Abstract
Issues remain to be elucidated in the developmental regulation of erythropoiesis. In particular the role of Fas, a member of the tumor necrosis factor family of receptors despite much work remains unclear. During erythropoiesis, Fas is expressed at low levels on erythroblasts. For most cell types, Fas to FasL interaction causes apoptotic cell death via caspase activation. Here, we show that in humans, early erythroid progenitors are refractory to apoptosis triggered through Fas. Further during early human erythropoiesis, Fas triggered caspase activation provides a positive stimulus for erythroid maturation, and does not alter cellular proliferation or trigger apoptosis.
Original language | English (US) |
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Pages (from-to) | 848-854 |
Number of pages | 7 |
Journal | FEBS Letters |
Volume | 583 |
Issue number | 4 |
DOIs | |
State | Published - Feb 18 2009 |
Externally published | Yes |
Keywords
- Cysteine-aspartic acid protease
- Development
- Erythrocyte
- Fas
- Regulation
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology