| First Author | Muto T | Year | 2006 |
| Journal | Proc Natl Acad Sci U S A | Volume | 103 |
| Issue | 8 | Pages | 2752-7 |
| PubMed ID | 16477013 | Mgi Jnum | J:107317 |
| Mgi Id | MGI:3620611 | Doi | 10.1073/pnas.0510970103 |
| Citation | Muto T, et al. (2006) Negative regulation of activation-induced cytidine deaminase in B cells. Proc Natl Acad Sci U S A 103(8):2752-7 |
| abstractText | Both class switch recombination (CSR) and somatic hypermutation (SHM) of the Ig genes require the activity of activation-induced cytidine deaminase (AID). Expression of AID is restricted to B cells in the germinal centers of the lymphoid organs, where activated B cells undergo CSR and SHM. We previously showed that constitutive and systemic expression of AID leads to tumorigenesis in T cells and lung epithelium, but not in B cells. This finding led us to suspect that transgenic AID may be inactivated at least in part in B cells. To address this issue, we generated conditional AID-transgenic mice that constitutively express AID only in B cells. Studies on the cross between the AID-transgenic and AID-deficient mice showed that abundant AID protein accumulated by constitutive expression is inactivated in B cells, possibly providing an explanation for the absence of deregulation of CSR and SHM in AID-transgenic B cells. |
