Relationship of the Aldosterone-lnduced Protein, GP7O, to the Conductive Na(cid:1) Channel1

Although one of the primary effects of aldosterone is to increase apical membrane Na(cid:1) conductance, as yet none of the proteins induced by the hormone in renal epithelia have been shown to be related to the conductive Na(cid:1) channel. Because the toad un-nary bladder aldosterone-induced glycoprotein, GP7O, has recently been localized to the apical surface of this Na(cid:1) transporting epithelium, whether GP7O is associated (cid:1) ith the Na(cid:1) channel was exam-med. The spe(cid:1),uiicities monoclonal used characterize GP7O polyclonal against the purified bovine renal papillary a central role Na(cid:1) channel modulation.

[1]  P. Law,et al.  Induction of citrate synthase by aldosterone in the rat kidney , 1978, The Journal of Membrane Biology.

[2]  A. Truscello,et al.  Thyroid hormone antagonizes an aldosterone-induced protein: A candidate mediator for the late mineralocorticoid response , 2005, The Journal of Membrane Biology.

[3]  D. Fambrough,et al.  Pre-translational regulation of the (Na+ + K+)-ATPase in response to demand for ion transport in cultured chicken skeletal muscle. , 1990, The Journal of biological chemistry.

[4]  M. Cox,et al.  Aldosterone-induced glycoproteins: further characterization. , 1989, Journal of steroid biochemistry.

[5]  D. Benos,et al.  Immunochemical localization of amiloride-sensitive sodium channels in sodium-transporting epithelia. , 1989, Journal of cell science.

[6]  J. Wade,et al.  Aldosterone-induced proteins: purification and localization of GP65,70. , 1989, The American journal of physiology.

[7]  K. Geering,et al.  Aldosterone-induced glycoproteins: electrophysiological-biochemical correlation. , 1988, Biochimica et biophysica acta.

[8]  U. Steckelings,et al.  Complex physiological and biochemical action of aldosterone in toad urinary bladder and mammalian renal collecting duct cells. , 1987, Renal physiology.

[9]  K. Kawakami,et al.  The transmembrane segment of the human Na,K-ATPase beta-subunit acts as the membrane incorporation signal. , 1988, Journal of biochemistry.

[10]  I. Edelman,et al.  Dual action of aldosterone on toad bladder: Na+ permeability and Na+ pump modulation. , 1984, The American journal of physiology.

[11]  A. Owen,et al.  Steroid-induced protein synthesis in giant-toad (Bufo marinus) urinary bladders. Correlation with natriferic activity. , 1984, The Biochemical journal.

[12]  D. Fanestil,et al.  Modification of carboxyl of Na+ channel inhibits aldosterone action on Na+ transport. , 1983, The American journal of physiology.

[13]  B. Blazer-Yost,et al.  Aldosterone-induced proteins in renal epithelia. , 1982, Biochimica et biophysica acta.

[14]  K. Geering,et al.  Hormonal regulation of (Na+,K+)-ATPase biosynthesis in the toad bladder. Effect of aldosterone and 3,5,3'-triiodo-L-thyronine. , 1982, The Journal of biological chemistry.

[15]  P. L. Jørgensen.  Mechanism of the Na+, K+ pump. Protein structure and conformations of the pure (Na+ +K+)-ATPase. , 1982, Biochimica et biophysica acta.

[16]  R. Snart.  The two stage nature of the aldosterone response. , 1972, Journal of steroid biochemistry.

[17]  J. Porath,et al.  Chemical Coupling of Peptides and Proteins to Polysaccharides by Means of Cyanogen Halides , 1967, Nature.