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10.1016/j.jmb.2017.06.004 http://scihub22266oqcxt.onion/10.1016/j.jmb.2017.06.004 C5659283!5659283 !28602818     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28602818 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Mol+Biol 2017 ; 429 (15 ): 2265-2277 Nephropedia Template TP {{tp|p=28602818 |t=2017. Cell Cycle Control by PTEN |pdf=|usr=}}{{28602818 }} gab.com Text Cell Cycle Control by PTEN JO: J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=28602818 #FOAvip Continuous and error-free chromosome inheritance through the cell cycle is essential for genomic stability and tumor suppression. However, accumulation of aberrant genetic materials often causes the cell cycle to go awry, leading to malignant transformation. In response to genotoxic stress, cells employ diverse adaptive mechanisms to halt or exit the cell cycle temporarily or permanently. The intrinsic machinery of cycling, resting, and exiting shapes the cellular response to extrinsic stimuli, whereas prevalent disruption of the cell cycle machinery in tumor cells often confers resistance to anticancer therapy. Phosphatase and tensin homolog (PTEN) is a tumor suppressor and a guardian of the genome that is frequently mutated or deleted in human cancer. Moreover, it is increasingly evident that PTEN deficiency disrupts the fundamental processes of genetic transmission. Cells lacking PTEN exhibit cell cycle deregulation and cell fate reprogramming. Here, we review the role of PTEN in regulating the key processes in and out of cell cycle to optimize genomic integrity. Twit Text FOAVip Cell Cycle Control by PTEN ????J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=28602818 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28602818 #FOAvip English Wikipedia <ref>{{Cite pmid|28602818 }}</ref> Cell Cycle Control by PTEN #MMPMID28602818 Brandmaier A ; Hou SQ ; Shen WH J Mol Biol 2017[Jul]; 429 (15 ): 2265-2277 PMID28602818 show ga Continuous and error-free chromosome inheritance through the cell cycle is essential for genomic stability and tumor suppression. However, accumulation of aberrant genetic materials often causes the cell cycle to go awry, leading to malignant transformation. In response to genotoxic stress, cells employ diverse adaptive mechanisms to halt or exit the cell cycle temporarily or permanently. The intrinsic machinery of cycling, resting, and exiting shapes the cellular response to extrinsic stimuli, whereas prevalent disruption of the cell cycle machinery in tumor cells often confers resistance to anticancer therapy. Phosphatase and tensin homolog (PTEN) is a tumor suppressor and a guardian of the genome that is frequently mutated or deleted in human cancer. Moreover, it is increasingly evident that PTEN deficiency disrupts the fundamental processes of genetic transmission. Cells lacking PTEN exhibit cell cycle deregulation and cell fate reprogramming. Here, we review the role of PTEN in regulating the key processes in and out of cell cycle to optimize genomic integrity. |*Cell Cycle Checkpoints [MESH] |Animals [MESH] |Carcinogenesis [MESH] |Humans [MESH] |Neoplasms/physiopathology [MESH]Cell Cycle Control by PTEN (epmc).pdf DeepDyve Pubget Overpricing