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, Yusaku Nakabeppu

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)4097-4103
Number of pages7
JournalBlood
Volume104
Issue number13
DOIs
Publication statusPublished - Dec 15 2004

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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