Growth factor independence-1B (Gfi-1B) is a transcription factor with a highly 
conserved transcriptional repressor snail-Gfi-1 (SNAG) domain and 6 zinc-finger 
domains at the N- and C-terminus, respectively. Disruption of the Gfi-1B gene is 
lethal in the embryo with failure to produce definitive enucleated erythrocytes. 
In this study, we analyzed the role of Gfi-1B in human erythropoiesis. We 
observed an increase of Gfi-1B expression during erythroid maturation of human 
primary progenitor cells. We studied the consequences of variations in Gfi-1B 
expression in 2 transformed cell lines (K562 and UT7 cells), as well as in 
primary CD36(+)/GPA(-) progenitors. A knock-down of Gfi-1B delayed the terminal 
differentiation of K562 and primary cells. Forced expression of Gfi-1B in UT7 
and K562 cells led to an arrest of proliferation and an induction of erythroid 
differentiation. Enforced expression of Gfi-1B in primary cells at the 
colony-forming units-erythroid (CFU-E) stage led to a partial glycophorin A 
(GPA) induction after erythropoietin (EPO) withdrawal but failed to protect 
cells from apoptosis. Deletion of the SNAG repressor domain abolished 
Gfi-1B-induced erythroid maturation, strongly suggesting that Gfi-1B acts in the 
late stage of erythroid differentiation as a transcriptional repressor.