ArticlePLoS genetics2011
Uncoupling antisense-mediated silencing and DNA methylation in the imprinted Gnas cluster.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 94 citations in OpenAlex.
- Transcriptional interference drives intronic polyadenylation at the endogenous H13/Mcts2 locus.Nucleic acids research · 2026Article
- The superpowers of imprinting control regions.Genome research · 2026Review
- Imprinting and skeletal disorders: lessons from pseudohypoparathyroidism and related disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Review
- Bidirectional disruption ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A biallelically active embryonic enhancer dictates GNAS imprinting through allele-specific conformations.Nature communications · 2025Article
- Noncoding RNAs improve the predictive power of network medicine.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Imprinted Long Non-Coding RNAs in Mammalian Development and Disease.International journal of molecular sciences · 2023Review
- Novel epigenetic molecular therapies for imprinting disorders.Molecular psychiatry · 2023Review
- LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis.Molecular and cellular biochemistry · 2023Article
- Lack of GNAS Remethylation During Oogenesis May Be a Cause of Sporadic Pseudohypoparathyroidism Type Ib.The Journal of clinical endocrinology and metabolism · 2022Article
- Genetic Studies on Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
- Presence of H3K4me3 on Paternally Expressed Genes of the Paternal Genome From Sperm to Implantation.Frontiers in cell and developmental biology · 2022Article
- Intragenic CpG Islands and Their Impact on Gene Regulation.Frontiers in cell and developmental biology · 2022Review
- Diverse epigenetic mechanisms maintain parental imprints within the embryonic and extraembryonic lineages.Developmental cell · 2021Article
- High-throughput Molecular Analysis of Pseudohypoparathyroidism 1b Patients Reveals Novel Genetic and Epigenetic Defects.The Journal of clinical endocrinology and metabolism · 2021Article
- Exploring chromatin structural roles of non-coding RNAs at imprinted domains.Biochemical Society transactions · 2021Review
- Genomic Imprinting at the PorcineGenes · 2021Article
- Canonical and Non-canonical Genomic Imprinting in Rodents.Frontiers in cell and developmental biology · 2021Review
- Brain and Pituitary Transcriptome Analyses Reveal the Differential Regulation of Reproduction-Related LncRNAs and mRNAs inFrontiers in genetics · 2021Article
- MaternalFrontiers in genetics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
There is increasing evidence that non-coding macroRNAs are major elements for silencing imprinted genes, but their mechanism of action is poorly understood. Within the imprinted Gnas cluster on mouse chromosome 2, Nespas is a paternally expressed macroRNA that arises from an imprinting control region and runs antisense to Nesp, a paternally repressed protein coding transcript. Here we report a knock-in mouse allele that behaves as a Nespas hypomorph. The hypomorph mediates down-regulation of Nesp in cis through chromatin modification at the Nesp promoter but in the absence of somatic DNA methylation. Notably there is reduced demethylation of H3K4me3, sufficient for down-regulation of Nesp, but insufficient for DNA methylation; in addition, there is depletion of the H3K36me3 mark permissive for DNA methylation. We propose an order of events for the regulation of a somatic imprint on the wild-type allele whereby Nespas modulates demethylation of H3K4me3 resulting in repression of Nesp followed by DNA methylation. This study demonstrates that a non-coding antisense transcript or its transcription is associated with silencing an overlapping protein-coding gene by a mechanism independent of DNA methylation. These results have broad implications for understanding the hierarchy of events in epigenetic silencing by macroRNAs.
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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.