The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The comparative effects of 5'-methylthioadenosine and some of its analogs on cells containing, and deficient in, 5'-methylthioadenosine phosphorylase.

The antiproliferative effects of 5'-methylthioadenosine and the 5'-methylthioadenosine analogs, 5'-isobutylthioadenosine, 5'-deoxyadenosine and 5'-methylthiotubercidin were examined using two mouse cell lines, one 5'-methylthioadenosine phosphorylase-deficient the other containing 5'-methylthioadenosine phosphorylase. All of the compounds were found to be growth inhibitory to both cell lines, demonstrating that these compounds need not be degraded to exert their inhibitory effects. A correlation was observed between the potency of the growth inhibitory effect and the ability of the cells to degrade these compounds. 5'-Methylthioadenosine, 5'-deoxyadenosine and 5'-isobutylthioadenosine, all of which are substrates for the 5'-methylthioadenosine phosphorylase in vitro, were more growth inhibitory to the 5'-methylthioadenosine phosphorylase-deficient cells than to the 5'-methylthioadenosine phosphorylase-containing cells, whereas, the 7-deaza analog, 5'-methylthiotubercidin, a nondegradable inhibitor of the 5'-methylthioadenosine phosphorylase, was a more potent inhibitor of the 5'-methylthioadenosine phosphorylase-containing cell line. Due to the inhibition by 5'-methylthiotubercidin on 5'-methylthioadenosine phosphorylase in vitro the disposition of cellularly-synthesized 5'-methylthioadenosine was explored using both cell types. 5'-Methylthiotubercidin inhibited the accumulation of exogenous 5'-methylthioadenosine from 5'-methylthioadenosine phosphorylase-deficient cells with no effect on intracellular 5'-methylthioadenosine. In contrast, 5'-methylthiotubercidin caused a large accumulation of extracellular 5'-methylthioadenosine with a concomitant smaller increase intracellularly in 5'-methylthioadenosine phosphorylase-containing cells. That cellularly-synthesized 5'-methylthioadenosine as well as the cellular excretion of this nucleoside are altered in response to treatment with 5'-methylthiotubercidin suggests two possible sites at which 5'-methylthiotubercidin may exert its effect.[1]

References

 
WikiGenes - Universities