ArticleNature communications2018
Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond Coding Variants: RNA-Level Mechanisms in Human Disease and Precision Therapeutics.Genes · 2026Review
- From chromatin to proteostasis: multilevel gene regulation in Mendelian diseases.Frontiers in epigenetics and epigenomics · 2026Review
- TheBiomolecules · 2025Review
- miRNA-based regulation in growth plate cartilage: mechanisms, targets, and therapeutic potential.Frontiers in endocrinology · 2025Review
- Genomic screening of fish-specific genes in gnathostomes and their functions in fin development.Development, growth & differentiation · 2024Article
- Article
- MYCN in human development and diseases.Frontiers in oncology · 2024Review
- Emerging concepts involving inhibitory and activating RNA functionalization towards the understanding of microcephaly phenotypes and brain diseases in humans.Frontiers in cell and developmental biology · 2023Review
- Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1.PLoS biology · 2022Article
- Article
- [Research progress of cellular senescence in the pathogenesis of osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2021Review
- Review
- Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling.Frontiers in molecular biosciences · 2020Article
- Molecular mechanisms underlying nuchal hump formation in dolphin cichlid, Cyrtocara moorii.Scientific reports · 2019Article
- Growth hormone deficiency, aortic dilation, and neurocognitive issues in Feingold syndrome 2.American journal of medical genetics. Part A · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Feingold syndrome is a skeletal dysplasia caused by loss-of-function mutations of either MYCN (type 1) or MIR17HG that encodes miR-17-92 microRNAs (type 2). Since miR-17-92 expression is transcriptionally regulated by MYC transcription factors, it has been postulated that Feingold syndrome type 1 and 2 may be caused by a common molecular mechanism. Here we show that Mir17-92 deficiency upregulates TGF-β signaling, whereas Mycn-deficiency downregulates PI3K signaling in limb mesenchymal cells. Genetic or pharmacological inhibition of TGF-β signaling efficiently rescues the skeletal defects caused by Mir17-92 deficiency, suggesting that upregulation of TGF-β signaling is responsible for the skeletal defect of Feingold syndrome type 2. By contrast, the skeletal phenotype of Mycn-deficiency is partially rescued by Pten heterozygosity, but not by TGF-β inhibition. These results strongly suggest that despite the phenotypical similarity, distinct molecular mechanisms underlie the pathoetiology for Feingold syndrome type 1 and 2.
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