Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intersubunit cross-linked creatine kinase (CK) has been prepared with the cross-linking reagent dithiobis(succinimidyl propionate) (DTSP). Unfolding of cross-linked CK during denaturation by guanidine hydrochloride (GuHCl), as monitored by intrinsic fluorescence, circular dichroism and fluorescence of the hydrophobic probe, 1-aniline-naphthalene-8-sulfonate (ANS), occurs in two stages with increasing GuHCl concentration. The process is similar to that of the unmodified enzyme, but in the second stage, conformational changes of the cross-linked enzyme need higher concentration of GuHCl, suggesting that there is a stable intermediate during its unfolding transition and the intermediate is stabilized by intersubunit cross-linkage.
Biochem Mol Biol Int 1997 Sep
PMID:The influence of intersubunit cross-linking on the conformational changes of creatine kinase during denaturation by guanidine hydrochloride. 931 99

The protective effects of alpha-Hederin on carbon tetrachloride-induced hepatotoxicities were investigated in mice. Pretreatment with alpha-Hederin prior to the administration of carbon tetrachloride significantly prevented the increase in serum alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activity and lipid peroxidation in a dose dependent manner. Hepatic glutathione levels and glutathione-S-transferase activities were not affected by pretreatment with alpha-Hederin alone but pretreatment with alpha-Hederin protects carbon tetrachloride-induced depletion of hepatic glutathione levels. The effects of alpha-Hederin on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon tetrachloride bioactivation were investigated. alpha-Hederin markedly decreased the P450 2E1-specific activities of p-nitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. These results demonstrate that treatment of mice with alpha-Hederin decreases the expression and activities of P450 2E1 enzyme, and reduces biotransformation of carbon tetrachloride, and diminished carbon tetrachloride-induced liver injury.
Biochem Mol Biol Int 1998 Jun
PMID:The prevention of carbon tetrachloride-induced hepatotoxicity in mice by alpha-hederin: inhibiton of cytochrome P450 2E1 expression. 963 40

Semisynthetic flavocytochromes, obtained by covalent binding of riboflavin with cytochromes P450 2B4, were able to catalyze the H2O2-mediated reactions of aniline p-hydroxylation, aminopyrine N-demethylation and p-nitroanizole' O-dealkylation. The rates of the flavocytochrome-catalyzed, H2O2-supported reactions far exceeded those of the appropriate NADH-dependent reactions and were comparable with the cytochrome P450 2B4-catalyzed, peroxide-mediated reaction rates. The kinetic parameters (kcat, K(m)) for the peroxide-dependent flavocytochrome P450 2B4 reactions were obtained. Sodium cyanide and SKF-525A, a specific P450 inhibitor, were both shown to inhibit these reactions. The generation of active oxygen species by flavocytochrome 2B4 was registered by chemiluminescence intensity.
Biochem Mol Biol Int 1998 Jun
PMID:Hydrogen peroxide-supported activities of semisynthetic flavocytochrome 2B4. 963 41

The rotational spectra of aniline-water and its 18O isotopomer have been studied in the microwave region between 3 and 26.5 GHz using a pulsed molecular beam FT microwave spectrometer. The spectra were described in terms of a centrifugally distorted asymmetric rotor. Assuming a linear hydrogen NellipsisH-O bond and that the water molecule was located in the symmetry plane of aniline, two structures turned out to be possible. In structure (I) the free water proton is directed toward the aniline ring. In structure (II) the proton is bent away from it. Ab initio calculations indicate that only structure (I) is supported by the experimental results. Copyright 1998 Academic Press.
J Mol Spectrosc 1998 Aug
PMID:The Aniline-Water Complex. 966 21

The chemical modifications induced by trifluoperazine (TFP) in erythrocyte ghosts have been investigated by fluorescence quenching. The apparent distance separating the membrane protein tryptophans and bound 1-aniline-8-naphthalene sulfonate (ANS) molecules decreased after treating erythrocyte membranes with TFP. This effect was accompanied by a significant decrease in the maximum efficiency of energy transfer. We conclude that TFP-induced alterations in the structure of membrane proteins lead to a rearrangement of the surrounding lipids, and consequently to local conformational changes in membrane organization.
Mol Genet Metab 1998 Jun
PMID:Effects of trifluoperazine on the conformation and dynamics of membrane proteins in human erythrocytes. 970 39

The effects of alpha-Hederin, a triterpenoid saponin which exists in some oriental herbs, on the expression of liver cytochrome P450s were examined in mice. The administration of alpha-Hederin to mice significantly decreased the hepatic content of P450 and the activities of microsomal ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, and aniline hydroxylase, representative activities of cytochrome-P4501A1, -P4501A2, and -P4502E1, respectively, in a dose- and time-dependent manner. However, pentoxyresorufin O-dealkylase, a representative activity of cytochrome P4502B1/2, was decreased to a lesser extent. alpha-Hederin also decreased inducible monooxygenase activities in the same manner. Suppressions of P450 isozyme expression occurred in alpha-Hederin treated hepatic microsomes, as determined by immunoblot analysis in a manner consistent with that of the enzyme activity levels. Levels of mRNA of P4501A1/2 and P4502B1/2 were also decreased by alpha-Hederin as shown by Northern blot analysis. In contrast, the level of P4502E1 mRNA in the liver of alpha-Hederin treated mice was unchanged. These results suggest that alpha-Hederin may act as a more specific suppressor for P4501A and P4502E1 than P4502B and that the suppression involves decreases in mRNA levels except in the case of P4502E1.
Biochem Mol Biol Int 1998 Dec
PMID:Suppression of constitutive and inducible cytochrome P450 gene expression by alpha-hederin in mice. 986 56

Molecularly imprinted polymers have been prepared against aniline and a bis-aniline compound, making use of a crown ether (18-crown-6) to solubilize the monomer-template complexes. Subsequent chromatographic rebinding studies in the absence of crown ether revealed regioselectivity for the templates in the respective polymers. This study indicates that crown ethers can be potentially useful in conjunction with molecular imprinting to solubilize and imprint organic solvent-insoluble compounds.
J Mol Recognit 1998
PMID:Crown ethers as a tool for the preparation of molecularly imprinted polymers. 1007 17

Trichomaglin, a novel ribosome-inactivating protein, has been isolated from root tuber of a plant Maganlin (Trichosanthes Lepiniate, Cucurbitaceae). The isolation and purification procedure included ammonium sulfate precipitation, Sephadex G-75 chromatography and CM-Sephadex C-50 chromatography. The protein was identified to be homogeneous by SDS-PAGE and FPLC analysis. Its molecular weight is 24,673 dalton and isoelectric point is 5.8, determined by electrospray ionization mass spectroscopy and isoelectric focusing gel electrophoresis respectively. Trichomaglin can inhibit protein synthesis in rabbit reticulocyte lysate with ID50 of 10.1 nM. When rat ribosome was incubated with trichomaglin, a diagnostic RNA fragment appeared on polyacrylamide gel after ribosomal RNAs were treated with acidic aniline. It was concluded that trichomaglin is an RNA N-glycosidase. In addition, it has been verified to be an abortifacient protein.
Biochem Mol Biol Int 1999 Feb
PMID:Purification and characterization of trichomaglin--a novel ribosome-inactivating protein with abortifacient activity. 1020 63

Testicular cytochrome P-450 was purified by a procedure including preparative isoelectrofocusing. The cytochrome P-450 was determined to have an isoelectric point of 6.47 on analytical isoelectric focusing. The purified cytochrome P-450 was found to be homogeneous and its molecular weight was estimated to be 52,000 on polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The carbon monoxide difference spectrum with a peak at 448 nm exhibited absorption spectrum of a typical cytochrome P-450. 284-fold purification was achieved with an yield of 10.6%. Following preparation of the microsomes, the purification is accomplished by a two-step procedure utilizing Aniline-Sepharose 4B column chromatography and preparative isoelectric focusing.
Biochem Mol Biol Int 1999 Feb
PMID:Purification of cytochrome P-450 from pig testis by aniline-sepharose 4B and isoelectric focusing. 1020 71

Toxic oil syndrome (TOS), a multisystemic epidemic outbreak in 1981 in Spain, was caused by the ingestion of a cooking oil mixture containing rapeseed oil denatured with aniline. The mechanisms and causative agents responsible for the TOS are still not known. Although primary lesions observed in TOS patients could not be reproduced experimentally, the levels of fatty acid anilides (FAAs) and aniline in TOS-related cooking oil were considered proximate markers of TOS. Aniline, available from free aniline and FAAs ingested with TOS-related cooking oil, and its reconjugation with endogenous fatty acids could be an early event leading to TOS. Therefore, the present study was undertaken to determine the formation of FAAs following an oral dose of 2 mmol/kg aniline hydrochloride (AH) via gavage in rats. Here, 16:0, 18:0, 18:1, 18:2, 18:3, and 20:4 FAAs were analyzed in the whole blood, brown fat, liver, and pancreas at 0 (control), 0.25, 0.5, 1, 3, 6, 12, 24, and 48 hours. Generally, 16:0 and 18:1 FAAs were detected in the whole blood, brown fat, and liver of AH-treated rats with highest mean levels at 0.25 or 0.5 hour, except 3 hours for the whole blood. Only 16:0 FAA was detectable in the pancreas of AH-treated animals. The 18:0 FAA was also detected frequently in the liver while other FAAs were either in trace amounts or not detectable in the tissues analyzed in the present study. Overall, highest formation of the 16:0 FAA was found in the liver followed by pancreas and of 18:1 FAA in the whole blood and brown fat. These results indicate a rapid formation and further metabolism and disposition of FAAs in rat model and support our previous findings that 18:1 and 16:0 fatty acids are better substrates for the conjugation with aniline. Surprisingly, a small or trace amount of a few FAAs also detected in the tissues of control rats indicates their endogenous biosynthesis and/or presence. Results of 18:1 fatty acid incubation and aniline in the presence of fatty acid ethyl ester synthase, purified to homogeneity from rat liver microsome, suggest that formation of FAAs is catalyzed by an enzyme involved in the conjugation of fatty acids with xenobiotic alcohols. Because the FAAs are known to exert a wide range of toxicity in experimental animals and primary cell cultures, in vivo formation of FAAs could be an early event leading to TOS.
J Biochem Mol Toxicol 1999
PMID:Fatty acid anilides: in vivo formation and relevance to toxic oil syndrome. 1040 61


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