Sickle hemoglobin (HbS), caused by a point mutation in the β-globin gene of hemoglobin,
polymerizes when deoxygenated. The pathophysiology of sickle cell disease results from …

The human polyomavirus BK (BKV) has a proven oncogenic potential, but its contribution to
tumorigenesis under natural conditions remains undetermined. As for other primate …

Techniques of comparative genomics are being used to identify candidate functional DNA
sequences, and objective evaluations are needed to assess their effectiveness. Different …

Despite considerable concerns with pharmacological stimulation of fetal hemoglobin (Hb F)
as a therapeutic option for the β-globin disorders, the molecular basis of action of Hb F …

Tissue-and developmental stage-specific expression of the human β-like globin genes is
regulated by a combination of ubiquitous and erythroid-restricted trans factors that bind to cis …

The short-chain fatty acid butyrate has been shown to elevate fetal hemoglobin (HbF) by
inducing expression of the γ-globin gene. Regulation of gene expression by butyrate is …

The developmental regulation of γ‐globin gene expression has shaped research efforts to
establish therapeutic modalities for individuals affected with sickle cell disease (SCD). Fetal …

The human beta-like globin gene locus contains embryonic, fetal, and adult globin genes
that are regulated in a developmentally timed, as well as a tissue-specific, manner. The …

We previously determined that a region between positions-228 and-189 upstream from the
human gamma-globin genes can form an intramolecular triplex (H-DNA) in supercoiled …

The mechanisms by which pharmacologic agents stimulate γ-globin gene expression in β-
globin disorders has not been fully established at the molecular level. In studies described …