PolyGA targets the ER stress-adaptive response by impairing GRP75 function at the MAM in C9ORF72-ALS/FTD.

Furthermore, as previously shown [ 11 ], we found a direct correlation between large PolyGA aggregates (volume > 1 μm 3 ) and the expression of P i -eIF2α in MNs, which became highly significant by P150 in mutant MNs coinciding with widespread UPR in MNs compared with P80, when highest GRP75 expression is observed.

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Transcripts of both GRP75 binding partners, i.e., ITPR3 and VDAC1, exhibited a significant trend toward higher expression (Fig. 1 b).

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