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1 whose expression was affected by DHEA and/or nafenopin.
2 DHEA or the classic peroxisome proliferator nafenopin.
3 id not affect negative regulation by DHEA or nafenopin.
4 ary for negative regulation by both DHEA and nafenopin.
5 the response of mouse hepatocytes to the PP, nafenopin.
6 urbation of hepatocyte growth by PPs such as nafenopin.
7 bodies were able to abrogate the response to nafenopin.
8 the presence of the peroxisome proliferator, nafenopin.
9 tion of CYP4A2 mRNA levels by either DHEA or nafenopin.
10 ephosphorylated upon treatment with DHEA and nafenopin.
11 ly abolished negative regulation by DHEA and nafenopin.
12 ession at this site must differ for DHEA and nafenopin.
14 tudy, we demonstrate that various PPARalpha (nafenopin) and gamma (ciglitazone and troglitazone) agon
15 bited the induction of CYP4A2 mRNA levels by nafenopin but had little effect on induction of CYP4A1 o
16 an altered expression pattern in response to nafenopin differed from those showing altered expression
17 ith altered expression upon stimulation with nafenopin, including muscarinic acetylcholine receptor 3
18 factor (EGF) and the peroxisome proliferator nafenopin induce DNA replication in primary rat hepatocy
19 ary rat hepatocytes decreased both DHEA- and nafenopin-induced FACO activity in primary rat hepatocyt
22 pared with those induced by a single dose of nafenopin (NAF), a direct mitogen which does not induce
23 h was induced by DHEA and to a lesser extent nafenopin, nuclear tyrosine phosphatase, which was induc
25 ive regulation of a CYP2C11 reporter gene by nafenopin required coexpression of PPARalpha, whereas ne
28 the suppression of apoptosis in response to nafenopin was abrogated completely by blocking antibodie
29 that the responsive region for both DHEA and nafenopin was between -108 and -60 relative to the trans
30 ation by DHEA or the peroxisome proliferator nafenopin was in large part unaffected by treatment of a
31 e induction of peroxisomal beta-oxidation by nafenopin was not blocked by the anti-TNFR1 antibody.
32 induction of hepatic CYP4A2 mRNA by DHEA or nafenopin was significantly inhibited (> 80%) compared w
33 ffects of a classic peroxisome proliferator, nafenopin, with those of the steroid dehydroepiandroster
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