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10.1681/ASN.2013101102 http://scihub22266oqcxt.onion/10.1681/ASN.2013101102 C4243352!4243352!24854272     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2014 ; 25 (12): 2822-34 Nephropedia Template TP {{tp|p=24854272|t=2014. Renal Phosphate Wasting in the Absence of Adenylyl Cyclase 6 |pdf=|usr=}}{{24854272}} gab.com Text Renal Phosphate Wasting in the Absence of Adenylyl Cyclase 6 JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24854272 #FOAvip Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) enhance phosphate excretion by the proximal tubule of the kidney by retrieval of the sodium-dependent phosphate transporters (Npt2a and Npt2c) from the apical plasma membrane. PTH activates adenylyl cyclase (AC) through PTH 1 receptors and stimulates the cAMP/PKA signaling pathway. However, the precise role and isoform(s) of AC in phosphate homeostasis are not known. We report here that mice lacking AC6 (AC6?/?) have increased plasma PTH and FGF-23 levels compared with wild-type (WT) mice but comparable plasma phosphate concentrations. Acute activation of the calcium-sensing receptor or feeding a zero phosphate diet almost completely suppressed plasma PTH levels in both AC6?/? and WT mice, indicating a secondary cause for hyperparathyroidism. Pharmacologic blockade of FGF receptors resulted in a comparable increase in plasma phosphate between genotypes, whereas urinary phosphate remained significantly higher in AC6?/? mice. Compared with WT mice, AC6?/? mice had reduced renal Npt2a and Npt2c protein abundance, with approximately 80% of Npt2a residing in lysosomes. WT mice responded to exogenous PTH with redistribution of Npt2a from proximal tubule microvilli to intracellular compartments and lysosomes alongside a PTH-induced dose?response relationship for fractional phosphate excretion and urinary cAMP excretion. These responses were absent in AC6?/? mice. In conclusion, AC6 in the proximal tubule modulates cAMP formation, Npt2a trafficking, and urinary phosphate excretion, which are highlighted by renal phosphate wasting in AC6?/? mice. Twit Text FOAVip Renal Phosphate Wasting in the Absence of Adenylyl Cyclase 6 ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24854272 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24854272 #FOAvip English Wikipedia <ref>{{Cite pmid|24854272}}</ref> Renal Phosphate Wasting in the Absence of Adenylyl Cyclase 6 #MMPMID24854272 Fenton RA; Murray F; Dominguez Rieg JA; Tang T; Levi M; Rieg T J Am Soc Nephrol 2014[Dec]; 25 (12): 2822-34 PMID24854272show ga Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) enhance phosphate excretion by the proximal tubule of the kidney by retrieval of the sodium-dependent phosphate transporters (Npt2a and Npt2c) from the apical plasma membrane. PTH activates adenylyl cyclase (AC) through PTH 1 receptors and stimulates the cAMP/PKA signaling pathway. However, the precise role and isoform(s) of AC in phosphate homeostasis are not known. We report here that mice lacking AC6 (AC6?/?) have increased plasma PTH and FGF-23 levels compared with wild-type (WT) mice but comparable plasma phosphate concentrations. Acute activation of the calcium-sensing receptor or feeding a zero phosphate diet almost completely suppressed plasma PTH levels in both AC6?/? and WT mice, indicating a secondary cause for hyperparathyroidism. Pharmacologic blockade of FGF receptors resulted in a comparable increase in plasma phosphate between genotypes, whereas urinary phosphate remained significantly higher in AC6?/? mice. Compared with WT mice, AC6?/? mice had reduced renal Npt2a and Npt2c protein abundance, with approximately 80% of Npt2a residing in lysosomes. WT mice responded to exogenous PTH with redistribution of Npt2a from proximal tubule microvilli to intracellular compartments and lysosomes alongside a PTH-induced dose?response relationship for fractional phosphate excretion and urinary cAMP excretion. These responses were absent in AC6?/? mice. In conclusion, AC6 in the proximal tubule modulates cAMP formation, Npt2a trafficking, and urinary phosphate excretion, which are highlighted by renal phosphate wasting in AC6?/? mice. äRenal Phosphate Wasting in the Absence of Adenylyl Cyclase 6 (epmc).pdf DeepDyve Pubget Overpricing