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To confirm whether an increase in UCK2 activity as a result of pyrimidine stress was the driving force behind mitochondrial biogenesis signalling, we knocked down UCK2 in cells using siRNA (Fig

doi: 10.1016/j.molmed.2021.06.002 14 MuellerCLinJCSheriffSMaudsleyAAYoungerJW

PMCID: PMC3845706

Animal models of depression show a decrease in cell proliferation (creation of new brain cells) as well as an increase in cell death (apoptosis).[ref] A relative lack of ATP due to mitochondrial dysfunction could also impact the ability of neurotransmitters to bind to their receptors

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