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The system that cuts off the fuel before the engine.
Slfn bactérien clive sélectivement les ARNt apportés par le phage, stoppant la traduction virale. Homologue fonctionnel direct de SLFN11 humain (restriction VIH + biomarqueur de réponse aux PARP inhibitors). Cible host-directed exceptionnelle.
Phages, like any virus, need the host's translation machinery to make their own proteins. Bacterial Schlafen found an elegant vulnerability: cleave tRNAs. No functional tRNA, no translation. No translation, no phage. And as a bonus, no bacterium either — it's abortive cell death, but it saves the neighbors. The beauty of the system is that it distinguishes phage tRNAs (modified differently) from endogenous tRNAs — at least partially. The name Schlafen ("to sleep" in German) comes from 1998: the first Schlafen genes identified were blocking T-lymphocyte proliferation in mice, as if putting them to sleep. It took 24 years to realize the same family existed in bacteria to put phages to sleep.
Reactivating SLFN11 in SLFN11-silenced tumors = making chemo effective again where it no longer is. That's a huge practical-oncology stake, and bacterial Schlafen gives us the mechanistic model to understand how to activate the human version.
Human SLFN11, the cancer-suppressor paralog, is abnormally active in cancer cells that are sensitive to topoisomerase chemotherapy, and silenced in resistant ones. It has become a routine biomarker in clinical oncology. And nobody knows exactly why it has this function — except now we know it probably comes from the bacterial anti-phage ancestor.
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