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Park, Cheol-Min
Synthetic & Medicinal Chemistry Lab
Research Interests
  • Organic synthesis, medicinal chemistry, chemical biology


N-AS-triggered SPMs are direct regulators of microglia in a model of Alzheimer’s disease

DC Field Value Language Lee, Ju Youn ko Han, Seung Hoon ko Park, Min Hee ko Song, Im-Sook ko Choi, Min-Koo ko Yu, Eunsoo ko Park, Cheol-Min ko Kim, Hee-Jin ko Kim, Seung Hyun ko Schuchman, Edward H. ko Jin, Hee Kyung ko Bae, Jae-sung ko 2020-06-08T01:40:00Z - 2020-06-05 ko 2020-05 ko
dc.identifier.citation NATURE COMMUNICATIONS, v.11, no.1 ko
dc.identifier.issn 2041-1723 ko
dc.identifier.uri -
dc.description.abstract Sphingosine kinase1 (SphK1) is an acetyl-CoA dependent acetyltransferase which acts on cyclooxygenase2 (COX2) in neurons in a model of Alzheimer's disease (AD). However, the mechanism underlying this activity was unexplored. Here we show that N-acetyl sphingosine (N-AS) is first generated by acetyl-CoA and sphingosine through SphK1. N-AS then acetylates serine 565 (S565) of COX2, and the N-AS-acetylated COX2 induces the production of specialized pro-resolving mediators (SPMs). In a mouse model of AD, microglia show a reduction in N-AS generation, leading to decreased acetyl-S565 COX2 and SPM production. Treatment with N-AS increases acetylated COX2 and N-AS-triggered SPMs in microglia of AD mice, leading to resolution of neuroinflammation, an increase in microglial phagocytosis, and improved memory. Taken together, these results identify a role of N-AS in the dysfunction of microglia in AD. Neuronal sphingosine kinase 1 (SphK1) acetylates COX2 which is needed for microglial phagocytosis activity, and release of pro-resolving mediators (SPMs) from neurons. Here the authors examine how SphK1-mediates COX2 acetylation, and how this leads to increased secretion of SPMs from neurons in the context of Alzheimer's disease models. ko
dc.language 영어 ko
dc.title N-AS-triggered SPMs are direct regulators of microglia in a model of Alzheimer’s disease ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-85084501724 ko
dc.identifier.wosid 000537248100001 ko
dc.type.rims ART ko
dc.identifier.doi 10.1038/s41467-020-16080-4 ko
dc.identifier.url ko
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