Aedes albopictus cells resistant to adenosine because of a defect in nucleoside transport.
By growing Aedes albopictus mosquito cells in media containing increasing concentrations of adenosine and subsequently plating low numbers of cells in the presence of EHNA (an inhibitor of adenosine deaminase), three clones were obtained which were resistant to adenosine. The adenosine-resistant clones contained level of adenosine and thymidine kinase similar to those in the parental cells, but were unable to incorporate labeled nucleotides (adenosine, uridine, thymidine, or guanosine) into TCA-precipitable material. The inability to incorporate nucleosides was also reflected in an enhanced resistance to several nucleoside analogs such as 5-fluorodeoxyuridine and tubercidin but not to the unribosylated base, 5-fluorouracil. Direct measurements over short time intervals indicated that the primary defect in these cells was at the level of nucleoside transport.
D000241:Adenosine / Q000494:pharmacology*; D000248:Adenosine Kinase / Q000032:analysis; D000330:Aedes / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D001693:Biological Transport, Active; D002999:Clone Cells / Q000378:metabolism; D004351:Drug Resistance; D009705:Nucleosides / Q000378:metabolism*; D013937:Thymidine Kinase / Q000032:analysis
D009705:Nucleosides; D000248:Adenosine Kinase; D013937:Thymidine Kinase; D000241:Adenosine