1. An international effort to cure a global health problem: A report on the 19th Hemoglobin Switching Conference 
Gerd A. Blobel, David Bodine, Marjorie Brand, John Crispino, Marella F.T.R. de Bruijn, David Nathan, Thalia Papayannopoulou, Catherine Porcher, John Strouboulis, Len Zon, Douglas R. Higgs, George Stamatoyannopoulos, James Douglas Engel 
Experimental Hematology 
Volume 43, Issue 10, Pages (October 2015)
DOI: /j.exphem
Copyright © 2015 ISEH - International Society for Experimental Hematology Terms and Conditions

2. Figure 1
(A) Top: Approximate timing (abscissa) and level (ordinate) of expression of the human α-type (ζ- and α-globin) and β-type (ε, γ, and β) globin genes during embryonic and postnatal development. Bottom: Diagrams depicting the physical order of the genes and adjacent DNase I hypersensitive sites (yellow squares that define the major transcriptional regulatory elements of the α- and β-globin loci) with each of the genes color coded to match their timing and abundance of expression as depicted above. (B) Top: Approximate abundance and timing of expression of the murine α- and β-type globin genes during embryonic and postnatal development. Bottom: Time line of expression diagram. The lines depict the relative positions of the hypersensitive site (HS) elements and the genes within the mouse globin loci.
Experimental Hematology  , DOI: ( /j.exphem )
Copyright © 2015 ISEH - International Society for Experimental Hematology Terms and Conditions

3. Figure 2
Simplified overview of the current network interactions that define γ-globin repression in adult, definitive erythroid cells. TR2/TR4 binds to the DR1 cis-elements found in the promoters of both the ε- and γ-globin genes [45]; mutation of either γ-globin cis-sequence results in HPFH (hereditary persistence of fetal hemoglobin) [46–48]. BCL11A binds to multiple sites within the β-globin locus [49,50] and associates with co-factor SOX6 to repress γ-globin transcription [50]. GATA1 has also been proposed to negatively regulate γ-globin transcription [51,52], but its mechanism of action is still unclear. Myb is an upstream activator of Tr2/Tr4, but does not seem to affect Bcl11a expression [57,58], whereas KLF1 is an upstream activator of Bcl11a [33,53–56], but is not known to affect Tr2/Tr4 transcription. These DNA-binding repressors of γ-globin transcription associate with an overlapping array of co-repressor enzymes (e.g., HDACs, PRMT5, mSIN3A, LSD1/Corest, DNMT1 and NuRD complex [59–61]) that epigenetically modify the chromatin environment to relieve repression of γ-globin transcription. HS = hypersensitive site.
Experimental Hematology  , DOI: ( /j.exphem )
Copyright © 2015 ISEH - International Society for Experimental Hematology Terms and Conditions