A non-apoptotic role for Fas/FasL in erythropoiesis

Graeme W. Carlile, Deborah H. Smith, Martin Wiedmann

Research output: Contribution to journalArticle

10 Scopus citations

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 languageEnglish (US)
Pages (from-to)848-854
Number of pages7
JournalFEBS Letters
Volume583
Issue number4
DOIs
StatePublished - Feb 18 2009

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Keywords

  • Cysteine-aspartic acid protease
  • Development
  • Erythrocyte
  • Fas
  • Regulation

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Carlile, G. W., Smith, D. H., & Wiedmann, M. (2009). A non-apoptotic role for Fas/FasL in erythropoiesis. FEBS Letters, 583(4), 848-854. https://doi.org/10.1016/j.febslet.2009.01.047