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pubmed:abstractText |
Mitochondrial uncoupling proteins (UCPs) can dissociate oxidative phosphorylation from respiration, and they appear to be critical for energy balance. One of these proteins, UCP2, is also expressed in neurons of subcortical brain regions of healthy subjects. Here, we report on the protective role of UCP2 in brain injury by revealing its early induction after lesions and its inverse relationship with activation of an apoptotic signal, caspase 3, in wild-type and UCP2 overexpressing transgenic mice.
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