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10.1016/j.celrep.2015.08.034 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.08.034 C5089067!5089067 !26365182     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26365182 &cmd=llinks): Failed to open stream: HTTP request failed! 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Off-Target V(D)J Recombination Drives Lymphomagenesis and Is Escalated by Loss of the Rag2 C Terminus |pdf=|usr=}}{{26365182 }} gab.com Text Off-Target V(D)J Recombination Drives Lymphomagenesis and Is Escalated by Loss of the Rag2 C Terminus JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365182 #FOAvip Genome-wide analysis of thymic lymphomas from Tp53(-/-) mice with wild-type or C-terminally truncated Rag2 revealed numerous off-target, RAG-mediated DNA rearrangements. A significantly higher fraction of these errors mutated known and suspected oncogenes/tumor suppressor genes than did sporadic rearrangements (p < 0.0001). This tractable mouse model recapitulates recent findings in human pre-B ALL and allows comparison of wild-type and mutant RAG2. Recurrent, RAG-mediated deletions affected Notch1, Pten, Ikzf1, Jak1, Phlda1, Trat1, and Agpat9. Rag2 truncation substantially increased the frequency of off-target V(D)J recombination. The data suggest that interactions between Rag2 and a specific chromatin modification, H3K4me3, support V(D)J recombination fidelity. Oncogenic effects of off-target rearrangements created by this highly regulated recombinase may need to be considered in design of site-specific nucleases engineered for genome modification. Twit Text FOAVip Off-Target V(D)J Recombination Drives Lymphomagenesis and Is Escalated by Loss of the Rag2 C Terminus ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365182 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26365182 #FOAvip English Wikipedia <ref>{{Cite pmid|26365182 }}</ref> Off-Target V(D)J Recombination Drives Lymphomagenesis and Is Escalated by Loss of the Rag2 C Terminus #MMPMID26365182 Miju?kovi? M ; Chou YF ; Gigi V ; Lindsay CR ; Shestova O ; Lewis SM ; Roth DB Cell Rep 2015[Sep]; 12 (11 ): 1842-52 PMID26365182 show ga Genome-wide analysis of thymic lymphomas from Tp53(-/-) mice with wild-type or C-terminally truncated Rag2 revealed numerous off-target, RAG-mediated DNA rearrangements. A significantly higher fraction of these errors mutated known and suspected oncogenes/tumor suppressor genes than did sporadic rearrangements (p < 0.0001). This tractable mouse model recapitulates recent findings in human pre-B ALL and allows comparison of wild-type and mutant RAG2. Recurrent, RAG-mediated deletions affected Notch1, Pten, Ikzf1, Jak1, Phlda1, Trat1, and Agpat9. Rag2 truncation substantially increased the frequency of off-target V(D)J recombination. The data suggest that interactions between Rag2 and a specific chromatin modification, H3K4me3, support V(D)J recombination fidelity. Oncogenic effects of off-target rearrangements created by this highly regulated recombinase may need to be considered in design of site-specific nucleases engineered for genome modification. |*V(D)J Recombination [MESH] |Animals [MESH] |DNA-Binding Proteins/*genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Lymphoma/*genetics/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Thymus Neoplasms/*genetics/metabolism [MESH]Off-Target V(D)J Recombination Drives Lymphomagenesis and Is Escalated(epmc).pdf DeepDyve Pubget Overpricing