ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Apurinic/apyrimidinic endonuclease 2 is necessary for normal B cell development and recovery of lymphoid progenitors after chemotherapeutic challenge.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Cisplatin-Induced APE2 Overexpression Disrupts MYH9 Function and Causes Hearing Loss.Cancer research communications · 2025Article
- APEX1 Nuclease and Redox Functions are Both Essential for Adult Mouse Hematopoietic Stem and Progenitor Cells.Stem cell reviews and reports · 2023Article
- APE1/Ref-1 Role in Inflammation and Immune Response.Frontiers in immunology · 2022Review
- A DNA damage repair gene-associated signature predicts responses of patients with advanced soft-tissue sarcoma to treatment with trabectedin.Molecular oncology · 2021Article
- Cisplatin-Mediated Upregulation of APE2 Binding to MYH9 Provokes Mitochondrial Fragmentation and Acute Kidney Injury.Cancer research · 2021Article
- Genomic alterations and abnormal expression of APE2 in multiple cancers.Scientific reports · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- Apn2 resolves blocked 3' ends and suppresses Top1-induced mutagenesis at genomic rNMP sites.Nature structural & molecular biology · 2019Article
- APE2 promotes DNA damage response pathway from a single-strand break.Nucleic acids research · 2018Article
- APE2 Zf-GRF facilitates 3'-5' resection of DNA damage following oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Genomically Incorporated 5-Fluorouracil that Escapes UNG-Initiated Base Excision Repair Blocks DNA Replication and Activates Homologous Recombination.Molecular pharmacology · 2016Article
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- Apurinic/apyrimidinic endonuclease 2 regulates the expansion of germinal centers by protecting against activation-induced cytidine deaminase-independent DNA damage in B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Base excision repair: a critical player in many games.DNA repair · 2014Review
- Differential expression of APE1 and APE2 in germinal centers promotes error-prone repair and A:T mutations during somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Base excision repair and cancer.Cancer letters · 2012Review
- The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim.The Journal of experimental medicine · 2012Article
- Function and molecular mechanisms of APE2 in genome and epigenome integrity.Mutation research. Reviews in mutation researchReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
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.
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Registered trials
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