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10.1111/cts.12480 http://scihub22266oqcxt.onion/10.1111/cts.12480 C5593168!5593168!28689374     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       Clin+Transl+Sci 2017 ; 10 (5): 412-20 Nephropedia Template TP {{tp|p=28689374|t=2017. Identification of OAT1/OAT3 as Contributors to Cisplatin Toxicity |pdf=|usr=}}{{28689374}} gab.com Text Identification of OAT1/OAT3 as Contributors to Cisplatin Toxicity JO: Clin Transl Sci http://www.kidney.de/pget.php?&tw=1&pmid=28689374 #FOAvip Cisplatin is among the most widely used anticancer drugs and known to cause a dose?limiting nephrotoxicity, which is partially dependent on the renal uptake carrier OCT2. We here report a previously unrecognized, OCT2?independent pathway of cisplatin?induced renal injury that is mediated by the organic anion transporters OAT1 and OAT3. Using transporter?deficient mouse models, we found that this mechanism regulates renal uptake of a mercapturic acid metabolite of cisplatin that acts as a precursor of a potent nephrotoxin. The function of these two transport systems can be simultaneously inhibited by the tyrosine kinase inhibitor nilotinib through noncompetitive mechanisms, without compromising the anticancer properties of cisplatin. Collectively, our findings reveal a novel pathway that explains the fundamental basis of cisplatin?induced nephrotoxicity, with potential implications for its therapeutic management. Twit Text FOAVip Identification of OAT1/OAT3 as Contributors to Cisplatin Toxicity ????Clin Transl Sci http://www.kidney.de/pget.php?&tw=1&pmid=28689374 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28689374 #FOAvip English Wikipedia <ref>{{Cite pmid|28689374}}</ref> Identification of OAT1/OAT3 as Contributors to Cisplatin Toxicity #MMPMID28689374 Hu S; Leblanc A; Gibson A; Hong K; Kim J; Janke L; Li L; Vasilyeva A; Finkelstein D; Sprowl J; Sweet D; Schlatter E; Ciarimboli G; Schellens J; Baker S; Pabla N; Sparreboom A Clin Transl Sci 2017[Sep]; 10 (5): 412-20 PMID28689374show ga Cisplatin is among the most widely used anticancer drugs and known to cause a dose?limiting nephrotoxicity, which is partially dependent on the renal uptake carrier OCT2. We here report a previously unrecognized, OCT2?independent pathway of cisplatin?induced renal injury that is mediated by the organic anion transporters OAT1 and OAT3. Using transporter?deficient mouse models, we found that this mechanism regulates renal uptake of a mercapturic acid metabolite of cisplatin that acts as a precursor of a potent nephrotoxin. The function of these two transport systems can be simultaneously inhibited by the tyrosine kinase inhibitor nilotinib through noncompetitive mechanisms, without compromising the anticancer properties of cisplatin. Collectively, our findings reveal a novel pathway that explains the fundamental basis of cisplatin?induced nephrotoxicity, with potential implications for its therapeutic management. äIdentification of OAT1/OAT3 as Contributors to Cisplatin Toxicity (epmc).pdf DeepDyve Pubget Overpricing