PMID: 6974904Mar 1, 1981Paper

Isolation and preliminary characterization of 9-beta-d-arabinofuranosyladenine-resistant mutants of baby hamster cells

Somatic Cell Genetics
V L Chan, P Juranka

Abstract

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.

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Citations

Aug 1, 1985·Journal of Cellular Physiology·S ArcherV L Chan
Mar 1, 1989·Somatic Cell and Molecular Genetics·J C PangV L Chan
Mar 29, 2001·BioFactors·R A MittalH E Khoo
Jan 1, 1985·Cancer Metastasis Reviews·V LingR P Hill
Apr 18, 2013·Pharmacological Reviews·Detlev Boison
Jan 3, 2008·The Journal of Biological Chemistry·Munender VodnalaAnders Hofer
Dec 13, 1983·Biochimica Et Biophysica Acta·P P Saunders, M M Lai

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