| First Author | Sastry KJ | Year | 1987 |
| Journal | Biochem Genet | Volume | 25 |
| Issue | 11-12 | Pages | 765-77 |
| PubMed ID | 2835956 | Mgi Jnum | J:306608 |
| Mgi Id | MGI:6717101 | Doi | 10.1007/BF00502597 |
| Citation | Sastry KJ, et al. (1987) Adenosine kinase deficiency in tritiated deoxyadenosine-resistant mouse S49 lymphoma cell lines. Biochem Genet 25(11-12):765-77 |
| abstractText | Mutant sublines were derived of S49 mouse T-lymphoma cells that were resistant to tritiated deoxyadenosine. Twenty-five isolates that were selected in 1 microCi/ml of the nucleoside were cross-resistant to 6-thioguanine, were sensitive to HAT (hypoxanthine, aminopterin, and thymidine), and contained less than 1% of hypoxanthine phosphoribosyltransferase activity in wild-type cells. One of the mutant clones, S49-dA2, was further subjected to selection in a medium containing 2 microCi/ml tritiated deoxyadenosine and 1 microgram/ml deoxycoformycin, an inhibitor of adenosine deaminase. All resistant subclones were cross-resistant to tubercidin, 6-methylmercaptopurine riboside, and arabinosyladenine. One of the subclones, S49-12, was completely devoid of adenosine kinase and was partially deficient in deoxyadenosine kinase. This subclone, however, contained wild-type levels of deoxycytidine kinase. DEAE chromatography of the wild-type cell extracts revealed two deoxyadenosine phosphorylating activities, one of which coeluted with adenosine kinase and was the enzyme missing in S49-12. The other species phosphorylated both deoxyadenosine and deoxycytidine, of which deoxycytidine was the preferred substrate. |
