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

Hui Chun Chu, Hsing Ying Lee, Yen Shu Huang, Wei Lien Tseng, Ching Ju Yen, Ju Chien Cheng*, Ching Ping Tseng

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

11 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)58-64
Number of pages7
JournalFEBS Letters
Volume588
Issue number1
DOIs
StatePublished - 03 01 2014

Keywords

  • Erythroid differentiation
  • K562 cell
  • Reeler mice
  • Reelin
  • Sodium butyrate

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