Disease relevance of Ehhadh

• All 12 neoplastic nodules and nine hepatocellular carcinomas (HCCs) that were analyzed for PBE mRNA by in situ hybridization showed an intense signal comparable to the adjacent non-neoplastic liver [1].
• Mutacin MT6223, a cell-free bacteriocin produced by Streptococcus sobrinus MT6223, was purified by ammonium sulphate precipitation, chromatofocusing with PBE 94 and column chromatography on SP Sephadex C-25 [2].

High impact information on Ehhadh

• Reconstitution of purified mu opioid receptors with purified guanine nucleotide-binding regulatory proteins (G proteins) was investigated. mu opioid receptors were purified by 6-succinylmorphine AF-AminoTOYOPEARL 650M affinity chromatography and by PBE isoelectric chromatography [3].
• All three peroxisome proliferators rapidly increased the rate of FAOxase and PBE gene transcription in liver, with near maximal rates (9-15 times control) reached by 1 hr and persisting until at least 16 hr after administration of the compound [4].
• Pretreatment of rats with dexamethasone (2 mg/kg) inhibited both hepatocyte DNA synthesis and the induction of the peroxisomal bifunctional enzyme gene [5].
• The radioactive material that eluted as pure IGF-I (40% acetonitrile) was further studied by chromatofocusing on a Pharmacia PBE 94 column [6].
• We have examined ciprofibrate and dehydroepiandrosterone (DHEA)-induced hepatic lesions for the peroxisomal beta-oxidation system enzyme peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (PBE) and its mRNA using SDS-polyacrylamide gel electrophoresis, antibodies and cDNA probe [1].

Biological context of Ehhadh

• The induction of cyt.P452 mRNA always preceded the induction of PBE mRNA, but for both, the maximal induction (10-20-fold over control) was obtained within 24 hr and was achieved by transcriptional activation [7].
• By transfection of cells with the putative PPRE-driven luciferase reporter vector and PPARalpha, we found no significant activation of the luciferase gene expression, in contrast to the case with reporter expression driven by the PPRE of the peroxisomal bifunctional enzyme [8].
• A DNA sequence that confers a response to a class of rodent hepatocarcinogens termed peroxisome proliferators has been identified 2947bp upstream of the rat peroxisomal bifunctional enzyme gene [9].

Anatomical context of Ehhadh

• Although peroxisomal bifunctional enzyme (enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase; BE) is a positive marker for peroxisome proliferation, it is completely absent or expressed very weakly in rat hepatic preneoplastic and neoplastic lesions induced by peroxisome proliferators (PP) [10].
• Significant differences were observed between enterocyte peroxisomal enzymatic activities (catalase and PBE: peroxisomal bifunctional enzyme) in treated and control females on the one hand, and in the foetus of treated and control mothers on the other [11].

Associations of Ehhadh with chemical compounds

• In addition, they maintained the ability to show induction of the peroxisome proliferator-inducible enzymes peroxisomal bifunctional enzyme (PBE) and cytochrome P450IVA1 in response to the peroxisome proliferator nafenopin [12].
• At early time points (1 and 2 hr after the addition of nafenopin), in the absence of on-going protein synthesis, the amount of cyt.P452 mRNA (and not of PBE mRNA) was transiently higher in the presence of cycloheximide and nafenopin than in the presence of nafenopin alone [7].
• These results indicate that the levels of peroxisomal bifunctional enzyme were regulated by thyroid hormone in vivo [13].
• PBE-induced constriction was attenuated by either concentration of halothane (P < 0.05) but was unaltered by isoflurane (P > 0.5) [14].
• Two up-regulated proteins, glutathione S-transferase with methapyrilene and peroxisomal bifunctional enzyme with SB-219994, were identified in this manner [15].

Enzymatic interactions of Ehhadh

• A new enoyl-CoA hydratase present in these early fractions catalyzes the conversion of D-3-hydroxyacyl-CoA to 2-trans-enoyl-CoA which can be hydrated by crotonase or the peroxisomal bifunctional enzyme to L-3-hydroxyacyl-CoA [16].

Other interactions of Ehhadh

• Interestingly, whereas the levels of peroxisome proliferator-induced Mr 80,000 polypeptide and catalase and peroxisomal bifunctional enzyme, and the corresponding mRNAs and peroxisome volume density were unaffected [17].
• There was limited overlap in observed protein abundance changes between the three groups, and where this was the case (cytosolic epoxide hydrolase, peroxisomal bifunctional enzyme, hydroxymethyl glutaryl CoA, synthase, long chain acyl-CoA thioesterase), expression of these proteins had previously been shown to be under the control of PPAR activity [18].

Analytical, diagnostic and therapeutic context of Ehhadh

• FAOxase and PBE mRNA levels, measured by blot-hybridization analysis and FAOxase and PBE protein content, analyzed by immunoblotting, increased concurrently up to at least 16 hr following a single dose of peroxisome proliferator [4].
• After 4 weeks, NPC cocultures showed a six- and a fourfold induction of PBE and cytochrome P450IVA1 expression, respectively, which compared well with the three- and fivefold induction seen in freshly isolated cells [12].
• Immunoblot and Northern blot analysis showed a marked increase in PBE enzyme and PBE mRNA respectively in HCC and adjacent non-neoplastic liver tissue [1].
• The amount of peroxisomal bifunctional enzyme was increased by thyroidectomy and decreased by 3,5,3'- triiodo-L-thyronine treatment in the whole homogenate of rat liver [13].
• Gel filtration chromatography confirmed higher molecular weight complexes of xanthine oxidase and xanthine dehydrogenase in the presence of PBE [19].

References