Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1096/fj.201800435R http://scihub22266oqcxt.onion/10.1096/fj.201800435R 30252533!6338637!30252533     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       FASEB+J 2019 ; 33 (2): 2156-2170 Nephropedia Template TP {{tp|p=30252533|t=2019. Urinary concentrating defect in mice lacking Epac1 or Epac2 |pdf=|usr=}}{{30252533}} gab.com Text Urinary concentrating defect in mice lacking Epac1 or Epac2 JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=30252533 #FOAvip cAMP is a universal second messenger regulating a plethora of processes in the kidney. Two downstream effectors of cAMP are PKA and exchange protein directly activated by cAMP (Epac), which, unlike PKA, is often linked to elevation of [Ca(2+)](i). While both Epac isoforms (Epac1 and Epac2) are expressed along the nephron, their relevance in the kidney remains obscure. We combined ratiometric calcium imaging with quantitative immunoblotting, immunofluorescent confocal microscopy, and balance studies in mice lacking Epac1 or Epac2 to determine the role of Epac in renal water-solute handling. Epac1(-/-) and Epac2(-/-) mice developed polyuria despite elevated arginine vasopressin levels. We did not detect major deficiencies in arginine vasopressin [Ca(2+)](i) signaling in split-opened collecting ducts or decreases in aquaporin water channel type 2 levels. Instead, sodium-hydrogen exchanger type 3 levels in the proximal tubule were dramatically reduced in Epac1(-/-) and Epac2(-/-) mice. Water deprivation revealed persisting polyuria, impaired urinary concentration ability, and augmented urinary excretion of Na(+) and urea in both mutant mice. In summary, we report a nonredundant contribution of Epac isoforms to renal function. Deletion of Epac1 and Epac2 decreases sodium-hydrogen exchanger type 3 expression in the proximal tubule, leading to polyuria and osmotic diuresis.-Cherezova, A., Tomilin, V., Buncha, V., Zaika, O., Ortiz, P. A., Mei, F., Cheng, X., Mamenko, M., Pochynyuk, O. Urinary concentrating defect in mice lacking Epac1 or Epac2. Twit Text FOAVip Urinary concentrating defect in mice lacking Epac1 or Epac2 ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=30252533 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30252533 #FOAvip English Wikipedia <ref>{{Cite pmid|30252533}}</ref> Urinary concentrating defect in mice lacking Epac1 or Epac2 #MMPMID30252533 Cherezova A; Tomilin V; Buncha V; Zaika O; Ortiz PA; Mei F; Cheng X; Mamenko M; Pochynyuk O FASEB J 2019[Feb]; 33 (2): 2156-2170 PMID30252533show ga cAMP is a universal second messenger regulating a plethora of processes in the kidney. Two downstream effectors of cAMP are PKA and exchange protein directly activated by cAMP (Epac), which, unlike PKA, is often linked to elevation of [Ca(2+)](i). While both Epac isoforms (Epac1 and Epac2) are expressed along the nephron, their relevance in the kidney remains obscure. We combined ratiometric calcium imaging with quantitative immunoblotting, immunofluorescent confocal microscopy, and balance studies in mice lacking Epac1 or Epac2 to determine the role of Epac in renal water-solute handling. Epac1(-/-) and Epac2(-/-) mice developed polyuria despite elevated arginine vasopressin levels. We did not detect major deficiencies in arginine vasopressin [Ca(2+)](i) signaling in split-opened collecting ducts or decreases in aquaporin water channel type 2 levels. Instead, sodium-hydrogen exchanger type 3 levels in the proximal tubule were dramatically reduced in Epac1(-/-) and Epac2(-/-) mice. Water deprivation revealed persisting polyuria, impaired urinary concentration ability, and augmented urinary excretion of Na(+) and urea in both mutant mice. In summary, we report a nonredundant contribution of Epac isoforms to renal function. Deletion of Epac1 and Epac2 decreases sodium-hydrogen exchanger type 3 expression in the proximal tubule, leading to polyuria and osmotic diuresis.-Cherezova, A., Tomilin, V., Buncha, V., Zaika, O., Ortiz, P. A., Mei, F., Cheng, X., Mamenko, M., Pochynyuk, O. Urinary concentrating defect in mice lacking Epac1 or Epac2. |Animals[MESH] |Aquaporin 2/metabolism[MESH] |Arginine Vasopressin/metabolism[MESH] |Calcium Signaling[MESH] |Diuresis[MESH] |Gene Deletion[MESH] |Guanine Nucleotide Exchange Factors/*genetics[MESH] |Kidney Concentrating Ability/*genetics[MESH] |Kidney/metabolism/physiology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Osmosis[MESH] |Polyuria/genetics[MESH]Urinary concentrating defect in mice lacking Epac1 or Epac2 (epmc).pdf DeepDyve Pubget Overpricing