Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.21037/tcr.2016.09.16 http://scihub22266oqcxt.onion/10.21037/tcr.2016.09.16 C5617345!5617345!28966916     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       Transl+Cancer+Res 2016 ; 5 (6): 664-75 Nephropedia Template TP {{tp|p=28966916|t=2016. The IGF-1R/AKT pathway determines cell fate in response to p53 |pdf=|usr=}}{{28966916}} gab.com Text The IGF-1R/AKT pathway determines cell fate in response to p53 JO: Transl Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28966916 #FOAvip p53 that is activated in response to DNA-damaging stress can induce apoptosis or either transient or permanent cell cycle arrests. Apoptosis and permanent cell cycle arrest (senescence) are bona-fide tumor suppressor mechanisms through which p53 inhibits cancer cell survival. In contrast, transient cell cycle arrests induced by p53 can increase survival by allowing cells time to repair their DNA before proceeding with cell division. Mechanisms that control the choice of response to p53 (apoptosis vs arrest) are not fully understood. There is abundant crosstalk between p53 and the IGF-1R/AKT/mTORC1 signaling pathway. Recent studies indicate this crosstalk can determine the choice of response to p53. These findings have clear implications for the potential use of IGF-1R pathway inhibitors against p53 wild-type or p53-null or mutant cancers. Twit Text FOAVip The IGF-1R/AKT pathway determines cell fate in response to p53 ????Transl Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28966916 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28966916 #FOAvip English Wikipedia <ref>{{Cite pmid|28966916}}</ref> The IGF-1R/AKT pathway determines cell fate in response to p53 #MMPMID28966916 Duan L; Maki CG Transl Cancer Res 2016[Dec]; 5 (6): 664-75 PMID28966916show ga p53 that is activated in response to DNA-damaging stress can induce apoptosis or either transient or permanent cell cycle arrests. Apoptosis and permanent cell cycle arrest (senescence) are bona-fide tumor suppressor mechanisms through which p53 inhibits cancer cell survival. In contrast, transient cell cycle arrests induced by p53 can increase survival by allowing cells time to repair their DNA before proceeding with cell division. Mechanisms that control the choice of response to p53 (apoptosis vs arrest) are not fully understood. There is abundant crosstalk between p53 and the IGF-1R/AKT/mTORC1 signaling pathway. Recent studies indicate this crosstalk can determine the choice of response to p53. These findings have clear implications for the potential use of IGF-1R pathway inhibitors against p53 wild-type or p53-null or mutant cancers. äThe IGF-1R/AKT pathway determines cell fate in response to p53 (epmc).pdf DeepDyve Pubget Overpricing