Roth David B
Howard Hughes Medical Institute and Department of Immunology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
Mol Cell. 2002 Jul;10(1):1-2. doi: 10.1016/s1097-2765(02)00573-7.
Mice doubly deficient for either XRCC4 or DNA ligase IV and p53 invariably develop lymphomas bearing characteristic chromosome translocations with gene amplification. A recent study highlights the importance of nonclassical end joining mechanisms in the formation of these oncogenic DNA rearrangements.
XRCC4或DNA连接酶IV以及p53双缺陷的小鼠总是会发生带有基因扩增的特征性染色体易位的淋巴瘤。最近的一项研究强调了非经典末端连接机制在这些致癌DNA重排形成中的重要性。
