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By contrast, the expression of mitochondrial fusion protein Mfn2 decreased in both in vivo and in vitro ischemic models, and reduced Mfn2 expression led to mitochondrial dysfunction and disruption of Ca 2+ homeostasis [49, 50]
Since mutations have been identified in some of these MTases and were associated with neurodevelopmental disorders, it will be also critical in the future to understand the role of the methyl group added by these TRMT112-MTase complexes on general cellular processes such as translation of specific proteins important for brain development for instance
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Despite its benefits in early clinical trials, the trials were halted due to limited efficiency and several side effects of the murine and chimeric types [142, 192, 193]
