[1] Bhalla V, Hallows KR. Mechanisms of ENaC regulation and clinical implications[J]. J Am Soc Nephrol, 2008, 19(10): 1845–1854. doi:  10.1681/ASN.2008020225
[2] Thomas W, McEneaney V, Harvey BJ. Aldosterone-induced signalling and cation transport in the distal nephron[J]. Steroids, 2008, 73(9-10): 979–984. doi:  10.1016/j.steroids.2008.01.013
[3] Garty H, Palmer LG. Epithelial sodium channels: function, structure, and regulation[J]. Physiol Rev, 1997, 77(2): 359–396. doi:  10.1152/physrev.1997.77.2.359
[4] Bonny O, Rossier BC. Disturbances of Na/K balance: pseudohypoaldosteronism revisited[J]. J Am Soc Nephrol, 2002, 13(9): 2399–2414. doi:  10.1097/01.ASN.0000028641.59030.B2
[5] Lifton RP, Gharavi AG, Geller DS. Molecular mechanisms of human hypertension[J]. Cell, 2001, 104(4): 545–556. doi:  10.1016/S0092-8674(01)00241-0
[6] Schild L. The epithelial sodium channel: from molecule to disease[J]. Rev Physiol Biochem Pharmacol, 2004, 151: 93–107.
[7] Rossier BC. Epithelial sodium channel (ENaC) and the control of blood pressure[J]. Curr Opin Pharmacol, 2014, 15: 33–46. doi:  10.1016/j.coph.2013.11.010
[8] Randrianarison N, Escoubet B, Ferreira C, et al. β-Liddle mutation of the epithelial sodium channel increases alveolar fluid clearance and reduces the severity of hydrostatic pulmonary oedema in mice[J]. J Physiol, 2007, 582(2): 777–788. doi:  10.1113/jphysiol.2007.131078
[9] Van Huysse JW, Amin S, Yang BL, et al. Salt-induced hypertension in a mouse model of Liddle syndrome is mediated by epithelial sodium channels in the brain[J]. Hypertension, 2012, 60(3): 691–696. doi:  10.1161/HYPERTENSIONAHA.112.193045
[10] Bertog M, Cuffe JE, Pradervand S, et al. Aldosterone responsiveness of the Epithelial Sodium Channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome[J]. J Physiol, 2008, 586(2): 459–475. doi:  10.1113/jphysiol.2007.140459
[11] Canessa CM, Schild L, Buell G, et al. Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits[J]. Nature, 1994, 367(6462): 463–467. doi:  10.1038/367463a0
[12] Lingueglia E, Voilley N, Waldmann R, et al. Expression cloning of an epithelial amiloride-sensitive Na+ channel. A new channel type with homologies to Caenorhabditis elegans degenerins[J]. FEBS Lett, 1993, 318(1): 95–99. doi:  10.1016/0014-5793(93)81336-X
[13] Butterworth MB. Regulation of the Epithelial Sodium Channel (ENaC) by membrane trafficking[J]. Biochim Biophys Acta, 2010, 1802(12): 1166–1177. doi:  10.1016/j.bbadis.2010.03.010
[14] Loffing J, Zecevic M, Féraille E, et al. Aldosterone induces rapid apical translocation of ENaC in early portion of renal collecting system: possible role of SGK[J]. Am J Physiol Renal Physiol, 2001, 280(4): F675–F682. doi:  10.1152/ajprenal.2001.280.4.F675
[15] Bubien JK. Epithelial Na+ channel (ENaC), hormones, and hypertension[J]. J Biol Chem, 2010, 285(31): 23527–23531. doi:  10.1074/jbc.R109.025049
[16] Blazer-Yost BL, Esterman MA, Vlahos CJ. Insulin-stimulated trafficking of ENaC in renal cells requires PI 3-kinase activity[J]. Am J Physiol Cell Physiol, 2003, 284(6): C1645–C1653. doi:  10.1152/ajpcell.00372.2002
[17] Ilatovskaya DV, Levchenko V, Brands MW, et al. Cross-talk between insulin and IGF-1 receptors in the cortical collecting duct principal cells: implication for ENaC-mediated Na+ reabsorption[J]. Am J Physiol Renal Physiol, 2015, 308(7): F713–F719. doi:  10.1152/ajprenal.00081.2014
[18] Bernstein BW, Bamburg JR. ADF/cofilin: a functional node in cell biology[J]. Trends Cell Biol, 2010, 20(4): 187–195. doi:  10.1016/j.tcb.2010.01.001
[19] Endo M, Ohashi K, Sasaki Y, et al. Control of growth cone motility and morphology by LIM kinase and Slingshot via phosphorylation and dephosphorylation of cofilin[J]. J Neurosci, 2003, 23(7): 2527–2537. doi:  10.1523/JNEUROSCI.23-07-02527.2003
[20] Van Troys M, Huyck L, Leyman S, et al. Ins and outs of ADF/cofilin activity and regulation[J]. Eur J Cell Biol, 2008, 87(8-9): 649–667. doi:  10.1016/j.ejcb.2008.04.001
[21] Aitken A, Baxter H, Dubois T, et al. Specificity of 14-3-3 isoform dimer interactions and phosphorylation[J]. Biochem Soc Trans, 2002, 30(4): 351–360. doi:  10.1042/bst0300351
[22] Wilker E, Yaffe MB. 14-3-3 Proteins--a focus on cancer and human disease[J]. J Mol Cell Cardiol, 2004, 37(3): 633–642. doi:  10.1016/j.yjmcc.2004.04.015
[23] Yaffe MB. How do 14-3-3 proteins work?-- Gatekeeper phosphorylation and the molecular anvil hypothesis[J]. FEBS Lett, 2002, 513(1): 53–57. doi:  10.1016/S0014-5793(01)03288-4
[24] Liang XB, Butterworth MB, Peters KW, et al. AS160 modulates aldosterone-stimulated epithelial sodium channel forward trafficking[J]. Mol Biol Cell, 2010, 21(12): 2024–2033. doi:  10.1091/mbc.e10-01-0042
[25] Shen YC, Xu WF, You H, et al. FoxO1 inhibits transcription and membrane trafficking of epithelial Na+ channel[J]. J Cell Sci, 2015, 128(19): 3621–3630. doi:  10.1242/jcs.171876
[26] Liang XB, Peters KW, Butterworth MB, et al. 14-3-3 isoforms are induced by aldosterone and participate in its regulation of epithelial sodium channels[J]. J Biol Chem, 2006, 281(24): 16323–16332. doi:  10.1074/jbc.M601360200
[27] Staruschenko A. Regulation of transport in the connecting tubule and cortical collecting duct[J]. Compr Physiol, 2012, 2(2): 1541–1584.
[28] Knobler H, Elson A. Metabolic regulation by protein tyrosine phosphatases[J]. J Biomed Res, 2014, 28(3): 157–168.
[29] Iida K, Matsumoto S, Yahara I. The KKRKK sequence is involved in heat shock-induced nuclear translocation of the 18-kDa actin-binding protein, cofilin[J]. Cell Struct Funct, 1992, 17(1): 39–46. doi:  10.1247/csf.17.39
[30] Duc C, Farman N, Canessa CM, et al. Cell-specific expression of epithelial sodium channel alpha, beta, and gamma subunits in aldosterone-responsive epithelia from the rat: localization by in situ hybridization and immunocytochemistry[J]. J Cell Biol, 1994, 127(6): 1907–1921. doi:  10.1083/jcb.127.6.1907
[31] Volk KA, Sigmund RD, Snyder PM, et al. rENaC is the predominant Na+ channel in the apical membrane of the rat renal inner medullary collecting duct[J]. J Clin Invest, 1995, 96(6): 2748–2757. doi:  10.1172/JCI118344
[32] Masilamani S, Kim GH, Mitchell C, et al. Aldosterone-mediated regulation of ENaC α, β, and γ subunit proteins in rat kidney[J]. J Clin Invest, 1999, 104(7): R19-R23.
[33] Weisz OA, Wang JM, Edinger RS, et al. Non-coordinate regulation of endogenous Epithelial Sodium Channel (ENaC) subunit expression at the apical membrane of A6 cells in response to various transporting conditions[J]. J Biol Chem, 2000, 275(51): 39886–39893. doi:  10.1074/jbc.M003822200
[34] Pochynyuk O, Staruschenko A, Bugaj V, et al. Quantifying RhoA facilitated trafficking of the epithelial Na+ channel toward the plasma membrane with total internal reflection fluorescence-fluorescence recovery after photobleaching[J]. J Biol Chem, 2007, 282(19): 14576–14585. doi:  10.1074/jbc.M701348200
[35] Yip MF, Ramm G, Larance M, et al. CaMKⅡ-mediated phosphorylation of the myosin motor Myo1c is required for insulin-stimulated GLUT4 translocation in adipocytes[J]. Cell Metab, 2008, 8(5): 384–398. doi:  10.1016/j.cmet.2008.09.011