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10.1016/j.molcel.2014.08.002 http://scihub22266oqcxt.onion/10.1016/j.molcel.2014.08.002 C4398060!4398060!25201414     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell 2014 ; 55 (6): 829-42 Nephropedia Template TP {{tp|p=25201414|t=2014. Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining |pdf=|usr=}}{{25201414}} gab.com Text Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25201414 #FOAvip Breakpoint junctions of the chromosomal translocations that occur in human cancers display hallmarks of nonhomologous end-joining (NHEJ). In mouse cells, translocations are suppressed by canonical NHEJ (c-NHEJ) components, which include DNA ligase IV (LIG4), and instead arise from alternative NHEJ (alt-NHEJ). Here we used designer nucleases (ZFNs, TALENs, and CRISPR/Cas9) to introduce DSBs on two chromosomes to study translocation joining mechanisms in human cells. Remarkably, translocations were altered in cells deficient for LIG4 or its interacting protein XRCC4. Translocation junctions had significantly longer deletions and more microhomology, indicative of alt-NHEJ. Thus, unlike mouse cells, translocations in human cells are generated by c-NHEJ. Human cancer translocations induced by paired Cas9 nicks also showed a dependence on c-NHEJ, despite having distinct joining characteristics. These results demonstrate an unexpected and striking species-specific difference for common genomic rearrangements associated with tumorigenesis. Twit Text FOAVip Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25201414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25201414 #FOAvip English Wikipedia <ref>{{Cite pmid|25201414}}</ref> Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining #MMPMID25201414 Ghezraoui H; Piganeau M; Renouf B; Renaud JB; Sallmyr A; Ruis B; Oh S; Tomkinson A; Hendrickson EA; Giovannangeli C; Jasin M; Brunet E Mol Cell 2014[Sep]; 55 (6): 829-42 PMID25201414show ga Breakpoint junctions of the chromosomal translocations that occur in human cancers display hallmarks of nonhomologous end-joining (NHEJ). In mouse cells, translocations are suppressed by canonical NHEJ (c-NHEJ) components, which include DNA ligase IV (LIG4), and instead arise from alternative NHEJ (alt-NHEJ). Here we used designer nucleases (ZFNs, TALENs, and CRISPR/Cas9) to introduce DSBs on two chromosomes to study translocation joining mechanisms in human cells. Remarkably, translocations were altered in cells deficient for LIG4 or its interacting protein XRCC4. Translocation junctions had significantly longer deletions and more microhomology, indicative of alt-NHEJ. Thus, unlike mouse cells, translocations in human cells are generated by c-NHEJ. Human cancer translocations induced by paired Cas9 nicks also showed a dependence on c-NHEJ, despite having distinct joining characteristics. These results demonstrate an unexpected and striking species-specific difference for common genomic rearrangements associated with tumorigenesis. äChromosomal translocations in human cells are generated by canonical n(epmc).pdf DeepDyve Pubget Overpricing