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10.1126/science.aac5610 http://scihub22266oqcxt.onion/10.1126/science.aac5610 C5217461!5217461!26965628     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       Science 2016 ; 351 (6278): 1204-8 Nephropedia Template TP {{tp|p=26965628|t=2016. Schedule-dependent interaction between anticancer treatments |pdf=|usr=}}{{26965628}} gab.com Text Schedule-dependent interaction between anticancer treatments JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=26965628 #FOAvip The oncogene MDMX is overexpressed in many cancers leading to suppression of the tumor suppressor p53. MDMX inhibitors therefore might help reactivate p53 and enhance the efficacy of DNA damaging drugs. However, we currently lack a quantitative understanding of how MDMX inhibition affects the p53 signaling pathway and the sensitivity to DNA damage. Live cell imaging showed that MDMX depletion triggered two distinct phases of p53 accumulation in single cells: an initial post-mitotic pulse followed by low-amplitude oscillations. The response to DNA damage was sharply different in these two phases; in the first phase, MDMX depletion was synergistic with DNA damage in causing cell death, whereas in the second phase depletion of MDMX inhibited cell death. Thus a quantitative understanding of signal dynamics and cellular state is important for designing an optimal schedule of dual-drug administration. Twit Text FOAVip Schedule-dependent interaction between anticancer treatments ????Science http://www.kidney.de/pget.php?&tw=1&pmid=26965628 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26965628 #FOAvip English Wikipedia <ref>{{Cite pmid|26965628}}</ref> Schedule-dependent interaction between anticancer treatments #MMPMID26965628 Chen Sh; Forrester W; Lahav G Science 2016[Mar]; 351 (6278): 1204-8 PMID26965628show ga The oncogene MDMX is overexpressed in many cancers leading to suppression of the tumor suppressor p53. MDMX inhibitors therefore might help reactivate p53 and enhance the efficacy of DNA damaging drugs. However, we currently lack a quantitative understanding of how MDMX inhibition affects the p53 signaling pathway and the sensitivity to DNA damage. Live cell imaging showed that MDMX depletion triggered two distinct phases of p53 accumulation in single cells: an initial post-mitotic pulse followed by low-amplitude oscillations. The response to DNA damage was sharply different in these two phases; in the first phase, MDMX depletion was synergistic with DNA damage in causing cell death, whereas in the second phase depletion of MDMX inhibited cell death. Thus a quantitative understanding of signal dynamics and cellular state is important for designing an optimal schedule of dual-drug administration. äSchedule-dependent interaction between anticancer treatments (epmc).pdf DeepDyve Pubget Overpricing