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| Untersuchte Arbeit: Seite: 45, Zeilen: 6-12 |
Quelle: Lang et al 2006 Seite(n): 1156, Zeilen: r.col: 16ff |
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| As shown in Xenopus oocytes, SGK1 and SGK3 activate the renal epithelial Ca2+ channel TRPV5 by enhancing channel abundance in the plasma membrane, an effect again requiring cooperation with NHERF2 (Embark HM. et al., (2004) Cell Physiol Biochem; Palmada M. et al., (2005) Cell Physiol Biochem). The TRPV5 C-tail interacts in a Ca2+- independent manner with NHERF2. Deletion of the second, but not the first, PDZ domain in NHERF2 abrogates the stimulating effect of SGK1 on TRPV5 protein abundance (Palmada M. et al., (2005) Cell Physiol Biochem). | As shown in Xenopus oocytes, SGK1 and SGK3 activate the renal epithelial Ca2+ channel TRPV5 by enhancing channel abundance in the plasma membrane, an effect again requiring cooperation with NHERF2 (101, 246). The TRPV5 C-tail interacts in a Ca2+-independent manner with NHERF2. Deletion of the second, but not the first, PDZ domain in NHERF2 abrogates the stimulating effect of SGK1 on TRPV5 protein abundance (246).
101. Embark HM, Setiawan I, Poppendieck S, van de Graaf SF, Boehmer C, Palmada M, Wieder T, Gerstberger R, Cohen P, Yun CC, Bindels RJ, and Lang F. Regulation of the epithelial Ca2+ channel TRPV5 by the NHE regulating factor NHERF2 and the serum and glucocorticoid inducible kinase isoforms SGK1 and SGK3 expressed in Xenopus oocytes. Cell Physiol Biochem 14: 203–212, 2004. 246. Palmada M, Poppendieck S, Embark HM, van de Graaf SF, Boehmer C, Bindels RJ, and Lang F. Requirement of PDZ domains for the stimulation of the epithelial Ca2+ channel TRPV5 by the NHE regulating factor NHERF2 and the serum and glucocorticoid inducible kinase SGK1. Cell Physiol Biochem 15: 175–182, 2005. |
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