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Journal of Lipid Research
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    • Research Article
      Open Access

      Lipid droplet-mitochondria coupling via perilipin 5 augments respiratory capacity but is dispensable for FA oxidation

      Journal of Lipid Research
      Vol. 63Issue 3100172Published online: January 20, 2022
      • Benedikt Kien
      • Stephanie Kolleritsch
      • Natalia Kunowska
      • Christoph Heier
      • Gabriel Chalhoub
      • Anna Tilp
      • and others
      Cited in Scopus: 5
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        Disturbances in lipid homeostasis can cause mitochondrial dysfunction and lipotoxicity. Perilipin 5 (PLIN5) decorates intracellular lipid droplets (LDs) in oxidative tissues and controls triacylglycerol (TG) turnover via its interactions with adipose triglyceride lipase and the adipose triglyceride lipase coactivator, comparative gene identification-58. Furthermore, PLIN5 anchors mitochondria to the LD membrane via the outermost part of the carboxyl terminus. However, the role of this LD-mitochondria coupling (LDMC) in cellular energy catabolism is less established.
        Lipid droplet-mitochondria coupling via perilipin 5 augments respiratory capacity but is dispensable for FA oxidation
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