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Publication : Erythroid differentiation is augmented in Reelin-deficient K562 cells and homozygous reeler mice.

First Author  Chu HC Year  2014
Journal  FEBS Lett Volume  588
Issue  1 Pages  58-64
PubMed ID  24239537 Mgi Jnum  J:206162
Mgi Id  MGI:5548025 Doi  10.1016/j.febslet.2013.11.002
Citation  Chu HC, et al. (2014) Erythroid differentiation is augmented in Reelin-deficient K562 cells and homozygous reeler mice. FEBS Lett 588(1):58-64
abstractText  Reelin is an extracellular glycoprotein that is highly conserved in mammals. In addition to its expression in the nervous system, Reelin is present in erythroid cells but its function there is unknown. We report in this study that Reelin is up-regulated during erythroid differentiation of human erythroleukemic K562 cells and is expressed in the erythroid progenitors of murine bone marrow. Reelin deficiency promotes erythroid differentiation of K562 cells and augments erythroid production in murine bone marrow. In accordance with these findings, Reelin deficiency attenuates AKT phosphorylation of the Ter119(+)CD71(+) erythroid progenitors and alters the cell number and frequency of the progenitors at different erythroid differentiation stages. A regulatory role of Reelin in erythroid differentiation is thus defined.
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