dc.citation.conferencePlace |
KO |
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dc.citation.conferencePlace |
International Convention Center Jeju |
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dc.citation.title |
ICKSMCB 2023 |
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dc.contributor.author |
Kim, Yeonjoo |
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dc.contributor.author |
Lee, Jieun |
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dc.contributor.author |
Myung, Kyungjae |
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dc.contributor.author |
Lee, Seungeun |
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dc.contributor.author |
Kim, Jae-Ick |
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dc.date.accessioned |
2024-01-31T18:06:40Z |
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dc.date.available |
2024-01-31T18:06:40Z |
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dc.date.created |
2023-11-27 |
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dc.date.issued |
2023-11-07 |
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dc.description.abstract |
O- GlcNAcylation is a post-translational modification critical for various cellular functions such as regulation of gene expression, signal transduction, and protein homeostasis. Notably, it has been shown that O-GlcNAcylation modulates neuronal functions through "on-demand" protein modification. Despite this fact, it remains to be determined whether O-GlcNAcylation is essential for glial cells. In this study, we generated microglia-specific OGlcNAc transferase (OGT) knockout (KO) mice to reveal the physiological roles of microglial O-GlcNAcylation in the brain. We found that the loss of O-GlcNAcylation in microglia alters the innate biology. Interestingly, the potassium channel Kv1.3, which is known to be O-GlcNAcylated, exhibited an elevated expression level and channel conductance in hippocampal OGT cKO microglia. We also found that these Kv1.3 abundant microglia specifically modulate hippocampal GABAergic synapses and inhibitory tone, causing a shift in E/I balance. Collectively, these data demonstrate that microglia are important for tuning inhibitory tone in the hippocampus via O-GlcNAcylation of the microglial proteins including the Kv1.3 channel. |
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dc.identifier.bibliographicCitation |
ICKSMCB 2023 |
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dc.identifier.uri |
https://scholarworks.unist.ac.kr/handle/201301/74464 |
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dc.language |
영어 |
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dc.publisher |
Korean Society for Molecular and Cellular Biology |
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dc.title |
Microglial O-GlcNAcylation regulates inhibitory tone in the hippocampus via the Kv1.3 channel |
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dc.type |
Conference Paper |
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dc.date.conferenceDate |
2023-11-06 |
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