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10.1038/ncomms15772 http://scihub22266oqcxt.onion/10.1038/ncomms15772 C5472749!5472749!28598431     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28598431&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28598431|t=2017. A covalent PIN1 inhibitor selectively targets cancer cells by a dual mechanism of action |pdf=|usr=}}{{28598431}} gab.com Text A covalent PIN1 inhibitor selectively targets cancer cells by a dual mechanism of action JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28598431 #FOAvip The prolyl isomerase PIN1, a critical modifier of multiple signalling pathways, is overexpressed in the majority of cancers and its activity strongly contributes to tumour initiation and progression. Inactivation of PIN1 function conversely curbs tumour growth and cancer stem cell expansion, restores chemosensitivity and blocks metastatic spread, thus providing the rationale for a therapeutic strategy based on PIN1 inhibition. Notwithstanding, potent PIN1 inhibitors are still missing from the arsenal of anti-cancer drugs. By a mechanism-based screening, we have identified a novel covalent PIN1 inhibitor, KPT-6566, able to selectively inhibit PIN1 and target it for degradation. We demonstrate that KPT-6566 covalently binds to the catalytic site of PIN1. This interaction results in the release of a quinone-mimicking drug that generates reactive oxygen species and DNA damage, inducing cell death specifically in cancer cells. Accordingly, KPT-6566 treatment impairs PIN1-dependent cancer phenotypes in vitro and growth of lung metastasis in vivo. Twit Text FOAVip A covalent PIN1 inhibitor selectively targets cancer cells by a dual mechanism of action ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28598431 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28598431 #FOAvip English Wikipedia <ref>{{Cite pmid|28598431}}</ref> A covalent PIN1 inhibitor selectively targets cancer cells by a dual mechanism of action #MMPMID28598431 Campaner E; Rustighi A; Zannini A; Cristiani A; Piazza S; Ciani Y; Kalid O; Golan G; Baloglu E; Shacham S; Valsasina B; Cucchi U; Pippione AC; Lolli ML; Giabbai B; Storici P; Carloni P; Rossetti G; Benvenuti F; Bello E; D'Incalci M; Cappuzzello E; Rosato A; Del Sal G Nat Commun 2017[]; 8 (ä): ä PMID28598431show ga The prolyl isomerase PIN1, a critical modifier of multiple signalling pathways, is overexpressed in the majority of cancers and its activity strongly contributes to tumour initiation and progression. Inactivation of PIN1 function conversely curbs tumour growth and cancer stem cell expansion, restores chemosensitivity and blocks metastatic spread, thus providing the rationale for a therapeutic strategy based on PIN1 inhibition. Notwithstanding, potent PIN1 inhibitors are still missing from the arsenal of anti-cancer drugs. By a mechanism-based screening, we have identified a novel covalent PIN1 inhibitor, KPT-6566, able to selectively inhibit PIN1 and target it for degradation. We demonstrate that KPT-6566 covalently binds to the catalytic site of PIN1. This interaction results in the release of a quinone-mimicking drug that generates reactive oxygen species and DNA damage, inducing cell death specifically in cancer cells. Accordingly, KPT-6566 treatment impairs PIN1-dependent cancer phenotypes in vitro and growth of lung metastasis in vivo. äA covalent PIN1 inhibitor selectively targets cancer cells by a dual m(epmc).pdf DeepDyve Pubget Overpricing