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10.1038/nm.4287 http://scihub22266oqcxt.onion/10.1038/nm.4287 C5603285!5603285!28218918     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Med 2017 ; 23 (4): 429-38 Nephropedia Template TP {{tp|p=28218918|t=2017. Transgenic Expression of Human APOL1 Risk Variants in Podocytes Induces Kidney Disease in Mice |pdf=|usr=}}{{28218918}} gab.com Text Transgenic Expression of Human APOL1 Risk Variants in Podocytes Induces Kidney Disease in Mice JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=28218918 #FOAvip African-Americans have an increased risk of developing chronic and end-stage kidney disease, with much of it attributed to two common genetic variants in the APOL1 gene, termed G1 and G2. Direct evidence demonstrating that these APOL1 risk alleles are pathogenic is still lacking as the APOL1 gene is only present in some primates and humans; thus experimental proof of causality of these risk alleles for renal disease has been challenging. Here, we generated mice with podocyte-specific inducible expression of the APOL1 reference allele (termed G0) or each of the risk alleles (G1 or G2). We show that mice with podocyte-specific expression of either APOL1 risk allele, but not the G0 allele, develop functional (albuminuria, azotemia), structural (foot process effacement and glomerulosclerosis) and molecular (gene expression) changes that closely resemble the human kidney disease. Disease development was cell-type specific, and likely reversible, and the severity correlated with the level of expression of the risk allele. We further found that expression of the APOL1 risk alleles interferes with endosomal trafficking and blocks autophagic flux, leading ultimately to inflammatory-mediated podocyte death and glomerular scarring. In summary, this is the first in vivo demonstration that expression of APOL1 risk alleles are causal for altered podocyte function and glomerular disease. Twit Text FOAVip Transgenic Expression of Human APOL1 Risk Variants in Podocytes Induces Kidney Disease in Mice ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=28218918 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28218918 #FOAvip English Wikipedia <ref>{{Cite pmid|28218918}}</ref> Transgenic Expression of Human APOL1 Risk Variants in Podocytes Induces Kidney Disease in Mice #MMPMID28218918 Beckerman P; Bi-Karchin J; Park ASD; Qiu C; Dummer PD; Soomro I; Boustany-Kari CM; Pullen SS; Miner JH; Hu CAA; Rohacs T; Inoue K; Ishibe S; Saleem MA; Palmer MB; Cuervo AM; Kopp JB; Susztak K Nat Med 2017[Apr]; 23 (4): 429-38 PMID28218918show ga African-Americans have an increased risk of developing chronic and end-stage kidney disease, with much of it attributed to two common genetic variants in the APOL1 gene, termed G1 and G2. Direct evidence demonstrating that these APOL1 risk alleles are pathogenic is still lacking as the APOL1 gene is only present in some primates and humans; thus experimental proof of causality of these risk alleles for renal disease has been challenging. Here, we generated mice with podocyte-specific inducible expression of the APOL1 reference allele (termed G0) or each of the risk alleles (G1 or G2). We show that mice with podocyte-specific expression of either APOL1 risk allele, but not the G0 allele, develop functional (albuminuria, azotemia), structural (foot process effacement and glomerulosclerosis) and molecular (gene expression) changes that closely resemble the human kidney disease. Disease development was cell-type specific, and likely reversible, and the severity correlated with the level of expression of the risk allele. We further found that expression of the APOL1 risk alleles interferes with endosomal trafficking and blocks autophagic flux, leading ultimately to inflammatory-mediated podocyte death and glomerular scarring. In summary, this is the first in vivo demonstration that expression of APOL1 risk alleles are causal for altered podocyte function and glomerular disease. äTransgenic Expression of Human APOL1 Risk Variants in Podocytes Induce(epmc).pdf DeepDyve Pubget Overpricing