The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
And this is unrelated to DAF2? Although, interestingly, in the screens that gave the DAF mutants, one of the DAF mutants, in retrospect, one of the ones actually had never been identified what the gene was. It was simply a mutant that had a mutation. It turns out to be raptor. I think it's DAF15.
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
It was an important paper in worms where there was a mutant in the C. elegans version of mTORC1 that had longevity effects.
Even at the time you didn't appreciate what you do now, which is that effectively mTORC1 sits at the center of the universe for at least some of the things that we care a lot about, including potentially longevity. We did not.
his group published a nice paper not that long ago where they knocked out several components of the torque 1 complex inhibition of torque 1 extends life span and health span and rodents if you do that to torque 2 it accelerates death
and the first breakthrough for us was the Discover of a protein that that got this name Raptor um which at the time people didn't like this name but now is is a well studied protein and as Matt alluded there's actually genetics on Raptor that connect it to to lifespan in the aging process and so that defined what we now call torque 1 or M torque 1
and the first breakthrough for us was the discovery of a protein that that got this name Raptor um which at the time people didn't like this name but now is is a well-studied protein and as Matt alluded there's actually genetics on Raptor that connected to to lifespan in the aging process and so that defined what we now call torque 1 or M torque 1