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Literature summary for 4.2.99.18 extracted from

  • Guikema, J.E.; Gerstein, R.M.; Linehan, E.K.; Cloherty, E.K.; Evan-Browning, E.; Tsuchimoto, D.; Nakabeppu, Y.; Schrader, C.E.
    Apurinic/apyrimidinic endonuclease 2 is necessary for normal B cell development and recovery of lymphoid progenitors after chemotherapeutic challenge (2011), J. Immunol., 186, 1943-1950.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Mus musculus
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Synonyms

Synonyms Comment Organism
Ape2
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Mus musculus

General Information

General Information Comment Organism
physiological function mice deficient for the base excision repair enzyme, apurinic/apyrimidinic endonuclease APE2 protein develop relatively normally, but they display defects in lymphopoiesis. Mice nullizygous for APE2 show an inhibition of the pro-B to pre-B cell transition. APE2 is not required for V(D)J recombination and the turnover rate of APE2-deficient progenitor B cells is nearly normal. The production rate of pro- and pre-B cells is reduced due to a p53-dependent DNA damage response. 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. 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 weeks after a single treatment Mus musculus