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10.1038/s41467-018-04193-w http://scihub22266oqcxt.onion/10.1038/s41467-018-04193-w C5958119!5958119!29773874     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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=29773874|t=2018. Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment |pdf=|usr=}}{{29773874}} gab.com Text Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29773874 #FOAvip No efficient treatment exists for nephrotic syndrome (NS), a frequent cause of chronic kidney disease. Here we show mutations in six different genes (MAGI2, TNS2, DLC1, CDK20, ITSN1, ITSN2) as causing NS in 17 families with partially treatment-sensitive NS (pTSNS). These proteins interact and we delineate their roles in Rho-like small GTPase (RLSG) activity, and demonstrate deficiency for mutants of pTSNS patients. We find that CDK20 regulates DLC1. Knockdown of MAGI2, DLC1, or CDK20 in cultured podocytes reduces migration rate. Treatment with dexamethasone abolishes RhoA activation by knockdown of DLC1 or CDK20 indicating that steroid treatment in patients with pTSNS and mutations in these genes is mediated by this RLSG module. Furthermore, we discover ITSN1 and ITSN2 as podocytic guanine nucleotide exchange factors for Cdc42. We generate Itsn2-L knockout mice that recapitulate the mild NS phenotype. We, thus, define a functional network of RhoA regulation, thereby revealing potential therapeutic targets. Twit Text FOAVip Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29773874 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29773874 #FOAvip English Wikipedia <ref>{{Cite pmid|29773874}}</ref> Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment #MMPMID29773874 Ashraf S; Kudo H; Rao J; Kikuchi A; Widmeier E; Lawson JA; Tan W; Hermle T; Warejko JK; Shril S; Airik M; Jobst-Schwan T; Lovric S; Braun DA; Gee HY; Schapiro D; Majmundar AJ; Sadowski CE; Pabst WL; Daga A; van der Ven AT; Schmidt JM; Low BC; Gupta AB; Tripathi BK; Wong J; Campbell K; Metcalfe K; Schanze D; Niihori T; Kaito H; Nozu K; Tsukaguchi H; Tanaka R; Hamahira K; Kobayashi Y; Takizawa T; Funayama R; Nakayama K; Aoki Y; Kumagai N; Iijima K; Fehrenbach H; Kari JA; El Desoky S; Jalalah S; Bogdanovic R; Staji? N; Zappel H; Rakhmetova A; Wassmer SR; Jungraithmayr T; Strehlau J; Kumar AS; Bagga A; Soliman NA; Mane SM; Kaufman L; Lowy DR; Jairajpuri MA; Lifton RP; Pei Y; Zenker M; Kure S; Hildebrandt F Nat Commun 2018[]; 9 (ä): ä PMID29773874show ga No efficient treatment exists for nephrotic syndrome (NS), a frequent cause of chronic kidney disease. Here we show mutations in six different genes (MAGI2, TNS2, DLC1, CDK20, ITSN1, ITSN2) as causing NS in 17 families with partially treatment-sensitive NS (pTSNS). These proteins interact and we delineate their roles in Rho-like small GTPase (RLSG) activity, and demonstrate deficiency for mutants of pTSNS patients. We find that CDK20 regulates DLC1. Knockdown of MAGI2, DLC1, or CDK20 in cultured podocytes reduces migration rate. Treatment with dexamethasone abolishes RhoA activation by knockdown of DLC1 or CDK20 indicating that steroid treatment in patients with pTSNS and mutations in these genes is mediated by this RLSG module. Furthermore, we discover ITSN1 and ITSN2 as podocytic guanine nucleotide exchange factors for Cdc42. We generate Itsn2-L knockout mice that recapitulate the mild NS phenotype. We, thus, define a functional network of RhoA regulation, thereby revealing potential therapeutic targets. äMutations in six nephrosis genes delineate a pathogenic pathway amenab(epmc).pdf DeepDyve Pubget Overpricing