| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Li, Wei Yuan, Yefeng Zhang, Zhao Feng, Yaqin Wang, Hao Yan, Hui |
| Description |
Author Affiliation: Wang H ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the University of Chinese Academy of Sciences, Beijing 100039.); Yuan Y ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the University of Chinese Academy of Sciences, Beijing 100039.); Zhang Z ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the University of Chinese Academy of Sciences, Beijing 100039.); Yan H ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the Department of Histology and Embryology, Shanxi Medical University, Taiyuan 030001, and.); Feng Y ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the Department of Histology and Embryology, Shanxi Medical University, Taiyuan 030001, and.); Li W ( From the State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, the Center of Alzheimer's Disease, Beijing Institute for Brain Disorders, Beijing 100053, China wli@genetics.ac.cn.) |
| Abstract |
DTNBP1 (dystrobrevin-binding protein 1), which encodes dysbindin-1, is one of the leading susceptibility genes for schizophrenia. Both dysbindin-1B and -1C isoforms are decreased, but the dysbindin-1A isoform is unchanged in schizophrenic hippocampal formation, suggesting dysbindin-1 isoforms may have distinct roles in schizophrenia. We found that mouse dysbindin-1C, but not dysbindin-1A, is localized in the hilar glutamatergic mossy cells of the dentate gyrus. The maturation rate of newborn neurons in sandy (sdy) mice, in which both dysbindin-1A and -1C are deleted, is significantly delayed when compared with that in wild-type mice or with that in muted (mu) mice in which dysbindin-1A is destabilized but dysbindin-1C is unaltered. Dysbindin-1C deficiency leads to a decrease in mossy cells, which causes the delayed maturation of newborn neurons. This suggests that dysbindin-1C, rather than dysbindin-1A, regulates adult hippocampal neurogenesis in a non-cell autonomous manner. |
| ISSN |
00219258 |
| e-ISSN |
1083351X |
| Journal |
Journal of Biological Chemistry |
| Issue Number |
42 |
| Volume Number |
289 |
| Language |
English |
| Publisher |
American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date |
2014-10-17 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Carrier Proteins Physiology Dentate Gyrus Cytology Neurons Animals Animals, Newborn Apoptosis Autophagy Cell Proliferation Cell Survival Cognition Disorders Metabolism Crosses, Genetic Growth & Development Dystrophin-Associated Proteins Mice Mice, Inbred C57BL Mice, Inbred DBA Mutation Schizophrenia Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Cell Biology Biochemistry Molecular Biology |
