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Disruption of ROS homeostasis either pharmacologically or genetically has been shown to cause abnormal tubulin polymerization or impaired cell plate formation in Arabidopsis and wheat root tip cells, resulting in defective cytokinesis ( 2 O 2 , OH, and O 2 present in the apoplast affect cell wall stiffness and extensibility, thereby determining cell expansion rates

This generally agrees with the flood-gate model of ROS dynamics 70,71 , where a prolonged ROS stimulus (e.g., rotenone) can be cleared over time, but a sudden larger insult of ROS (e.g., pulsed KR stimulation) overwhelms redox machinery and leads to diffusion between compartments and ROS release into the cytosol

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In 2005, the proportion of neonatal CM was estimated at 5,2% based on the analysis of 57 newborns with mitochondrial cytopathy [145]

NOTCH2NLC GGC repeat expansion in patients with vascular leukoencephalopathy

A role for the NLRP3 inflammasome in metabolic diseasesdid Warburg miss inflammation