Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models

Feingold syndrome is a skeletal dysplasia caused by mutations in MYCN or MIR17HG, but it is not clear if these mutations lead to pathology via a common molecular mechanism. Here, the authors show that mutations in MIR17HG lead to upregulated TGF-β signaling in limb mesenchymal cells, while mutations...

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Autores principales: Fatemeh Mirzamohammadi, Anastasia Kozlova, Garyfallia Papaioannou, Elena Paltrinieri, Ugur M. Ayturk, Tatsuya Kobayashi
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/cce31e82791243b5bd7fb58a95b1fffa
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spelling oai:doaj.org-article:cce31e82791243b5bd7fb58a95b1fffa2021-12-02T15:34:26ZDistinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models10.1038/s41467-018-03788-72041-1723https://doaj.org/article/cce31e82791243b5bd7fb58a95b1fffa2018-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-03788-7https://doaj.org/toc/2041-1723Feingold syndrome is a skeletal dysplasia caused by mutations in MYCN or MIR17HG, but it is not clear if these mutations lead to pathology via a common molecular mechanism. Here, the authors show that mutations in MIR17HG lead to upregulated TGF-β signaling in limb mesenchymal cells, while mutations in MYCN downregulate PI3K signaling.Fatemeh MirzamohammadiAnastasia KozlovaGaryfallia PapaioannouElena PaltrinieriUgur M. AyturkTatsuya KobayashiNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-10 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Fatemeh Mirzamohammadi
Anastasia Kozlova
Garyfallia Papaioannou
Elena Paltrinieri
Ugur M. Ayturk
Tatsuya Kobayashi
Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
description Feingold syndrome is a skeletal dysplasia caused by mutations in MYCN or MIR17HG, but it is not clear if these mutations lead to pathology via a common molecular mechanism. Here, the authors show that mutations in MIR17HG lead to upregulated TGF-β signaling in limb mesenchymal cells, while mutations in MYCN downregulate PI3K signaling.
format article
author Fatemeh Mirzamohammadi
Anastasia Kozlova
Garyfallia Papaioannou
Elena Paltrinieri
Ugur M. Ayturk
Tatsuya Kobayashi
author_facet Fatemeh Mirzamohammadi
Anastasia Kozlova
Garyfallia Papaioannou
Elena Paltrinieri
Ugur M. Ayturk
Tatsuya Kobayashi
author_sort Fatemeh Mirzamohammadi
title Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
title_short Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
title_full Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
title_fullStr Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
title_full_unstemmed Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models
title_sort distinct molecular pathways mediate mycn and myc-regulated mir-17-92 microrna action in feingold syndrome mouse models
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/cce31e82791243b5bd7fb58a95b1fffa
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