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10.4161/mco.29901 http://scihub22266oqcxt.onion/10.4161/mco.29901 C4905175!4905175!27308311     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell+Oncol 2014 ; 1 (1): ä Nephropedia Template TP {{tp|p=27308311|t=2014. Telomere uncapping at the crossroad between cell cycle arrest and carcinogenesis |pdf=|usr=}}{{27308311}} gab.com Text Telomere uncapping at the crossroad between cell cycle arrest and carcinogenesis JO: Mol Cell Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27308311 #FOAvip Telomeres are nucleoprotein complexes that protect the natural ends of chromosomes from fusion and degradation and prevent them eliciting a checkpoint response. This protective function, which is called telomere capping, is largely mediated by telomere-binding proteins that suppress checkpoint activation and DNA repair activities. Telomere dysfunction through progressive shortening or removal of capping proteins leads to a checkpoint-mediated block of cell proliferation, which acts as a cancer-suppressor mechanism. However, genetic alterations that inactivate the checkpoint can lead to further telomere erosion and increased genomic instability that, coupled with the activation of mechanisms to restabilize telomeres, can drive the oncogenic process. Twit Text FOAVip Telomere uncapping at the crossroad between cell cycle arrest and carcinogenesis ????Mol Cell Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27308311 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27308311 #FOAvip English Wikipedia <ref>{{Cite pmid|27308311}}</ref> Telomere uncapping at the crossroad between cell cycle arrest and carcinogenesis #MMPMID27308311 Gobbini E; Trovesi C; Cassani C; Longhese MP Mol Cell Oncol 2014[]; 1 (1): ä PMID27308311show ga Telomeres are nucleoprotein complexes that protect the natural ends of chromosomes from fusion and degradation and prevent them eliciting a checkpoint response. This protective function, which is called telomere capping, is largely mediated by telomere-binding proteins that suppress checkpoint activation and DNA repair activities. Telomere dysfunction through progressive shortening or removal of capping proteins leads to a checkpoint-mediated block of cell proliferation, which acts as a cancer-suppressor mechanism. However, genetic alterations that inactivate the checkpoint can lead to further telomere erosion and increased genomic instability that, coupled with the activation of mechanisms to restabilize telomeres, can drive the oncogenic process. äTelomere uncapping at the crossroad between cell cycle arrest and carc(epmc).pdf DeepDyve Pubget Overpricing