Böhmer C, Palmada M, Kenngott C, Lindner R, Klaus F, Laufer J, Lang F
Department of Physiology I, University of Tübingen, Germany.
FEBS Lett. 2007 Dec 11;581(29):5586-90. doi: 10.1016/j.febslet.2007.11.006. Epub 2007 Nov 20.
Epithelial calcium (re)absorption is mediated by TRPV5 and TRPV6 channels. TRPV5 is modulated by the SGK1 kinase, a process requiring the PDZ-domain containing scaffold protein NHERF2. The present study explored whether TRPV6 is similarly regulated by SGKs and the scaffold proteins NHERF1/2. In Xenopus oocytes, SGKs activate TRPV6 by increasing its plasma membrane abundance. Deletion of the putative PDZ binding motif on TRPV6 did not abolish channel activation by SGKs. Furthermore, coexpression of neither NHERF1 nor NHERF2 affected TRPV6 or potentiated the SGKs stimulating effect. The present observations disclose a novel TRPV6 regulatory mechanism which presumably participates in calcium homeostasis.
上皮钙(再)吸收由TRPV5和TRPV6通道介导。TRPV5受SGK1激酶调节,这一过程需要含PDZ结构域的支架蛋白NHERF2。本研究探讨了TRPV6是否同样受SGKs和支架蛋白NHERF1/2的调节。在非洲爪蟾卵母细胞中,SGKs通过增加TRPV6的质膜丰度来激活它。TRPV6上假定的PDZ结合基序的缺失并没有消除SGKs对通道的激活作用。此外,NHERF1和NHERF2的共表达既不影响TRPV6,也不增强SGKs的刺激作用。本研究结果揭示了一种新的TRPV6调节机制,该机制可能参与钙稳态。