Deoxycoformycin Resistant Mammalian Cells That Overproduce Adenosine Deaminase

Abstract

Adenosine deaminase (ADA) catalyzes the deamination of adenosine and deoxyadenosine to inosine and deoxyinosine, respectively. The study of ADA in mammalian cells is of particular importance because of (a) its indicated association with combined immunodeficiency disease in which patients with a deficiency of ADA activity exhibit a loss of both B and T cell function (1); (b) the occurrence of patients with hereditary hemolytic anemia who have a 40-70-fold increase in erythrocyte ADA levels (2); and (c) recent reports that in acute lymphoblastic leukemia high levels of ADA are found in T lymphoblast cells (3). It would be extremely useful, therefore, to have available a model cell culture system in which cells with elevated levels of ADA could be isolated and used to study the regulation and expression of ADA.