By David Michaels
A continual video-game tie-in novel sequence "created by" Tom Clancy, yet written via a variety of authors lower than the pseudonym David Michaels
Third Echlon operative related Fisher is aware that numerous disastrous missions have depleted the ranks of the Splinter Cells. What he doesn't comprehend is attractive piece of facts has been exposed that issues to the mole who bought out his government...
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Extra resources for Endgame (Tom Clancy's Splinter Cell, Book 6)
This MeMPR-induced stimulation of MP anabolism is apparently related to inhibition of phosphoribosylpyrophosphate amidotransferase by methylthio-IMP accompanied by accummulation of increased concentration of PRPP. Since methylthio-IMP is an analogue of AMP, it may interfere with other reactions involving formation or participation of AMP. Such effects as well as any possible incorporation of the analogue into nucleic acids remain to be investigated. Resistance: MeMPR-resistant sublines have been isolated from Ehrlich ascites carcinoma (CALDWELL, HENDERSON and PATERSON, 1967; Ho and FREI, 1968), and from H.
Thus, interference by xyl-ATP with the formation of PRPP is likely to cause inhibition of cellular growth and multiplication. In addition to the above major inhibitory site, there are other reactions which are known to be affected by xyl-A. It is as effective as adenosine as a feedback inhibitor of purine synthesis in mice by preventing 5' -phosphoribosyl-N-formylglycineamide formation. The feedback inhibition is probably not significant in vivo since adenosine cannot produce the increased survival times observed in mice treated with xyl-A.
However, it should be noted that inosine or guanosine kinases ha ve not been reported to occur in mammalian cells. All facets of the metabolism and inhibitory action of MeMPR are not known; however, it can be said at present that methylthio-IMP is the active form of the inhibitor (Fig. >- Methylthio-IMP _ _ Thio-IMP-E<------MP Fig. 12. Phosphorylation of MeMPR to the active metabolite and the known site of inhibition as indicated by ~ in mouse tissues, Ehrlich ascites carcinoma cells or in cell-free extracts of tumors (CALDWELL, HENDERSON and PATERSON, 1966).