Chan V L, Juranka P
Somatic Cell Genet. 1981 Mar;7(2):147-60. doi: 10.1007/BF01567654.
A large number of 9-beta-D-arabinofuranosyladenine (araA) -resistant mutants of baby hamster kidney cells (BHK 21/Cl3) were isolated. These mutants can be grouped into three mechanistically distinct classes. All the mutants showed cross-resistance to deoxyadenosine (dAdo). The mechanism of resistance to araA and dAdo in the class I mutants can be attributed to a mutation to adenosine kinase (AK) deficiency. The class II mutants have normal levels of AK, adenosine deaminase, and deoxyadenosine kinase. These mutants also show resistance to 1-beta-D-arabinofuranosylcytosine (araC), and the mechanism of resistance is probably due to a mutation in the ribonucleotide reductase gene producing an enzyme that has an increased resistance to the inhibition by 9-beta-D-arabinofuranosyladenine 5'-triphosphate (araATP) and 2'-deoxyadenosine 5'-triphosphate (dATP). The class III mutants, unlike those of classes I and II, show extreme adenosine (Ado) sensitivity. The Ados/araAr/dAdor phenotypic properties can be attributed to a single mutation. Classes II and III are novel araA-resistant mutants.
分离出了大量对9-β-D-阿拉伯呋喃糖基腺嘌呤（araA）具有抗性的幼仓鼠肾细胞（BHK 21/Cl3）突变体。这些突变体可分为三个机制不同的类别。所有突变体均对脱氧腺苷（dAdo）表现出交叉抗性。I类突变体对araA和dAdo的抗性机制可归因于腺苷激酶（AK）缺陷的突变。II类突变体的AK、腺苷脱氨酶和脱氧腺苷激酶水平正常。这些突变体也对1-β-D-阿拉伯呋喃糖基胞嘧啶（araC）表现出抗性，其抗性机制可能是由于核糖核苷酸还原酶基因突变产生了一种对9-β-D-阿拉伯呋喃糖基腺嘌呤5'-三磷酸（araATP）和2'-脱氧腺苷5'-三磷酸（dATP）抑制作用具有更高抗性的酶。与I类和II类突变体不同，III类突变体表现出对腺苷（Ado）极度敏感。Ados/araAr/dAdor表型特性可归因于单个突变。II类和III类是新型的araA抗性突变体。
