Eva Bentmann

TL;DR: It is proposed that two pathological hits, namely nuclear import defects and cellular stress, are involved in the pathogenesis of FUS‐opathies.

TL;DR: This study shows that arginine methylation modulates nuclear import of FUS via a novel TRN‐binding epitope and provides evidence that these two diseases may be initiated by distinct pathomechanisms and implicates alterations in arginin methylation in pathogenesis.

TL;DR: Data imply different pathological processes underlying inclusion formation and cell death between both conditions; the pathogenesis in amyotrophic lateral sclerosis with FUS mutations appears to be more restricted to dysfunction of fused in sarcoma, while a more global and complex dysregulation of all FET proteins is involved in the subtypes of frontotemporal lobar degeneration with fused in Sarcoma pathology.

TL;DR: The requirements for SG recruitment of FUS and TDP-43 were determined and it was found that cytoplasmic mislocalization is a common prerequisite for SG recruited of F US and T DP-43.

TL;DR: It is proposed that pathological inclusions containing RNA‐binding proteins, such as TDP‐43 and FUS, might arise from SGs and discussed how SGs might contribute to neurodegeneration via toxic gain or loss‐of‐function mechanisms.