Figure 7From: Molecular Characterization of Chinese Hamster Cells Mutants Affected in Adenosine Kinase and Showing Novel Genetic and Biochemical CharacteristicsA model to account for the lack of AdK activity in the cell extracts of the FomR-4 mutant and dominant expression of its drug-resistance phenotype. (A) In the WT cells, AdK converts Ado and various Ado-analogs (e.g. FoA, Tub) into their corresponding monophosphates; subsequently AMP-kinase (AMPK) and other enzymes convert them into di- and tri-phosphates. (B) and (C), In the FomR-4 mutant or the cell hybrids formed between FomR-4 and the WT cells, the Ser191Phe mutation in AdK (indicated by âœ) leads to its complex formation with AMPK. This mutation is also postulated to specifically prevent the binding of FoA and FoA-MP to the AdK-AMPK complex. As a result of this complex formation, AMP (or Tub-MP) formed by AdK is not released but directly transferred to the AMPK for conversion into ADP. These account for the unusual properties of the FomR-4 mutant.Back to article page