title: A non-apoptotic role for Fas/FasL in erythropoiesis.
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.
authors.affiliation: Department of Biochemistry, McGill University, McIntyre Medical Sciences Building, 3655 Sir William Osler Promenade, Montreal, Quebec, Canada.
authors.forename: Graeme W
authors.initials: GW
authors.lastname: Carlile
authors.forename: Deborah H
authors.initials: DH
authors.lastname: Smith
authors.forename: Martin
authors.initials: M
authors.lastname: Wiedmann
mesh_terms: D017209:Apoptosis / Q000276:immunology* / Q000502:physiology*; D053148:Caspase 3 / Q000032:analysis / Q000378:metabolism; D053181:Caspase 8 / Q000032:analysis / Q000378:metabolism; D053453:Caspase 9 / Q000032:analysis / Q000378:metabolism; D016923:Cell Death / Q000276:immunology; D002478:Cells, Cultured; D004789:Enzyme Activation; D004900:Erythroblasts / Q000276:immunology / Q000378:metabolism; D015672:Erythroid Precursor Cells / Q000166:cytology / Q000378:metabolism; D004920:Erythropoiesis / Q000276:immunology* / Q000502:physiology*; D053222:Fas Ligand Protein / Q000276:immunology*; D006801:Humans; D034741:RNA, Small Interfering / Q000494:pharmacology; D013997:Time Factors; D014162:Transfection
chemical_list: D053222:Fas Ligand Protein; D034741:RNA, Small Interfering; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9