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| Content Provider | Springer Nature Link |
|---|---|
| Author | Ning, Xiaojin Tao, Tao Shen, Jianhong Ji, Yuteng Xie, Lili Wang, Hongmei Liu, Ning Xu, Xide Sun, Chi Zhang, Dongmei Shen, Aiguo Ke, Kaifu |
| Copyright Year | 2016 |
| Abstract | Contrary to cell cycle-associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling processes in regulating mammalian CNS development. Studies of CDK5 have focused on its phosphorylation, although the diversity of CDK5 functions in the brain suggests additional forms of regulation. Here we expanded on the functional roles of CDK5 glycosylation in neurons. We showed that CDK5 was dynamically modified with O-GlcNAc in response to neuronal activity and that glycosylation represses CDK5-dependent apoptosis by impairing its association with p53 pathway. Blocking glycosylation of CDK5 alters cellular function and increases neuronal apoptosis in the cell model of the ICH. Our findings demonstrated a new role for O-glycosylation in neuronal apoptosis and provided a mechanistic understanding of how glycosylation contributes to critical neuronal functions. Moreover, we identified a previously unknown mechanism for the regulation of activity-dependent gene expression, neural development, and apoptosis. |
| Starting Page | 527 |
| Ending Page | 536 |
| Page Count | 10 |
| File Format | |
| ISSN | 02724340 |
| Journal | Cellular and Molecular Neurobiology |
| Volume Number | 37 |
| Issue Number | 3 |
| e-ISSN | 15736830 |
| Language | English |
| Publisher | Springer US |
| Publisher Date | 2016-06-17 |
| Publisher Place | New York |
| Access Restriction | Subscribed |
| Subject Keyword | CDK5 O-GlcNAc modification Intracerebral hemorrhage Neuronal apoptosis Neurosciences Cell Biology Neurobiology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Medicine Cellular and Molecular Neuroscience |
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