@article {42,
	title = {Expression of the yeast PIS1 gene requires multiple regulatory elements including a Rox1p binding site.},
	journal = {J Biol Chem},
	volume = {278},
	year = {2003},
	month = {2003 Oct 3},
	pages = {38646-52},
	abstract = {The PIS1 gene is required for de novo synthesis of phosphatidylinositol (PI), an essential phospholipid in Saccharomyces cerevisiae. PIS1 gene expression is unusual because it is uncoupled from the other phospholipid biosynthetic genes, which are regulated in response to inositol and choline. Relatively little is known about regulation of transcription of the PIS1 gene. We reported previously that PIS1 transcription is sensitive to carbon source. To further our understanding of the regulation of PIS1 transcription, we carried out a promoter deletion analysis that identified three regions required for PIS1 gene expression (upstream activating sequence (UAS) elements 1-3). Deletion of either UAS1 or UAS2 resulted in an approximately 45\% reduction in expression, whereas removal of UAS3 yielded an 84\% decrease in expression. A comparison of promoters among several Saccharomyces species shows that these sequences are highly conserved. Curiously, the UAS3 element region (-149 to -138) includes a Rox1p binding site. Rox1p is a repressor of hypoxic genes under aerobic growth conditions. Consistent with this, we have found that expression of a PIS1-cat reporter was repressed under aerobic conditions, and this repression was dependent on both Rox1p and its binding site. Furthermore, PI levels were elevated under anaerobic conditions. This is the first evidence that PI levels are affected by regulation of PIS1 transcription.},
	keywords = {Anoxia, Base Sequence, Binding Sites, Carbon, Chloramphenicol O-Acetyltransferase, Choline, Chromatography, Thin Layer, Conserved Sequence, DNA, DNA, Complementary, DNA-Binding Proteins, Gene Deletion, Gene Expression Regulation, Fungal, Genes, Reporter, Inositol, Lipid Metabolism, Models, Biological, Models, Genetic, Molecular Sequence Data, Oxygen, Phospholipids, Plasmids, Promoter Regions, Genetic, Protein Binding, Repressor Proteins, RNA, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Transcription, Genetic, Transferases (Other Substituted Phosphate Groups)},
	issn = {0021-9258},
	doi = {10.1074/jbc.M305251200},
	author = {Gardocki, Mary Elizabeth and Lopes, John M}
}
@article {1731,
	title = {Disposition of (15,16-3H)naltrexone in the central nervous system of the rat.},
	journal = {Drug Metab Dispos},
	volume = {4},
	year = {1976},
	month = {1976 May-Jun},
	pages = {276-80},
	abstract = {<p>After injection of (15,16-3H)naltrexone (10 mg/kg s.c.) in male Wistar rats, peak concentrations of drug occurred in brain and plasma within 0.5 hr. Levels of naltrexone were sustained in brain between 2 and 24 hr and were barely detectable at 48 hr. Significant amounts of metabolities were present in brain and plasma at longer time periods. The t1/2 of naltrexone in brain and plasma were approximately 8.0 and 11.4 hr. respectively. The brain/plasma ratios of naltrexone at earlier times (0.5-1 hr) were higher than those at later times. The binding of naltrexone in vitro with rat plasma proteins in concentrations of 1-10 mug/ml ranged between 41 and 59\% 6beta-Naltrexol was present in very small amounts in brain but not in plasma. In addition to 7,8-dihydro-14-hydroxynormophinone and 7,8-dihydro-14-hydroxynormophine, tentative evidence was obtained for three other metabolites of naltrexone in brain. These metabolites were also present in plasma in addition to free and conjugated naltrexone and its N-dealkylated metabolites.</p>},
	keywords = {Animals, Blood-Brain Barrier, Brain, Chromatography, Thin Layer, Male, Naloxone, Naltrexone, Rats},
	issn = {0090-9556},
	author = {Misra, A L and Bloch, R and Vardy, J and Mul{\'e}, S J and Verebely, K}
}
@article {1706,
	title = {Digitoxin metabolism by rat liver microsomes.},
	journal = {Biochem Pharmacol},
	volume = {24},
	year = {1975},
	month = {1975 Sep 1},
	pages = {1639-41},
	keywords = {Animals, Chromatography, Thin Layer, Digitoxigenin, Digitoxin, Hydroxylation, In Vitro Techniques, Male, Microsomes, Liver, NADP, Rats, Time Factors},
	issn = {0006-2952},
	author = {Schmoldt, A and Benthe, H F and Haberland, G}
}
