Human immunodeficiency virus protein Tat induces oligodendrocyte injury by enhancing outward K⁺ current conducted by K_V1.3

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• 作者：Han Liu^a ; Jianuo Liu^a ; Enquan Xu^a ; Guihua Tu^a ; Minglei Guo^a ; Shangdong Liang^b ; Huangui Xiong^a ; ^{hxiong@unmc.edu}
• 关键词：cART ; combination antiretroviral therapy ; GxTx ; Guangxi toxin ; HIV-1 ; human immunodeficiency virus type 1 ; HAND ; HIV-1-associated neurocognitive disorders ; MgTx ; Margatoxin ; Ol ; oligodendrocyte ; PAP ; 5-(4-phenoxybutoxy) psoralen ; PVD ; Pervanadate
• 刊名：Neurobiology of Disease
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：97
• 期：part_PA
• 页码：1-10
• 全文大小：1644 K
• 卷排序：97

文摘

HIV-1 brain infection causes cerebral white matter damage and the underlying mechanisms are not fully understood. Toxic virus trans-activator of transcription (Tat) protein can be released to the extracellular space during disease. Tat increases Kv1.3 current in rat oligodendrocytes via downregulation of channel protein phosphorylation. Tat-induced oligodendrocyte and myelin injury can be blocked by specific Kv1.3 antagonists or by knockdown of Kv1.3 gene.