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10.1016/j.cell.2013.01.007 http://scihub22266oqcxt.onion/10.1016/j.cell.2013.01.007 C4382911!4382911!23374339     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2013 ; 152 (3): 417-29 Nephropedia Template TP {{tp|p=23374339|t=2013. Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System |pdf=|usr=}}{{23374339}} gab.com Text Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=23374339 #FOAvip Chromosomal translocations involving antigen receptor loci are common in lymphoid malignancies. Translocations require DNA double-strand breaks (DSBs) at two chromosomal sites, their physical juxtaposition, and their fusion by end joining. Ability of lymphocytes to generate diverse repertoires of antigen receptors and effector antibodies derives from programmed genomic alterations that produce DSBs. We discuss these lymphocyte-specific processes, with a focus on mechanisms that provide requisite DSB target specificity and mechanisms that suppress DSB translocation. We also discuss recent work that provides new insights into DSB repair pathways and influences of three-dimensional genome organization on physiological processes and cancer genomes. Twit Text FOAVip Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=23374339 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23374339 #FOAvip English Wikipedia <ref>{{Cite pmid|23374339}}</ref> Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System #MMPMID23374339 Alt FW; Zhang Y; Meng FL; Guo C; Schwer B Cell 2013[Jan]; 152 (3): 417-29 PMID23374339show ga Chromosomal translocations involving antigen receptor loci are common in lymphoid malignancies. Translocations require DNA double-strand breaks (DSBs) at two chromosomal sites, their physical juxtaposition, and their fusion by end joining. Ability of lymphocytes to generate diverse repertoires of antigen receptors and effector antibodies derives from programmed genomic alterations that produce DSBs. We discuss these lymphocyte-specific processes, with a focus on mechanisms that provide requisite DSB target specificity and mechanisms that suppress DSB translocation. We also discuss recent work that provides new insights into DSB repair pathways and influences of three-dimensional genome organization on physiological processes and cancer genomes. äMechanisms of Programmed DNA Lesions and Genomic Instability in the Im(epmc).pdf DeepDyve Pubget Overpricing