These studies are designed to define and precisely characterize various molecular lesions occuring in the beta-globin gene cluster in patients with beta thalassemia or with syndromes associated with increased HbF production in adult life such as delta-beta thalassemia, or hereditary persistence of fetal hemoglobin (HPFH). To investigate the mechanism by which premature termination codons cause a quantitative deficiency of beta globin mRNA, precursor and spliced mRNA molecules are generated in vitro and in vivo. The processing and nuclear to cytoplasmic transport of these RNA molecules are studied by microinjection into nuclei of Xenopus oocytes.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Intramural Research (Z01)
Project #
1Z01HL002322-01
Application #
4694585
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
U.S. National Heart Lung and Blood Inst
Department
Type
DUNS #
City
State
Country
United States
Zip Code