scholarly journals Kinks in the chain: examining recombination‐activating gene scanning during V(D)J recombination

2019 ◽  
Vol 97 (10) ◽  
pp. 859-861
Author(s):  
Timothy M Johanson ◽  
Rhys S Allan
Immunobiology ◽  
2021 ◽  
pp. 152090
Author(s):  
Ibtihal Benhsaien ◽  
Soukaina Essadssi ◽  
Lamiae Elkhattabi ◽  
Amina Bakhchane ◽  
Houria Abdelghaffar ◽  
...  

2012 ◽  
Vol 16 (5) ◽  
pp. 406-411 ◽  
Author(s):  
Jurat Obul ◽  
Sakae Itoga ◽  
Maynur Abliz ◽  
Kenichi Sato ◽  
Takayuki Ishige ◽  
...  

2002 ◽  
Vol 196 (4) ◽  
pp. 469-480 ◽  
Author(s):  
Michael J. Difilippantonio ◽  
Simone Petersen ◽  
Hua Tang Chen ◽  
Roger Johnson ◽  
Maria Jasin ◽  
...  

Nonreciprocal translocations and gene amplifications are commonly found in human tumors. Although little is known about the mechanisms leading to such aberrations, tissue culture models predict that they can arise from DNA breakage, followed by cycles of chromatid fusion, asymmetric mitotic breakage, and replication. Mice deficient in both a nonhomologous end joining (NHEJ) DNA repair protein and the p53 tumor suppressor develop lymphomas at an early age harboring amplification of an IgH/c-myc fusion. Here we report that these chromosomal rearrangements are initiated by a recombination activating gene (RAG)-induced DNA cleavage. Subsequent DNA repair events juxtaposing IgH and c-myc are mediated by a break-induced replication pathway. Cycles of breakage-fusion-bridge result in amplification of IgH/c-myc while chromosome stabilization occurs through telomere capture. Thus, mice deficient in NHEJ provide excellent models to study the etiology of unbalanced translocations and amplification events during tumorigenesis.


1989 ◽  
pp. 385-388
Author(s):  
D. Baltimore ◽  
M. Oettinger ◽  
D. Schatz

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