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| Untersuchte Arbeit: Seite: 20, Zeilen: 1ff (entire page) |
Quelle: Rajamanickam 2007 Seite(n): 13, Zeilen: 1ff |
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Figure 5. Schematic model showing molecular mechanisms of ENaC regulation by SGK1. Aldosterone binding to the mineralocorticoid receptor (MR) can stimulates the transcription of SGK1 as well as ENaC. Insulin or Insulin-like growth factor (IGF-1) phosphorylates SGK1 at Ser422 through PI3 kinase and PDK2/H-motify kinase signaling cascade. Activated (phosphorylated) SGK1 enhances ENaC plasma membrane abundance either directly by phosphorylating the channel or indirectly by inhibiting the downregulating effect of the ubiquitin ligase Nedd4-2. |
Figure 1 Schematic model showing molecular mechanisms of ENaC regulation by SGK1. Aldosterone binding to the mineralocorticoid receptor (MR) can stimulates the transcription of SGK1 as well as ENaC. Insulin or Insulin-like growth factor (IGF-1) phosphorylates SGK1 at Ser422 through PI3 kinase and PDK2/H-motify kinase signaling cascade. Activated (phosphorylated) SGK1 enhances ENaC plasma membrane abundance either directly by phosphorylating the channel or indirectly by inhibiting the downregulating effect of the ubiquitin ligase Nedd4-2. |
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