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10.1371/journal.pone.0119142 http://scihub22266oqcxt.onion/10.1371/journal.pone.0119142 C4370407!4370407!25799508     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (3): ä Nephropedia Template TP {{tp|p=25799508|t=2015. Selective Dicer Suppression in the Kidney Alters GSK3?/?-Catenin Pathways Promoting a Glomerulocystic Disease |pdf=|usr=}}{{25799508}} gab.com Text Selective Dicer Suppression in the Kidney Alters GSK3 / -Catenin Pathways Promoting a Glomerulocystic Disease JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799508 #FOAvip Dicer is a crucial enzyme for the maturation of miRNAs. Mutations in the Dicer gene are highly associated with Pleuro Pulmonary Blastoma-Family Dysplasia Syndrome (PPB-FDS, OMIM 601200), recently proposed to be renamed Dicer syndrome. Aside from the pulmonary phenotype (blastoma), renal nephroma and thyroid goiter are frequently part of Dicer syndrome. To investigate the renal phenotype, conditional knockout (cKO) mice for Dicer in Pax8 expressing cells were generated. Dicer cKO mice progressively develop a glomerulocystic phenotype coupled with urinary concentration impairment, proteinuria and severe renal failure. Higher cellular turnover of the parietal cells of Bowman?s capsule precedes the development of the cysts and the primary cilium progressively disappears with cyst-enlargement. Upregulation of GSK3? precedes the development of the glomerulocystic phenotype. Downregulation of ?-catenin in the renal cortex and its cytosolic removal in the cells lining the cysts may be associated with observed accumulation of GSK3?. Alterations of ?-catenin regulating pathways could promote cystic degeneration as in other models. Thus, miRNAs are fundamental in preserving renal morphology and function. Alteration of the GSK3?/?-catenin pathway could be a crucial mechanism linking miRNA dysregulation and the development of a glomerulocystic disease. Twit Text FOAVip Selective Dicer Suppression in the Kidney Alters GSK3 / -Catenin Pathways Promoting a Glomerulocystic Disease ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799508 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25799508 #FOAvip English Wikipedia <ref>{{Cite pmid|25799508}}</ref> Selective Dicer Suppression in the Kidney Alters GSK3?/?-Catenin Pathways Promoting a Glomerulocystic Disease #MMPMID25799508 Iervolino A; Trepiccione F; Petrillo F; Spagnuolo M; Scarfò M; Frezzetti D; De Vita G; De Felice M; Capasso G PLoS One 2015[]; 10 (3): ä PMID25799508show ga Dicer is a crucial enzyme for the maturation of miRNAs. Mutations in the Dicer gene are highly associated with Pleuro Pulmonary Blastoma-Family Dysplasia Syndrome (PPB-FDS, OMIM 601200), recently proposed to be renamed Dicer syndrome. Aside from the pulmonary phenotype (blastoma), renal nephroma and thyroid goiter are frequently part of Dicer syndrome. To investigate the renal phenotype, conditional knockout (cKO) mice for Dicer in Pax8 expressing cells were generated. Dicer cKO mice progressively develop a glomerulocystic phenotype coupled with urinary concentration impairment, proteinuria and severe renal failure. Higher cellular turnover of the parietal cells of Bowman?s capsule precedes the development of the cysts and the primary cilium progressively disappears with cyst-enlargement. Upregulation of GSK3? precedes the development of the glomerulocystic phenotype. Downregulation of ?-catenin in the renal cortex and its cytosolic removal in the cells lining the cysts may be associated with observed accumulation of GSK3?. Alterations of ?-catenin regulating pathways could promote cystic degeneration as in other models. Thus, miRNAs are fundamental in preserving renal morphology and function. Alteration of the GSK3?/?-catenin pathway could be a crucial mechanism linking miRNA dysregulation and the development of a glomerulocystic disease. äSelective Dicer Suppression in the Kidney Alters GSK3?/?-Catenin Pathw(epmc).pdf DeepDyve Pubget Overpricing