Persistent Fetal γ-Globin Expression in Adult Transgenic Mice following Deletion of Two Silencer Elements Located 3’ to the Human Aγ-Globin Gene

Maria Gazouli, Eleni Katsantoni, Theodoros Kosteas, and Nicholas P Anagnou
 
Thalassemia is a hereditary hemolytic disease that is caused by reduced production of globin proteins in the blood. Gazouli et al. set out to define the regulatory elements controlling fetal γ-globin gene expression, because exogenous activation of this gene may have therapeutic benefit for thalassemia patients. The authors found that selective deletion of the Enh and F regulatory elements in the γ-globin gene loci resulted in high levels of fetal Aγ-globin gene expression in adult mice. These results identify specific repressing elements in the globin gene locus, a finding that may assist in the development of targeted therapeutic strategies for thalassemia and related disorders.

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Posted by MolMed Editor on Dec 2, 2009 12:00 AM CST