AID mutant analyses indicate requirement for class-switch-specific cofactors
AID mutant analyses indicate requirement for class-switch-specific cofactors
复制标题
DOI：
10.1038/ni964
复制
发表时间：
2003-09-01
影响因子：
30.5
通讯作者：
Honjo, T
中科院分区：
文献类型：
--
作者：
Ta, VT;Nagaoka, H;Honjo, T
激活诱导的胞苷脱氨酶（AID）是类别转换重组（CSR）和体细胞超突变（SHM）所必需的唯一B细胞特异性因子。然而，目前还不知道艾滋病署如何区别调节这两个独立的事件。与AID相互作用的几个辅因子的参与已被指示的分散分布的功能丧失的点突变和进化保守的整个198个氨基酸的蛋白质。在这里，我们报告说，人类艾滋病突变蛋白的插入，替换或截断的C-末端区域保留了强大的SHM活性，但几乎完全失去了CSR活动。这些结果表明，AID需要与CSR特异性辅因子相互作用。
Activation-induced cytidine deaminase (AID) is the essential and sole B cell-specific factor required for class-switch recombination (CSR) and somatic hypermutation (SHM). However, it is not known how AID differentially regulates these two independent events. Involvement of several cofactors interacting with AID has been indicated by scattered distribution of loss-of-function point mutations and evolutionary conservation of the entire 198-amino-acid protein. Here, we report that human AID mutant proteins with insertions, replacements or truncations in the C-terminal region retained strong SHM activity but almost completely lost CSR activity. These results indicate that AID requires interaction with a cofactor(s) specific to CSR.