Premium
Erythroid differentiation is augmented in Reelin‐deficient K562 cells and homozygous reeler mice
Author(s) -
Chu Hui-Chun,
Lee Hsing-Ying,
Huang Yen-Shu,
Tseng Wei-Lien,
Yen Ching-Ju,
Cheng Ju-Chien,
Tseng Ching-Ping
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.11.002
Subject(s) - reelin , dab1 , reeler , microbiology and biotechnology , progenitor cell , biology , cellular differentiation , bone marrow , k562 cells , erythropoiesis , phosphorylation , stem cell , immunology , leukemia , genetics , gene , medicine , extracellular matrix , anemia
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.