PKC epsilon facilitates recovery of exocytosis after an exhausting stimulation
It has been well documented that protein kinase Cs (PKCs) play multifaceted roles in regulating exocytosis of neurotransmitters and hormones. But the isoform-specific PKC effects are still poorly elucidated mainly because of the large variety of PKC isoforms and the dubious specificity of the common...
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| Main Authors: | , , , , |
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| Other Authors: | |
| Format: | Article |
| Language: | English |
| Published: |
2012
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| Subjects: | |
| Online Access: | https://hdl.handle.net/10356/94373 http://hdl.handle.net/10220/7523 |
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| Institution: | Nanyang Technological University |
| Language: | English |
| Summary: | It has been well documented that protein kinase Cs (PKCs) play multifaceted roles in regulating exocytosis of neurotransmitters and hormones. But the isoform-specific PKC effects are still poorly elucidated mainly because of the large variety of PKC isoforms and the dubious specificity of the commonly used
pharmacological agents. In the present study, based on
overexpression of wild-type or dominant negative PKCε, we demonstrate in neuroendocrine PC12 cells that PKCε, but not PKCα, facilitates recovery of exocytosis after an exhausting stimulation. Specifically, PKCε mediates fast recovery of the extent of exocytosis in a phosphatidylinositol biphosphate-dependent manner, likely through enhancing the rate of vesicle delivery and reorganization of cortical actin network. In addition,
PKCε promotes fast recovery of vesicle release kinetics
that is slowed after a strong stimulation. These experimental results may suggest a PKC-dependent mechanism relevant to the short-term plasticity of exocytosis in both neurons and neuroendocrine cells. |
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