PARP-2 sustains erythropoiesis in mice by limiting replicative stress in erythroid progenitors

@article{Farrs2015PARP2SE,
  title={PARP-2 sustains erythropoiesis in mice by limiting replicative stress in erythroid progenitors},
  author={Jordi Arrey i Farr{\'e}s and Laura Llacuna and Juan Dvm Mart{\'i}n-Caballero and Concepci{\'o}n Huertas Mart{\'i}nez and Juan Jos{\'e} Lozano and Coral Ampurdan{\'e}s and Andr{\'e}s J L{\'o}pez-Contreras and Luis Marcelo Florensa and Judith Espinoza Navarro and Eleonora Ottina and Françoise Dantzer and Valerie K. Schreiber and Andreas Villunger and Oscar Fern{\'a}ndez-Capetillo and Jos{\'e} F. Murillo Y{\'e}lamos},
  journal={Cell Death and Differentiation},
  year={2015},
  volume={22},
  pages={1144-1157}
}
Erythropoiesis is a tightly regulated process in which multipotential hematopoietic stem cells produce mature red blood cells. Here we show that deletion of poly(ADP-ribose) polymerase-2 (PARP-2) in mice leads to chronic anemia at steady state, despite increased erythropoietin plasma levels, a phenomenon not observed in mice lacking PARP-1. Loss of PARP-2 causes shortened lifespan of erythrocytes and impaired differentiation of erythroid progenitors. In erythroblasts, PARP-2 deficiency triggers… CONTINUE READING
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