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10.1681/ASN.2009040421 http://scihub22266oqcxt.onion/10.1681/ASN.2009040421 20075061!2831854!20075061     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\20075061.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Am+Soc+Nephrol 2010 ; 21 (3): 489-97 Nephropedia Template TP {{tp|p=20075061|t=2010. Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1 |pdf=|usr=}}{{20075061}} gab.com Text Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1 JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=20075061 #FOAvip Aberrant activation of the mammalian target of rapamycin (mTOR) pathway occurs in polycystic kidney disease (PKD). mTOR inhibitors, such as rapamycin, are highly effective in several rodent models of PKD, but these models result from mutations in genes other than Pkd1 and Pkd2, which are the primary genes responsible for human autosomal dominant PKD. To address this limitation, we tested the efficacy of rapamycin in a mouse model that results from conditional inactivation of Pkd1. Mosaic deletion of Pkd1 resulted in PKD and replicated characteristic features of human PKD including aberrant mTOR activation, epithelial proliferation and apoptosis, and progressive fibrosis. Treatment with rapamycin was highly effective: It reduced cyst growth, preserved renal function, inhibited epithelial cell proliferation, increased apoptosis of cyst-lining cells, and inhibited fibrosis. These data provide in vivo evidence that rapamycin is effective in a human-orthologous mouse model of PKD. Twit Text FOAVip Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1 ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=20075061 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20075061 #FOAvip English Wikipedia <ref>{{Cite pmid|20075061}}</ref> Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1 #MMPMID20075061 Shillingford JM; Piontek KB; Germino GG; Weimbs T J Am Soc Nephrol 2010[Mar]; 21 (3): 489-97 PMID20075061show ga Aberrant activation of the mammalian target of rapamycin (mTOR) pathway occurs in polycystic kidney disease (PKD). mTOR inhibitors, such as rapamycin, are highly effective in several rodent models of PKD, but these models result from mutations in genes other than Pkd1 and Pkd2, which are the primary genes responsible for human autosomal dominant PKD. To address this limitation, we tested the efficacy of rapamycin in a mouse model that results from conditional inactivation of Pkd1. Mosaic deletion of Pkd1 resulted in PKD and replicated characteristic features of human PKD including aberrant mTOR activation, epithelial proliferation and apoptosis, and progressive fibrosis. Treatment with rapamycin was highly effective: It reduced cyst growth, preserved renal function, inhibited epithelial cell proliferation, increased apoptosis of cyst-lining cells, and inhibited fibrosis. These data provide in vivo evidence that rapamycin is effective in a human-orthologous mouse model of PKD. |Animals[MESH] |Apoptosis/physiology[MESH] |Blood Urea Nitrogen[MESH] |Cell Division/physiology[MESH] |Disease Models, Animal[MESH] |Fibrosis[MESH] |Gene Expression/drug effects[MESH] |Humans[MESH] |Immunosuppressive Agents/pharmacology[MESH] |Intermediate Filament Proteins/genetics[MESH] |Intracellular Signaling Peptides and Proteins/metabolism[MESH] |Kidney Tubules, Collecting/pathology/physiopathology[MESH] |Kidney Tubules, Distal/pathology/physiopathology[MESH] |Mice[MESH] |Mosaicism[MESH] |Nerve Tissue Proteins/genetics[MESH] |Nestin[MESH] |Phenotype[MESH] |Polycystic Kidney Diseases/*genetics/pathology/*physiopathology[MESH] |Protein Serine-Threonine Kinases/metabolism[MESH] |Sirolimus/*pharmacology[MESH] |TOR Serine-Threonine Kinases[MESH]Rapamycin ameliorates PKD resulting from conditional inactivation of P(epmc).pdf DeepDyve Pubget Overpricing