1985
DOI: 10.1016/0006-291x(85)91866-2
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The regulation of cytosolic epoxide hydrolase in mice

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Cited by 15 publications
(2 citation statements)
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“…This suggested that in EPXH2, the Sp1 site immediately upstream of the putative transcriptional start site is essential for expression. Because Sp1 expression is generally ubiquitous [64] such a promoter system could explain the ubiquitous expression of sEH in numerous tissues in mammals [17,20,21,23,[25][26][27][28][29][30][65][66][67]. However, it does not explain the regulation of EPHX2 by PPAR-alpha agonists and testosterone as predicted from in vivo induction studies in rodents.…”
Section: Discussionmentioning
confidence: 99%
“…This suggested that in EPXH2, the Sp1 site immediately upstream of the putative transcriptional start site is essential for expression. Because Sp1 expression is generally ubiquitous [64] such a promoter system could explain the ubiquitous expression of sEH in numerous tissues in mammals [17,20,21,23,[25][26][27][28][29][30][65][66][67]. However, it does not explain the regulation of EPHX2 by PPAR-alpha agonists and testosterone as predicted from in vivo induction studies in rodents.…”
Section: Discussionmentioning
confidence: 99%
“…Another reasonable consideration is that the two immunorelated forms of sEH are the products of two genes. Administration of the hypolipidemic drug clofibrate in the diets of rodents causes an increase in cytosolic sEH activity in liver cells, whereas peroxisomal sEH activity appears to be unaltered [33–36]. Hollinshead and Meijer [9], on the other hand, showed that clofibrate treatment did not lead to an increase in the cytosolic form of sEH.…”
Section: Discussionmentioning
confidence: 99%