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10.1074/jbc.M116.734194 http://scihub22266oqcxt.onion/10.1074/jbc.M116.734194 C4938184!4938184!27226630     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2016 ; 291 (28): 14628-38 Nephropedia Template TP {{tp|p=27226630|t=2016. Unraveling Growth Factor Signaling and Cell Cycle Progression in Individual Fibroblasts* |pdf=|usr=}}{{27226630}} gab.com Text Unraveling Growth Factor Signaling and Cell Cycle Progression in Individual Fibroblasts* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27226630 #FOAvip Cultured cells require the actions of growth factors to enter the cell cycle, but how individual members of a population respond to the same stimulus remains unknown. Here we have employed continuous monitoring by live cell imaging in a dual-reporter cell model to investigate the regulation of short-term growth factor signaling (protein kinase B (PKB/Akt) activity) and longer-term progression through the cell cycle (cyclin-dependent kinase 2 activity). In the total population, insulin-like growth factor-I (IGF-I)-enhanced cell cycle entry by >5-fold compared with serum-free medium (from 13.5 to 78%), but at the single cell level we observed a broad distribution in the timing of G1 exit (4?24 h, mean ?12 h) that did not vary with either the amount or duration of IGF-I treatment. Cells that failed to re-enter the cell cycle exhibited similar responses to IGF-I in terms of integrated Akt activity and migration distance compared with those that did. We made similar observations with EGF, PDGF-AA, and PDGF-BB. As potential thresholds of growth factor-mediated cell cycle progression appeared to be heterogeneous within the population, the longer-term proliferative outcomes of individual cells to growth factor stimulation could not be predicted based solely on acute Akt signaling responses, no matter how robust these might be. Thus, although we could define a relationship at the population level between growth factor-induced Akt signaling dynamics and cell cycle progression, we could not predict the fate of individual cells. Twit Text FOAVip Unraveling Growth Factor Signaling and Cell Cycle Progression in Individual Fibroblasts* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27226630 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27226630 #FOAvip English Wikipedia <ref>{{Cite pmid|27226630}}</ref> Unraveling Growth Factor Signaling and Cell Cycle Progression in Individual Fibroblasts* #MMPMID27226630 Gross SM; Rotwein P J Biol Chem 2016[Jul]; 291 (28): 14628-38 PMID27226630show ga Cultured cells require the actions of growth factors to enter the cell cycle, but how individual members of a population respond to the same stimulus remains unknown. Here we have employed continuous monitoring by live cell imaging in a dual-reporter cell model to investigate the regulation of short-term growth factor signaling (protein kinase B (PKB/Akt) activity) and longer-term progression through the cell cycle (cyclin-dependent kinase 2 activity). In the total population, insulin-like growth factor-I (IGF-I)-enhanced cell cycle entry by >5-fold compared with serum-free medium (from 13.5 to 78%), but at the single cell level we observed a broad distribution in the timing of G1 exit (4?24 h, mean ?12 h) that did not vary with either the amount or duration of IGF-I treatment. Cells that failed to re-enter the cell cycle exhibited similar responses to IGF-I in terms of integrated Akt activity and migration distance compared with those that did. We made similar observations with EGF, PDGF-AA, and PDGF-BB. As potential thresholds of growth factor-mediated cell cycle progression appeared to be heterogeneous within the population, the longer-term proliferative outcomes of individual cells to growth factor stimulation could not be predicted based solely on acute Akt signaling responses, no matter how robust these might be. Thus, although we could define a relationship at the population level between growth factor-induced Akt signaling dynamics and cell cycle progression, we could not predict the fate of individual cells. äUnraveling Growth Factor Signaling and Cell Cycle Progression in Indiv(epmc).pdf DeepDyve Pubget Overpricing