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    Apurinic/apyrimidinic endonuclease 2 is necessary for normal B cell development and recovery of lymphoid progenitors after chemotherapeutic challenge

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    Authors
    Guikema, Jeroen E. J.
    Gerstein, Rachel M.
    Linehan, Erin K.
    Cloherty, Erin K.
    Evan-Browning, Eric
    Tsuchimoto, Daisuke
    Nakabeppu, Yusaku
    Schrader, Carol E.
    UMass Chan Affiliations
    Program in Immunology and Virology
    Department of Molecular Genetics and Microbiology
    Document Type
    Journal Article
    Publication Date
    2011-02-15
    Keywords
    Animals
    B-Lymphocyte Subsets
    Cells, Cultured
    Coculture Techniques
    DNA Damage
    DNA Repair
    DNA-(Apurinic or Apyrimidinic Site) Lyase
    Endonucleases
    Fluorouracil
    Hematopoietic Stem Cells
    Lymphocyte Depletion
    Lymphocyte Subsets
    Lymphopoiesis
    Mice
    Mice, Knockout
    Myelopoiesis
    Tumor Suppressor Protein p53
    Life Sciences
    Medicine and Health Sciences
    Women's Studies
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4041036/
    Abstract
    B cell development involves rapid cellular proliferation, gene rearrangements, selection, and differentiation, and it provides a powerful model to study DNA repair processes in vivo. Analysis of the contribution of the base excision repair pathway in lymphocyte development has been lacking primarily owing to the essential nature of this repair pathway. However, mice deficient for the base excision repair enzyme, apurinic/apyrimidinic endonuclease 2 (APE2) protein develop relatively normally, but they display defects in lymphopoiesis. In this study, we present an extensive analysis of bone marrow hematopoiesis in mice nullizygous for APE2 and find an inhibition of the pro-B to pre-B cell transition. We find that APE2 is not required for V(D)J recombination and that the turnover rate of APE2-deficient progenitor B cells is nearly normal. However, the production rate of pro- and pre-B cells is reduced due to a p53-dependent DNA damage response. FACS-purified progenitors from APE2-deficient mice differentiate normally in response to IL-7 in in vitro stromal cell cocultures, but pro-B cells show defective expansion. Interestingly, APE2-deficient mice show a delay in recovery of B lymphocyte progenitors following bone marrow depletion by 5-fluorouracil, with the pro-B and pre-B cell pools still markedly decreased 2 wk after a single treatment. Our data demonstrate that APE2 has an important role in providing protection from DNA damage during lymphoid development, which is independent from its ubiquitous and essential homolog APE1.
    Source

    J Immunol. 2011 Feb 15;186(4):1943-50. Epub 2011 Jan 12. Link to article on publisher's site

    DOI
    10.4049/jimmunol.1002422
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/50982
    PubMed ID
    21228350
    Related Resources

    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.4049/jimmunol.1002422
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