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      Lipid raft proteome reveals a novel function of ATP synthase in HDL uptake

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      https://www.riss.kr/link?id=E1064360

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      Lipid rafts concentrate many cellular proteins to mediate different cellular events such as signal transduction, cholesterol homeostasis, cellular migration, pathogen invasion, and endocytosis. In order to identify ubiquitous lipid raft marker proteins, lipid rafts were isolated from different rat organs such as liver, cerebrum, kidney, and testis, and analyzed in two-dimensional gel electrophoresis. Many proteins were found in all lipid rafts and annotated by electrospray ionization tandem mass spectrometry(ESI-MS/MS). Among them, ATP synthase α and β were further proven to be enriched in lipid rafts, and then localized on cellular surface. High density lipoprotein(HDL) uptake was dramatically decreased after treating adipocytes with anti-ATP synthase β antibody, supporting that ATP synthase complex is a HDL receptor. Moreover, the HDL uptake was completely abolished upon cellular exposure to methyl-β-cyclodextrin that is a lipid raft destroyer. Taken all these data, we conclude that lipid raft ATP synthase complex is required for HDL uptake in adipocyte.
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      Lipid rafts concentrate many cellular proteins to mediate different cellular events such as signal transduction, cholesterol homeostasis, cellular migration, pathogen invasion, and endocytosis. In order to identify ubiquitous lipid raft marker protein...

      Lipid rafts concentrate many cellular proteins to mediate different cellular events such as signal transduction, cholesterol homeostasis, cellular migration, pathogen invasion, and endocytosis. In order to identify ubiquitous lipid raft marker proteins, lipid rafts were isolated from different rat organs such as liver, cerebrum, kidney, and testis, and analyzed in two-dimensional gel electrophoresis. Many proteins were found in all lipid rafts and annotated by electrospray ionization tandem mass spectrometry(ESI-MS/MS). Among them, ATP synthase α and β were further proven to be enriched in lipid rafts, and then localized on cellular surface. High density lipoprotein(HDL) uptake was dramatically decreased after treating adipocytes with anti-ATP synthase β antibody, supporting that ATP synthase complex is a HDL receptor. Moreover, the HDL uptake was completely abolished upon cellular exposure to methyl-β-cyclodextrin that is a lipid raft destroyer. Taken all these data, we conclude that lipid raft ATP synthase complex is required for HDL uptake in adipocyte.

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