Nature Communications (Mar 2021)
Pharmacological rescue in patient iPSC and mouse models with a rare DISC1 mutation
- Nam-Shik Kim,
- Zhexing Wen,
- Jing Liu,
- Ying Zhou,
- Ziyuan Guo,
- Chongchong Xu,
- Yu-Ting Lin,
- Ki-Jun Yoon,
- Junhyun Park,
- Michelle Cho,
- Minji Kim,
- Xinyuan Wang,
- Huimei Yu,
- Srilatha Salamuru,
- Kimberly M. Christian,
- Kuei-sen Hsu,
- Menghang Xia,
- Weidong Li,
- Christopher A. Ross,
- Russell L. Margolis,
- Xin-Yun Lu,
- Hongjun Song,
- Guo-li Ming
Affiliations
- Nam-Shik Kim
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Zhexing Wen
- Departments of Psychiatry and Behavioral Sciences, Cell Biology, and Neurology, Emory University School of Medicine
- Jing Liu
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
- Ying Zhou
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Ziyuan Guo
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Chongchong Xu
- Departments of Psychiatry and Behavioral Sciences, Cell Biology, and Neurology, Emory University School of Medicine
- Yu-Ting Lin
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Ki-Jun Yoon
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Junhyun Park
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Michelle Cho
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Minji Kim
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Xinyuan Wang
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Huimei Yu
- Institute for Cell Engineering, Johns Hopkins University School of Medicine
- Srilatha Salamuru
- National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive
- Kimberly M. Christian
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Kuei-sen Hsu
- Department of Pharmacology, College of Medicine, National Cheng Kung University
- Menghang Xia
- National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive
- Weidong Li
- Bio-X Institutes, Key Laboratory for the Genetics of Development and Neuropsychiatric Disorders, Shanghai Jiao Tong University
- Christopher A. Ross
- Division of Neurobiology, Department of Psychiatry, Johns Hopkins University School of Medicine
- Russell L. Margolis
- Division of Neurobiology, Department of Psychiatry, Johns Hopkins University School of Medicine
- Xin-Yun Lu
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
- Hongjun Song
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- Guo-li Ming
- Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania
- DOI
- https://doi.org/10.1038/s41467-021-21713-3
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 11
Abstract
Previous work has shown in iPSC derived neurons that synaptic impairments are associated with a 4bp DISC1 deletion. Here the authors demonstrate a role for the PDE4 signalling pathway in these synaptic impairments.
