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- W4281624249 abstract "Abstract Rapid Eye Movement Sleep (REM) maintains brain excitability by modulating the brain Na-K ATPase activity. Earlier, It was reported that REMS deprivation (REMSD) associated elevated NA increases the expression of Na-K ATPase subunit as well as its enzyme activity and that is likely to be the cause of REMSD associated increased brain excitability. The Na-K ATPase is a transmembrane protein present on the cell membrane surface as well as in many organelle membranes. To be responsible for increased excitability, the α1 subunit of the Na-K ATPase must be expressed on the outer surface of the neuronal membrane, which has been confirmed in this study. We used cell impermeable Enz-link-sulfo-NHS-SS biotin that exclusively labels external surface proteins. In this study, we have shown using the Neuro2a cell line that NA (50 µM) increased Na-K ATPase α1 protein abundance on the cell surface by acting on α 1 - as well as β-ARs (AR). It was also observed that Chelerythrine chloride (CC) or KT570, inhibitor of PKC and PKA, respectively blocked the effects. The results not only confirm our previous findings, but they offer molecular level explanations that REMSD-associated elevated NA acting on α- and β-AR increased Na-K ATPase α1 protein expression as well as its translocation on the neuronal membrane through PKC and PKA dependent process." @default.
- W4281624249 created "2022-06-13" @default.
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- W4281624249 date "2022-05-27" @default.
- W4281624249 modified "2023-09-26" @default.
- W4281624249 title "Noradrenaline induced PKC and PKA mediated translocation of Na-K ATPase α1-subunit to the plasma membrane in Neuro-2a cells" @default.
- W4281624249 doi "https://doi.org/10.21203/rs.3.rs-1693865/v1" @default.
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