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. 2019 Aug 6;11:207. doi: 10.3389/fnagi.2019.00207

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Copyright © 2019 Maulik, Mitra, Basmayor, Lu, Taylor and Bult-Ito.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Defects in stress resistance are ameliorated by silencing of fat-5 and fat-7 genes in C. elegans expressing human mutated α-synuclein (A53T mutation). Graphical representation of (A) mean lifespan (n = 44 animals per group) B) viable progeny (C) pharyngeal pump rate (D) body bends (E) heat tolerance and (F) osmotic tolerance of JVR203 animals (n = 10–15 animals per group) fed on different genetic RNAi treatments (L4440, fat-5, fat-7, nhr-49 and tub-1). Empty vector L4440 was considered as control. The data represent the mean ± SEM with significant differences between the control and treatments at ***p < 0.001. Each experiment was repeated three times.