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10.1038/nrm.2017.67 http://scihub22266oqcxt.onion/10.1038/nrm.2017.67 C5796526!5796526!28811666     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Rev+Mol+Cell+Biol 2017 ; 18 (10): 622-36 Nephropedia Template TP {{tp|p=28811666|t=2017. The essential kinase ATR: ensuring faithful duplication of a challenging genome |pdf=|usr=}}{{28811666}} gab.com Text The essential kinase ATR: ensuring faithful duplication of a challenging genome JO: Nat Rev Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28811666 #FOAvip One way to preserve a rare book is to lock it away from all potential sources of damage. Of course, an inaccessible book is also of little use, and the paper and ink will continue to degrade with age in any case. Like a book, the information stored in our DNA needs to be read, but it is also subject to continuous assault. In this review, we examine how the replication stress response that is controlled by the kinase ataxia telangiectasia and Rad3-related (ATR) senses and resolves threats to DNA integrity so the DNA remains available to read in all of our cells. We discuss the multiple data that have revealed an elegant yet increasingly complex mechanism of ATR activation. These involve a core set of components that recruit ATR to stressed replication forks, stimulate kinase activity and amplify ATR signaling. We focus on the activities of ATR in control of cell cycle checkpoints, origin firing and replication fork stability, and how proper regulation of these processes is crucial to ensure faithful duplication of a challenging genome. Twit Text FOAVip The essential kinase ATR: ensuring faithful duplication of a challenging genome ????Nat Rev Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28811666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28811666 #FOAvip English Wikipedia <ref>{{Cite pmid|28811666}}</ref> The essential kinase ATR: ensuring faithful duplication of a challenging genome #MMPMID28811666 Saldivar JC; Cortez D; Cimprich KA Nat Rev Mol Cell Biol 2017[Oct]; 18 (10): 622-36 PMID28811666show ga One way to preserve a rare book is to lock it away from all potential sources of damage. Of course, an inaccessible book is also of little use, and the paper and ink will continue to degrade with age in any case. Like a book, the information stored in our DNA needs to be read, but it is also subject to continuous assault. In this review, we examine how the replication stress response that is controlled by the kinase ataxia telangiectasia and Rad3-related (ATR) senses and resolves threats to DNA integrity so the DNA remains available to read in all of our cells. We discuss the multiple data that have revealed an elegant yet increasingly complex mechanism of ATR activation. These involve a core set of components that recruit ATR to stressed replication forks, stimulate kinase activity and amplify ATR signaling. We focus on the activities of ATR in control of cell cycle checkpoints, origin firing and replication fork stability, and how proper regulation of these processes is crucial to ensure faithful duplication of a challenging genome. äThe essential kinase ATR: ensuring faithful duplication of a challengi(epmc).pdf DeepDyve Pubget Overpricing