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Journal of Lipid Research
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    • Research Article
      Open Access

      The SARS-CoV2 envelope differs from host cells, exposes procoagulant lipids, and is disrupted in vivo by oral rinses

      Journal of Lipid Research
      Vol. 63Issue 6100208Published online: April 14, 2022
      • Zack Saud
      • Victoria J. Tyrrell
      • Andreas Zaragkoulias
      • Majd B. Protty
      • Evelina Statkute
      • Anzelika Rubina
      • and others
      Cited in Scopus: 9
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        The lipid envelope of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an essential component of the virus; however, its molecular composition is undetermined. Addressing this knowledge gap could support the design of antiviral agents as well as further our understanding of viral-host protein interactions, infectivity, pathogenicity, and innate immune system clearance. Lipidomics revealed that the virus envelope comprised mainly phospholipids (PLs), with some cholesterol and sphingolipids, and with cholesterol/phospholipid ratio similar to lysosomes.
        The SARS-CoV2 envelope differs from host cells, exposes procoagulant lipids, and is disrupted in vivo by oral rinses
      • Research Article
        Open Access

        Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver

        Journal of Lipid Research
        Vol. 62100031Published online: February 5, 2021
        • Mingfeng Xia
        • Preethi Chandrasekaran
        • Shunxing Rong
        • Xiaorong Fu
        • Matthew A. Mitsche
        Cited in Scopus: 0
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          Genetic variants that increase the risk of fatty liver disease and cirrhosis have recently been identified in the proximity of membrane-bound O-acyltransferase domain-containing 7 (MBOAT7). To elucidate the link between these variants and fatty liver disease, we characterized Mboat7 liver-specific KO mice (Mboat7 LSKO). Chow-fed Mboat7 LSKO mice developed fatty livers and associated liver injury. Lipidomic analysis of liver using MS revealed a pronounced reduction in 20-carbon PUFA content in phosphatidylinositols (PIs) but not in other phospholipids.
          Hepatic deletion of Mboat7 (LPIAT1) causes activation of SREBP-1c and fatty liver
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