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10.1038/onc.2015.427 http://scihub22266oqcxt.onion/10.1038/onc.2015.427 C4842010!4842010!26549024     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncogene 2016 ; 35 (30): 4009-19 Nephropedia Template TP {{tp|p=26549024|t=2016. RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress |pdf=|usr=}}{{26549024}} gab.com Text RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26549024 #FOAvip The DNA replication machinery invariably encounters obstacles that slow replication fork progression, and threaten to prevent complete replication and faithful segregation of sister chromatids. The resulting replication stress activates ATR, the major kinase involved in resolving impaired DNA replication. In addition, replication stress also activates the related kinase ATM, which is required to prevent mitotic segregation errors. However, the molecular mechanism of ATM activation by replication stress is not defined. Here we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts with the ATM cofactor ATMIN via WRN interacting protein 1 (WRNIP1). ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation. Thus, WRNIP1 connects PCNA monoubiquitination with ATMIN/ATM to activate ATM signalling in response to replication stress and contribute to the maintenance of genomic stability. Twit Text FOAVip RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26549024 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26549024 #FOAvip English Wikipedia <ref>{{Cite pmid|26549024}}</ref> RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress #MMPMID26549024 Kanu N; Zhang T; Burrell RA; Chakraborty A; Cronshaw J; Da Costa C; Grönroos E; Pemberton HN; Anderton E; Gonzalez L; Sabbioneda S; Ulrich HD; Swanton C; Behrens A Oncogene 2016[Jul]; 35 (30): 4009-19 PMID26549024show ga The DNA replication machinery invariably encounters obstacles that slow replication fork progression, and threaten to prevent complete replication and faithful segregation of sister chromatids. The resulting replication stress activates ATR, the major kinase involved in resolving impaired DNA replication. In addition, replication stress also activates the related kinase ATM, which is required to prevent mitotic segregation errors. However, the molecular mechanism of ATM activation by replication stress is not defined. Here we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts with the ATM cofactor ATMIN via WRN interacting protein 1 (WRNIP1). ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation. Thus, WRNIP1 connects PCNA monoubiquitination with ATMIN/ATM to activate ATM signalling in response to replication stress and contribute to the maintenance of genomic stability. äRAD18, WRNIP1 and ATMIN promote ATM signalling in response to replicat(epmc).pdf DeepDyve Pubget Overpricing