ArticleFrontiers in genetics2012
Non-Coding RNAs at the Gnas and Snrpn-Ube3a Imprinted Gene Loci and Their Involvement in Hereditary Disorders.
Article in Frontiers in genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
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- Dynamic allelic expression in mouse mammary glands across the adult developmental cycle.Nucleic acids research · 2025Article
- Tissue-specific Grb10/Ddc insulator drives allelic architecture for cardiac development.Molecular cell · 2022Article
- Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective.Non-coding RNA · 2021Review
- Basic biology and therapeutic implications of lncRNA.Advanced drug delivery reviews · 2015Review
- Microarray analysis reveals higher gestational folic Acid alters expression of genes in the cerebellum of mice offspring-a pilot study.Brain sciences · 2015Article
- IAOseq: inferring abundance of overlapping genes using RNA-seq data.BMC bioinformatics · 2015Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
Non-coding RNAs (ncRNAs) have long been recognized at imprinted gene loci and provided early paradigms to investigate their functions and molecular mechanisms of action. The characteristic feature of imprinted genes, their monoallelic, parental-origin-dependent expression, is achieved through complex epigenetic regulation, which is modulated by ncRNAs. This minireview focuses on two imprinted gene clusters, in which changes in ncRNA expression contribute to human disorders. At the GNAS locus loss of NESP RNA can cause autosomal dominant Pseudohypoparathyroidism type 1b (AD-PHP-Ib), while at the SNRPN-UBE3A locus a long ncRNA and processed snoRNAs play a role in Angelman-Syndrome (AS) and Prader-Willi-Syndrome (PWS). The ncRNAs silence overlapping protein-coding transcripts in sense or anti-sense orientation through changes in histone modifications as well as DNA methylation at CpG-rich sequence motifs. Their epigenetic modulatory functions are required in early development in the pre-implantation embryo or already in the parental germ cells. However, it remains unclear whether the sequence homology-carrying ncRNA itself is required, or whether the process of its transcription through other promoters causes the silencing effect.
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