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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-04-1476v1 104/13/4097    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ide, Y. Articles by Nakabeppu, Y. Search for Related Content PubMed PubMed Citation Articles by Ide, Y. Articles by Nakabeppu, Y. Related Collections Immunobiology Cell Cycle Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. E.J. Guikema, E. K. Linehan, D. Tsuchimoto, Y. Nakabeppu, P. R. Strauss, J. Stavnezer, and C. E. Schrader APE1- and APE2-dependent DNA breaks in immunoglobulin class switch recombination J. Exp. Med., November 26, 2007; 204(12): 3017 - 3026. [Abstract] [Full Text] [PDF] P. Burkovics, V. Szukacsov, I. Unk, and L. Haracska Human Ape2 protein has a 3'-5' exonuclease activity that acts preferentially on mismatched base pairs. Nucleic Acids Res., January 1, 2006; 34(9): 2508 - 2515. [Abstract] [Full Text] [PDF] K. Torisu, D. Tsuchimoto, Y. Ohnishi, and Y. Nakabeppu Hematopoietic Tissue-Specific Expression of Mouse Neil3 for Endonuclease VIII-Like Protein J. Biochem., December 1, 2005; 138(6): 763 - 772. [Abstract] [Full Text] [PDF]

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