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doi: 10.1080/15548627.2023.2170960 61 TasuJ-PTougeronDRolsM-P

In this aspect, it suggested that dysfunction of the mitochondria and oxidative stress might be the main factor behind the T-2 toxin-induced apoptosis in the fetal brain [105]

We noted that the prototypical conformational mutant R175H, which has previously been characterized as responsive to APR-246 [10], was neither significantly enriched nor depleted in the treated population (Supplementary Fig