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- W2017602532 abstract "Abstract Inositol depletion is an acute response to lithium and valproate, and aberrant inositol metabolism has been demonstrated in bipolar patients. While it is unlikely that the therapeutic response to inositol depleting drugs is associated with inositol depletion per se, the role of inositol as a metabolic sensor for the secretory, unfolded protein response and glucose response pathways suggests that treatment with inositol depleting drugs may lead to dramatic changes in complex cellular processes. Surprisingly, almost nothing is known about how inositol biosynthesis is regulated in human cells. In contrast, genetic, molecular, and biochemical studies in yeast for over three decades have elucidated intricate mechanisms underlying regulation of inositol biosynthesis in this model eukaryote. INO1 , the gene encoding 1D-myo-inositol 3-phosphate (MIP) synthase, is the most highly regulated of the genes required for phospholipid biosynthesis. This enzyme, which catalyzes the rate limiting step in inositol biosynthesis, is highly conserved from yeast to humans. A recent study has shown that the human INO1 gene is functional in yeast and complements the inositol deficiency of the yeast ino1 mutant. Similar to the yeast enzyme, human MIP synthase activity is decreased in vivo in the presence of valproate. Functional conservation of MIP synthase from yeast to humans underscores the power of the yeast model in understanding the effects of anti-bipolar drugs on inositol synthesis. Because inositol is a metabolic sensor for a variety of signal transduction pathways, MIP synthase may be an important target for new mood stabilizing drugs." @default.
- W2017602532 created "2016-06-24" @default.
- W2017602532 creator A5013405117 @default.
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- W2017602532 date "2004-12-01" @default.
- W2017602532 modified "2023-10-13" @default.
- W2017602532 title "1D-myo-inositol 3-phosphate synthase: conservation, regulation, and putative target of mood stabilizers" @default.
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- W2017602532 doi "https://doi.org/10.1016/j.cnr.2004.09.010" @default.
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