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MATSUURA Katsuhisa
Department School of Medicine, School of Medicine Position Professor and Division head |
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| Article types | Original article |
| Language | English |
| Peer review | Peer reviewed |
| Title | New Noonan syndrome model mice with RIT1 mutation exhibit cardiac hypertrophy and susceptibility to β-adrenergic stimulation-induced cardiac fibrosis. |
| Journal | Formal name：EBioMedicine Abbreviation：EBioMedicine ISSN code：(2352-3964)2352-3964(Linking) |
| Domestic / Foregin | Foregin |
| Volume, Issue, Page | 42,pp.43-53 |
| Author and coauthor | TAKAHARA Shingo†, INOUE Shin-ichi, MIYAGAWA-TOMITA Sachiko, MATSUURA Katsuhisa, NAKASHIMA Yasumi, NIIHORI Tetsuya, MATSUBARA Yoichi, SAIKI Yoshikatsu, AOKI Yoko* |
| Publication date | 2019/04 |
| Summary | The A57G mutation in Rit1 causes cardiac hypertrophy, fibrosis and other NS-associated features. Biochemical analysis indicates that the AKT signaling pathway might be related to downstream signaling in the RIT1 A57G mutant at a developmental stage and under β-adrenergic stimulation in the heart. FUND: The Grants-in-Aid were provided by the Practical Research Project for Rare/Intractable Diseases from the Japan Agency for Medical Research and Development, the Japan Society for the Promotion of Science KAKENHI Grant. |
| DOI | 10.1016/j.ebiom.2019.03.014 |
| PMID | 30898653 |