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10.1016/j.semnephrol.2008.03.004 http://scihub22266oqcxt.onion/10.1016/j.semnephrol.2008.03.004 18519083!2692584!18519083     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 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       Semin+Nephrol 2008 ; 28 (3): 217-26 Nephropedia Template TP {{tp|p=18519083|t=2008. Dissecting the roles of aquaporins in renal pathophysiology using transgenic mice |pdf=|usr=}}{{18519083}} gab.com Text Dissecting the roles of aquaporins in renal pathophysiology using transgenic mice JO: Semin Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18519083 #FOAvip Transgenic mice lacking renal aquaporins (AQPs), or containing mutated AQPs, have been useful in confirming anticipated AQP functions in renal physiology and in discovering new functions. Mice lacking AQPs 1-4 manifest defects in urinary concentrating ability to different extents. Mechanistic studies have confirmed the involvement of AQP1 in near-isosmolar fluid absorption in the proximal tubule, and in countercurrent multiplication and exchange mechanisms that produce medullary hypertonicity in the antidiuretic kidney. Deletion of AQPs 2-4 impairs urinary concentrating ability by reduction of transcellular water permeability in the collecting duct. Recently created transgenic mouse models of nephrogenic diabetes insipidus produced by AQP2 gene mutation offer exciting possibilities to test new drug therapies. Several unanticipated AQP functions in kidney have been discovered recently that are unrelated to their role in transcellular water transport. There is evidence for involvement of AQP1 in kidney cell migration after renal injury, of AQP7 in renal glycerol clearance, of AQP11 in prevention of renal cystic disease, and possibly of AQP3 in regulation of collecting duct cell proliferation. Future work in renal AQPs will focus on mechanisms responsible for these non-fluid-transporting functions, and on the development of small-molecule AQP inhibitors for use as aquaretic-type diuretics. Twit Text FOAVip Dissecting the roles of aquaporins in renal pathophysiology using transgenic mice ????Semin Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18519083 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18519083 #FOAvip English Wikipedia <ref>{{Cite pmid|18519083}}</ref> Dissecting the roles of aquaporins in renal pathophysiology using transgenic mice #MMPMID18519083 Verkman AS Semin Nephrol 2008[May]; 28 (3): 217-26 PMID18519083show ga Transgenic mice lacking renal aquaporins (AQPs), or containing mutated AQPs, have been useful in confirming anticipated AQP functions in renal physiology and in discovering new functions. Mice lacking AQPs 1-4 manifest defects in urinary concentrating ability to different extents. Mechanistic studies have confirmed the involvement of AQP1 in near-isosmolar fluid absorption in the proximal tubule, and in countercurrent multiplication and exchange mechanisms that produce medullary hypertonicity in the antidiuretic kidney. Deletion of AQPs 2-4 impairs urinary concentrating ability by reduction of transcellular water permeability in the collecting duct. Recently created transgenic mouse models of nephrogenic diabetes insipidus produced by AQP2 gene mutation offer exciting possibilities to test new drug therapies. Several unanticipated AQP functions in kidney have been discovered recently that are unrelated to their role in transcellular water transport. There is evidence for involvement of AQP1 in kidney cell migration after renal injury, of AQP7 in renal glycerol clearance, of AQP11 in prevention of renal cystic disease, and possibly of AQP3 in regulation of collecting duct cell proliferation. Future work in renal AQPs will focus on mechanisms responsible for these non-fluid-transporting functions, and on the development of small-molecule AQP inhibitors for use as aquaretic-type diuretics. |Animals[MESH] |Aquaporin 2/genetics[MESH] |Aquaporins/genetics/*physiology[MESH] |Cell Movement[MESH] |Disease Models, Animal[MESH] |Gene Deletion[MESH] |Glycerol/metabolism[MESH] |Kidney Diseases/genetics/metabolism/*physiopathology/urine[MESH] |Mice[MESH] |Mice, Transgenic[MESH]Dissecting the roles of aquaporins in renal pathophysiology using tran(epmc).pdf DeepDyve Pubget Overpricing