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Recent studies have implicated these mechanisms in the control of brain pathology, raising the possibility that altered regulation of fundamental mechanisms of oxidative stress may contribute to the pathogenesis of schizophrenia and related disorders (Floyd, 1999

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This stimulated the expression of the egr1 gene, as it appeared as a combined effect, along with increased expression of its repressor nab2 gene [98]

Together, these results suggest that the dramatically increased EC 50 of vitamin K for VKD carboxylation in DKO cells results from the cells losing the ability to recycle K epo by VKOR, supporting the essential role of VKOR in VKD carboxylation as previously reported 24,25,26

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