells
inferredcites →https://doi.org/10.1016/j.celrep.2018.03.018openalex-snapshot
A Transcriptomic Signature of the Hypothalamic Response to Fasting and BDNF Deficiency in Prader-Willi Syndrome
inferredcites →https://doi.org/10.1016/j.ijdevneu.2012.05.005openalex-snapshot
Hypothalamic expression of snoRNASnord116is consistent with a link to the hyperphagia and obesity symptoms of Prader–Willi syndrome
inferredcites →https://doi.org/10.1016/j.molcel.2007.01.017openalex-snapshot
Reversal of H3K9me2 by a Small-Molecule Inhibitor for the G9a Histone Methyltransferase
inferredcites →https://doi.org/10.1016/j.nbd.2010.04.004openalex-snapshot
Mice with altered serotonin 2C receptor RNA editing display characteristics of Prader–Willi syndrome
inferredcites →https://doi.org/10.1016/j.neuron.2013.05.029openalex-snapshot
Rapid Single-Step Induction of Functional Neurons from Human Pluripotent Stem Cells
inferredcites →https://doi.org/10.1016/j.scr.2016.08.008openalex-snapshot
Induced pluripotent stem cells (iPSC) created from skin fibroblasts of patients with Prader-Willi syndrome (PWS) retain the molecular signature of PWS
inferredcites →https://doi.org/10.1038/nm.4257openalex-snapshot
Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader–Willi syndrome
inferredcites →https://doi.org/10.1038/srep06445openalex-snapshot
Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
inferredcites →https://doi.org/10.1038/srep18614openalex-snapshot
Snord116 is critical in the regulation of food intake and body weight
inferredcites →https://doi.org/10.1073/pnas.1004487107openalex-snapshot
Induced pluripotent stem cell models of the genomic imprinting disorders Angelman and Prader–Willi syndromes
inferredcites →https://doi.org/10.1073/pnas.1815279116openalex-snapshot
A bipartite boundary element restricts UBE3A imprinting to mature neurons
inferredcites →https://doi.org/10.1074/jbc.m110.183392openalex-snapshot
Induced Pluripotent Stem Cells Can Be Used to Model the Genomic Imprinting Disorder Prader-Willi Syndrome
inferredcites →https://doi.org/10.1074/jbc.m211753200openalex-snapshot
Role of Histone Methyltransferase G9a in CpG Methylation of the Prader-Willi Syndrome Imprinting Center
inferredcites →https://doi.org/10.1086/302177openalex-snapshot
Prader-Willi Syndrome Is Caused by Disruption of the SNRPN Gene
inferredcites →https://doi.org/10.1086/302917openalex-snapshot
Parent-of-Origin Specific Histone Acetylation and Reactivation of a Key Imprinted Gene Locus in Prader-Willi Syndrome
inferredcites →https://doi.org/10.1086/342408openalex-snapshot
Evidence for the Role of PWCR1/HBII-85 C/D Box Small Nucleolar RNAs in Prader-Willi Syndrome
inferredcites →https://doi.org/10.1093/hmg/10.6.645openalex-snapshot
Association of acetylated histones with paternally expressed genes in the Prader-Willi deletion region
inferredcites →https://doi.org/10.1093/hmg/ddn344openalex-snapshot
Necdin, a Prader-Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during development
inferredcites →https://doi.org/10.1093/hmg/ddp277openalex-snapshot
Histone methylation is mechanistically linked to DNA methylation at imprinting control regions in mammals
inferredcites →https://doi.org/10.1093/hmg/ddt628openalex-snapshot
Imprinted expression of UBE3A in non-neuronal cells from a Prader–Willi syndrome patient with an atypical deletion
inferredcites →https://doi.org/10.1093/hmg/ddu187openalex-snapshot
Reactivation of maternal SNORD116 cluster via SETDB1 knockdown in Prader-Willi syndrome iPSCs
inferredcites →https://doi.org/10.1093/hmg/ddx311openalex-snapshot
The Prader-Willi syndrome proteins MAGEL2 and necdin regulate leptin receptor cell surface abundance through ubiquitination pathways
inferredcites →https://doi.org/10.1093/hmg/ddx342openalex-snapshot
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
inferredcites →https://doi.org/10.1093/hmg/ddx420openalex-snapshot
Zinc finger protein 274 regulates imprinted expression of transcripts in Prader-Willi syndrome neurons
inferredcites →https://doi.org/10.1093/hmg/ddy274openalex-snapshot
Loss of hierarchical imprinting regulation at the Prader–Willi/Angelman syndrome locus in human iPSCs
inferredcites →https://doi.org/10.1093/jmcb/mjs007openalex-snapshot
Molecular analysis of FMR1 reactivation in fragile-X induced pluripotent stem cells and their neuronal derivatives
inferredcites →https://doi.org/10.1093/nar/gks321openalex-snapshot
The SNORD115 (H/MBII-52) and SNORD116 (H/MBII-85) gene clusters at the imprinted Prader-Willi locus generate canonical box C/D snoRNAs
inferredcites →https://doi.org/10.1126/science.1118265openalex-snapshot
The snoRNA HBII-52 Regulates Alternative Splicing of the Serotonin Receptor 2C
inferredcites →https://doi.org/10.1172/jci.insight.98333openalex-snapshot
Intranasal carbetocin reduces hyperphagia in individuals with Prader-Willi syndrome
inferredcites →https://doi.org/10.1172/jci79220openalex-snapshot
Differentiation of hypothalamic-like neurons from human pluripotent stem cells
inferredcites →https://doi.org/10.1172/jci88648openalex-snapshot
Deficiency in prohormone convertase PC1 impairs prohormone processing in Prader-Willi syndrome
inferredcites →https://doi.org/10.1172/jci97007openalex-snapshot
Hypothalamic loss of Snord116 recapitulates the hyperphagia of Prader-Willi syndrome
inferredcites →https://doi.org/10.1186/s13041-016-0277-4openalex-snapshot
Increased alternate splicing of Htr2c in a mouse model for Prader-Willi syndrome leads disruption of 5HT2C receptor mediated appetite
inferredcites →https://doi.org/10.1242/jcs.122754openalex-snapshot
Conversion of genomic imprinting by reprogramming and redifferentiation
inferredcites →https://doi.org/10.1371/journal.pone.0001709openalex-snapshot
SnoRNA Snord116 (Pwcr1/MBII-85) Deletion Causes Growth Deficiency and Hyperphagia in Mice
inferredcites →https://doi.org/10.1373/clinchem.2005.065086openalex-snapshot
Quantitative Analysis of SRNPN Gene Methylation by Pyrosequencing as a Diagnostic Test for Prader–Willi Syndrome and Angelman Syndrome
inferredcites →https://doi.org/10.1542/peds.2016-2976openalex-snapshot
The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome
inferredcites →https://doi.org/10.3389/fnins.2015.00252openalex-snapshot
Turning over DNA methylation in the mind
inferredcites →https://doi.org/10.7554/elife.32640openalex-snapshot
Necdin shapes serotonergic development and SERT activity modulating breathing in a mouse model for Prader-Willi syndrome
inferredcites →https://doi.org/10.7554/elife.32640.024openalex-snapshot
Author response: Necdin shapes serotonergic development and SERT activity modulating breathing in a mouse model for Prader-Willi syndrome

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.1098/rsob.200195openalex-snapshot
Prader-Willi syndrome: reflections on seminal studies and future therapies
inferred← citeshttps://doi.org/10.1126/sciadv.aej5702openalex-snapshot
SMCHD1 is a target for gene activation therapy to treat Prader-Willi syndrome
inferred← citeshttps://doi.org/10.3389/fgene.2021.624581openalex-snapshot
Epigenetics in Prader-Willi Syndrome
inferred← citeshttps://doi.org/10.64898/2026.05.13.725051openalex-snapshot
SMCHD1 is a novel target for gene-activation therapy to treat Prader-Willi Syndrome
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