| First Author | Ide Y | Year | 2004 |
| Journal | Blood | Volume | 104 |
| Issue | 13 | Pages | 4097-103 |
| PubMed ID | 15319281 | Mgi Jnum | J:95267 |
| Mgi Id | MGI:3525764 | Doi | 10.1182/blood-2004-04-1476 |
| Citation | Ide Y, et al. (2004) Growth retardation and dyslymphopoiesis accompanied by G2/M arrest in APEX2-null mice. Blood 104(13):4097-103 |
| abstractText | APEX2/APE2 is a secondary mammalian apurinic/apyrimidinic endonuclease that associates with proliferating cell nuclear antigen (PCNA), and the progression of S phase of the cell cycle is accompanied by its expression. To determine the biologic significance of APEX2, we established APEX2-null mice. These mice were about 80% the size of their wild-type littermates and exhibited a moderate dyshematopoiesis and a relatively severe defect in lymphopoiesis. A significant accumulation of both thymocytes and mitogen-stimulated splenocytes in G(2)/M phase was seen in APEX2-null mice compared with the wild type, indicating that APEX2 is required for proper cell cycle progression of proliferating lymphocytes. Although APEX2-null mice exhibited an attenuated immune response against ovalbumin in comparison with wild-type mice, they produced both antiovalbumin immunoglobulin M (IgM) and IgG, indicating that class switch recombination can occur even in the absence of APEX2. |
