Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease
Sphingosine kinase (SphK) converts sphingosine into lipids, and is implicated in inflammation. Here the authors show that SphK1 functions as an acetyltransferase, regulates microglial phagocytosis and is reduced in a model of Alzheimer’s Disease, such that its restoration ameliorates pathology
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2018-04-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-018-03674-2 |
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doaj-98b2523a54044a18a2edc80a341e17562021-05-11T09:30:42ZengNature Publishing GroupNature Communications2041-17232018-04-019111410.1038/s41467-018-03674-2Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s DiseaseJu Youn Lee0Seung Hoon Han1Min Hee Park2Bosung Baek3Im-Sook Song4Min-Koo Choi5Yoh Takuwa6Hoon Ryu7Seung Hyun Kim8Xingxuan He9Edward H. Schuchman10Jae-Sung Bae11Hee Kyung Jin12Stem Cell Neuroplasticity Research Group, Kyungpook National UniversityStem Cell Neuroplasticity Research Group, Kyungpook National UniversityStem Cell Neuroplasticity Research Group, Kyungpook National UniversityStem Cell Neuroplasticity Research Group, Kyungpook National UniversityCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Kyungpook National UniversityCollege of Pharmacy, Dankook UniversityDepartment of Physiology, Kanazawa University School of MedicineVA Boston Healthcare System, Department of Neurology and Boston University Alzheimer’s Disease Centre, Boston University School of MedicineDepartment of Neurology, Hanyang University College of MedicineDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount SinaiStem Cell Neuroplasticity Research Group, Kyungpook National UniversityStem Cell Neuroplasticity Research Group, Kyungpook National UniversitySphingosine kinase (SphK) converts sphingosine into lipids, and is implicated in inflammation. Here the authors show that SphK1 functions as an acetyltransferase, regulates microglial phagocytosis and is reduced in a model of Alzheimer’s Disease, such that its restoration ameliorates pathologyhttps://doi.org/10.1038/s41467-018-03674-2 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ju Youn Lee Seung Hoon Han Min Hee Park Bosung Baek Im-Sook Song Min-Koo Choi Yoh Takuwa Hoon Ryu Seung Hyun Kim Xingxuan He Edward H. Schuchman Jae-Sung Bae Hee Kyung Jin |
spellingShingle |
Ju Youn Lee Seung Hoon Han Min Hee Park Bosung Baek Im-Sook Song Min-Koo Choi Yoh Takuwa Hoon Ryu Seung Hyun Kim Xingxuan He Edward H. Schuchman Jae-Sung Bae Hee Kyung Jin Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease Nature Communications |
author_facet |
Ju Youn Lee Seung Hoon Han Min Hee Park Bosung Baek Im-Sook Song Min-Koo Choi Yoh Takuwa Hoon Ryu Seung Hyun Kim Xingxuan He Edward H. Schuchman Jae-Sung Bae Hee Kyung Jin |
author_sort |
Ju Youn Lee |
title |
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease |
title_short |
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease |
title_full |
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease |
title_fullStr |
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease |
title_full_unstemmed |
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease |
title_sort |
neuronal sphk1 acetylates cox2 and contributes to pathogenesis in a model of alzheimer’s disease |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2018-04-01 |
description |
Sphingosine kinase (SphK) converts sphingosine into lipids, and is implicated in inflammation. Here the authors show that SphK1 functions as an acetyltransferase, regulates microglial phagocytosis and is reduced in a model of Alzheimer’s Disease, such that its restoration ameliorates pathology |
url |
https://doi.org/10.1038/s41467-018-03674-2 |
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