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...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2018-04-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-018-03788-7 |
| _version_ | 1819039895928176640 |
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| 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 |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-12-21T09:00:29Z |
| format | Article |
| id | doaj.art-cce31e82791243b5bd7fb58a95b1fffa |
| institution | Directory Open Access Journal |
| issn | 2041-1723 |
| language | English |
| last_indexed | 2024-12-21T09:00:29Z |
| publishDate | 2018-04-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj.art-cce31e82791243b5bd7fb58a95b1fffa2022-12-21T19:09:29ZengNature PortfolioNature Communications2041-17232018-04-019111010.1038/s41467-018-03788-7Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse modelsFatemeh Mirzamohammadi0Anastasia Kozlova1Garyfallia Papaioannou2Elena Paltrinieri3Ugur M. Ayturk4Tatsuya Kobayashi5Endocrine Unit, Massachusetts General Hospital, and Harvard Medical SchoolEndocrine Unit, Massachusetts General Hospital, and Harvard Medical SchoolEndocrine Unit, Massachusetts General Hospital, and Harvard Medical SchoolEndocrine Unit, Massachusetts General Hospital, and Harvard Medical SchoolMusculoskeletal Integrity Program, Hospital for Special SurgeryEndocrine Unit, Massachusetts General Hospital, and Harvard Medical SchoolFeingold 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.https://doi.org/10.1038/s41467-018-03788-7 |
| spellingShingle | 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 Nature Communications |
| title | 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_short | 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 |
| url | https://doi.org/10.1038/s41467-018-03788-7 |
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