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Susanne Brodesser and the CECAD Lipidomics Facility for their support

This condensin-mediator interaction facilitates condensin recruitment to highly transcribed genes and mitotically activated genes, the latter of which demarcate condensin-mediated domains

Additional strategies aim to disrupt mitochondrial function through VDAC1 blockade or to reduce tumor hypoxia using hypoxia-activated prodrugs, hyperbaric oxygen therapy, and oxygen-transporting agents

Mutant FUS R495X dysregulates the expression of genes associated with oxidative mitochondrial metabolism in neurons, and significantly reduces the size of mitochondria, which induces neurotoxicity (Nakaya and Maragkakis, 2018)