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Blood, 15 December 2004, Vol. 104, No. 13, pp. 4097-4103.
Prepublished online as a Blood First Edition Paper on August 19, 2004; DOI 10.1182/blood-2004-04-1476.
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IMMUNOBIOLOGY
Growth retardation and dyslymphopoiesis accompanied by G2/M arrest in APEX2-null mice
Yasuhito Ide,
Daisuke Tsuchimoto,
Yohei Tominaga,
Manabu Nakashima,
Takeshi Watanabe,
Kunihiko Sakumi,
Mizuki Ohno, and
Yusaku Nakabeppu
From the Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation; the Department of Orthopedic Surgery, Graduate School of Medicine; and the Division of Molecular Immunology, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
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 G2/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. (Blood. 2004;104: 4097-4103)
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