MRC DTG Studentship: The role of a novel sequence element in activation of the murine beta globin locus

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Hemoglobinopathies are the most common genetics diseases world-wide and represent an enormous clinical burden. To date there are no effective strategies for hemoglobin defects that do not have serious unwanted side effects. A promising strategy is to re-activate the fetal globin genes which, if expressed in adults, can alleviate the symptoms of most hemoglobinopathies, including sickle cell anemia. We have recently obtained a mouse mutant that has a single base defect in the globin locus that renders the entire locus inactive in adult erythroid cells. We are investigating the basic molecular mechanisms controlled by this sequence element in activation and transcription control of globin gene expression during development and differentiation.

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