FUS regulates RAN translation through modulating the G-quadruplex structure of GGGGCC repeat RNA in <i>C9orf72</i>-linked ALS/FTD.

So when they call FUS an RNA chaperone, are they simply meaning it is changing the structure of the repeat, or could it just be interacting with the repeat to coat the repeat and prevent it from folding into whatever in vivo structures? Can they speculate on why some RNA chaperones lead to presumed decay of the repeat and others do not? Can they discuss these points in the discussion? Detailed mechanistic understanding of RNA chaperones that ultimately promote decay of the repeat might be of highly significant therapeutic benefit.

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