Jacob R. Mann

TL;DR: The formation of pathologically relevant inclusions is driven by aberrant interactions between low-complexity domains of TDP-43 that are antagonized by RNA binding, and it is shown that aberrant phase transitions of cytoplasmic TTP are neurotoxic and that treatment with oligonucleotides composed of T DP-43 target sequences prevent inclusions and rescue neurotoxicity.

TL;DR: In this paper, the authors describe the mechanisms underlying RNA-mediated phase transitions of RBPs and examine the molecular properties of these interactions, such as RNA length, sequence, and secondary structure, that mediate physiological or pathological LLPS.

TL;DR: WNK kinases are physiological crowding sensors that phase separate to coordinate a cell volume rescue response and bypass a strengthened ionic milieu that favors kinase inactivity and reclaim cell volume through condensate-mediated signal amplification.

TL;DR: The medium from hypoxic-preconditioned BMSCs robustly restored retinal function and prevented cell loss after ischemia when injected 24 hours after isChemia, and prosurvival signals triggered by the secretome may play a role in this neuroprotective effect.

TL;DR: In this paper , the authors show that NUP62 mislocalization contributes to TDP-43 proteinopathy in ALS/FTLD iPSC neurons, which is the most common genetic cause of ALS and FTLD, with cytoplasmic inclusions observed in regions of neurodegeneration.