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10.1016/j.celrep.2015.02.059 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.02.059 C4386026!4386026!25818292     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2015 ; 10 (12): 2006-18 Nephropedia Template TP {{tp|p=25818292|t=2015. Direct Involvement of Retinoblastoma Family Proteins in DNA Repair by Non-homologous End-Joining |pdf=|usr=}}{{25818292}} gab.com Text Direct Involvement of Retinoblastoma Family Proteins in DNA Repair by Non-homologous End-Joining JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=25818292 #FOAvip Deficiencies in DNA double-strand break (DSB) repair lead to genetic instability, a recognized cause of cancer initiation and evolution. We report that the retinoblastoma tumor suppressor protein (RB1) is required for DNA DSB repair by canonical non-homologous end-joining (cNHEJ). Support of cNHEJ involves a mechanism independent of RB1?s cell-cycle function and depends on its amino terminal domain with which it binds to NHEJ components XRCC5 and XRCC6. Cells with engineered loss of RB family function as well as cancer-derived cells with mutational RB1 loss show substantially reduced levels of cNHEJ. RB1 variants disabled for the interaction with XRCC5 and XRCC6, including a cancer-associated variant, are unable to support cNHEJ despite being able to confer cell-cycle control. Our data identify RB1 loss as a candidate driver of structural genomic instability and a causative factor for cancer somatic heterogeneity and evolution. Twit Text FOAVip Direct Involvement of Retinoblastoma Family Proteins in DNA Repair by Non-homologous End-Joining ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=25818292 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25818292 #FOAvip English Wikipedia <ref>{{Cite pmid|25818292}}</ref> Direct Involvement of Retinoblastoma Family Proteins in DNA Repair by Non-homologous End-Joining #MMPMID25818292 Cook R; Zoumpoulidou G; Luczynski M; Rieger S; Moquet J; Spanswick V; Hartley J; Rothkamm K; Huang P; Mittnacht S Cell Rep 2015[Mar]; 10 (12): 2006-18 PMID25818292show ga Deficiencies in DNA double-strand break (DSB) repair lead to genetic instability, a recognized cause of cancer initiation and evolution. We report that the retinoblastoma tumor suppressor protein (RB1) is required for DNA DSB repair by canonical non-homologous end-joining (cNHEJ). Support of cNHEJ involves a mechanism independent of RB1?s cell-cycle function and depends on its amino terminal domain with which it binds to NHEJ components XRCC5 and XRCC6. Cells with engineered loss of RB family function as well as cancer-derived cells with mutational RB1 loss show substantially reduced levels of cNHEJ. RB1 variants disabled for the interaction with XRCC5 and XRCC6, including a cancer-associated variant, are unable to support cNHEJ despite being able to confer cell-cycle control. Our data identify RB1 loss as a candidate driver of structural genomic instability and a causative factor for cancer somatic heterogeneity and evolution. äDirect Involvement of Retinoblastoma Family Proteins in DNA Repair by (epmc).pdf DeepDyve Pubget Overpricing