ArticleCell & bioscience2021
Deletion at an 1q24 locus reveals a critical role of long noncoding RNA DNM3OS in skeletal development.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Detection of a complex chromosomal rearrangement in a novel mouse mutant by optical genome mapping.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Biomarker Landscape in RASopathies.International journal of molecular sciences · 2024Review
- Long Non-coding RNA DNM3OS: Pathogenic Roles and Molecular Mechanisms in Pathophysiological Processes.Current medicinal chemistry · 2024Review
- Identification and characterization of factors associated with short stature and pre-shortness in Chinese preschool-aged children.Endocrine connections · 2021Article
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13 authors.
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Abstract
backgroundSkeletal development and maintenance are complex processes known to be coordinated by multiple genetic and epigenetic signaling pathways. However, the role of long non-coding RNAs (lncRNAs), a class of crucial epigenetic regulatory molecules, has been under explored in skeletal biology.
resultsHere we report a young patient with short stature, hypothalamic dysfunction and mild macrocephaly, who carries a maternally inherited 690 kb deletion at Chr.1q24.2 encompassing a noncoding RNA gene, DNM3OS, embedded on the opposite strand in an intron of the DYNAMIN 3 (DNM3) gene. We show that lncRNA DNM3OS sustains the proliferation of chondrocytes independent of two co-cistronic microRNAs miR-199a and miR-214. We further show that nerve growth factor (NGF), a known factor of chondrocyte growth, is a key target of DNM3OS-mediated control of chondrocyte proliferation.
conclusionsThis work demonstrates that DNM3OS is essential for preventing premature differentiation of chondrocytes required for bone growth through endochondral ossification.
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