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Publication : Abnormal differentiation of erythroid precursors in p45 NF-E2(-/-) mice.

First Author  Gasiorek JJ Year  2012
Journal  Exp Hematol Volume  40
Issue  5 Pages  393-400
PubMed ID  22265708 Mgi Jnum  J:196767
Mgi Id  MGI:5489863 Doi  10.1016/j.exphem.2012.01.007
Citation  Gasiorek JJ, et al. (2012) Abnormal differentiation of erythroid precursors in p45 NF-E2(-/-) mice. Exp Hematol 40(5):393-400
abstractText  The transcription factor p45 nuclear factor-erythroid-derived 2 (NF-E2) plays major roles in erythroid and megakaryocytic lineages. Here, we investigated the role of p45 NF-E2 in erythroid differentiation in vivo. Absence of p45 NF-E2 in mice leads to a twofold increase in serum erythropoietin levels. In the bone marrow of these animals, we found a different distribution of precursor populations compared to wild-type mice, suggesting abnormal differentiation. Loss of p45 NF-E2 was also associated with an increase in splenic erythropoiesis, as evidenced by an accumulation of early precursors, namely, late basophilic and polychromatic erythroblasts. These observations are consistent with a stress erythropoiesis phenotype and indicate that the spleen is likely compensating for ineffective erythropoiesis in the bone marrow. Analysis of bone marrow samples revealed increased GATA1 levels, as well as an increased proportion of erythroid cells arrested at the G(1) stage of cell cycle in p45 NF-E2-deficient mice. These results suggest that p45 NF-E2 is required for the differentiation of erythroid precursors.
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