Growth retardation and dyslymphopoiesis accompanied by G2/M arrest in APEX2-null mice
Growth retardation and dyslymphopoiesis accompanied by G2/M arrest in APEX2-null mice
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DOI：
10.1182/blood-2004-04-1476
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发表时间：
2004-12-15
期刊：
影响因子：
20.3
通讯作者：
Nakabeppu, Y
中科院分区：
文献类型：
--
作者：
Ide, Y;Tsuchimoto, D;Nakabeppu, Y
APEX2/APE2是一种与增殖细胞核抗原相关的次级哺乳动物脱嘌呤/脱嘧啶核酸内切酶，其表达伴随着细胞周期的S期的进展。为了确定APEX2的生物学意义，我们建立了APEX2缺失的小鼠。这些小鼠的体型约为野生型小鼠的80%，表现出中度的造血功能障碍和相对严重的淋巴系缺陷。与野生型相比，APEX2缺失型小鼠胸腺细胞和有丝分裂原刺激的脾细胞均显著聚集在G(2)/M期，表明APEX2是增殖淋巴细胞正常细胞周期进程所必需的。尽管APEX2基因缺失的小鼠与野生型小鼠相比表现出较弱的表现，但它们同时产生抗卵清蛋白免疫球蛋白M(IgM)和免疫球蛋白G，这表明即使没有APEX2基因，也可以发生类别转换重组。
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 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.