Benserazide racemate and enantiomers induce fetal globin gene expression in vivo: Studies to guide clinical development for beta thalassemia and sickle cell disease
Authors:
- 12 March 2021
- journal article
- research article
- Published by Elsevier in Blood Cells, Molecules, and Diseases
- Vol. 89, 102561
Abstract
No abstract availableKeywords
Funding Information
- Boston University School of Medicine
- National Center for Advancing Translational Sciences
This publication has 59 references indexed in Scilit:
- Lysine-specific demethylase 1 is a therapeutic target for fetal hemoglobin inductionNature Medicine, 2013
- Hydroxycarbamide in very young children with sickle-cell anaemia: a multicentre, randomised, controlled trial (BABY HUG)The Lancet, 2011
- KLF1 regulates BCL11A expression and γ- to β-globin gene switchingNature Genetics, 2010
- Haploinsufficiency for the erythroid transcription factor KLF1 causes hereditary persistence of fetal hemoglobinNature Genetics, 2010
- The inherited diseases of hemoglobin are an emerging global health burdenBlood, 2010
- The risks and benefits of long‐term use of hydroxyurea in sickle cell anemia: A 17.5 year follow‐upAmerican Journal of Hematology, 2010
- DNA polymorphisms at the BCL11A , HBS1L-MYB , and β- globin loci associate with fetal hemoglobin levels and pain crises in sickle cell diseaseProceedings of the National Academy of Sciences, 2008
- Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of β-thalassemiaProceedings of the National Academy of Sciences, 2008
- Short-chain fatty acids induce γ-globin gene expression by displacement of a HDAC3-NCoR repressor complexBlood, 2006
- The effect of fetal hemoglobin on the survival characteristics of sickle cellsBlood, 2006