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1 tisol was detected in dog, human, and monkey liver microsomes.
2 og liver microsomes than in human and monkey liver microsomes.
3 alkylation activity of human, mouse, and rat liver microsomes.
4 ster hydrolase activity from solubilized rat liver microsomes.
5 ronidation activity of mouse, rat, and human liver microsomes.
6 ylation takes place in both rodent and human liver microsomes.
7         The product was also formed in human liver microsomes.
8 bited cytochrome P450 3A4 enzyme (CYP3A4) in liver microsomes.
9 ncentrations but had no effect on cardiac or liver microsomes.
10 d proteins that bind apolipoprotein B in rat liver microsomes.
11  degradation similar to that observed in rat liver microsomes.
12 rapidly and selectively degraded in isolated liver microsomes.
13 S analysis of metabolites generated from rat liver microsomes.
14 etabolites was demonstrated in rat and human liver microsomes.
15 ctivity exhibited by CYP4F2 and rat or human liver microsomes.
16  substrates for cytochrome P450 2D6 in human liver microsomes.
17 ed by erythromycin N-demethylase activity in liver microsomes.
18 h activities similar to those found in human liver microsomes.
19 tabolically activated in the presence of rat liver microsomes.
20 tics was analyzed in both patients and human liver microsomes.
21  impairment of nifedipine oxidation by human liver microsomes.
22 ed conversion of TAX to 6-HT by 41% in human liver microsomes.
23 ficantly improved metabolic stability to rat liver microsomes.
24 idine 5'-diphosphoglucuronic acid and rabbit liver microsomes.
25  led to an increase in total SCD activity in liver microsomes.
26 ize UDP-GlcA in cartilage microsomes and rat liver microsomes.
27 e (DCCY) from cyclophosphamide (CY) in human liver microsomes.
28 roximately 30%) the 4-hydroxylation in human liver microsomes.
29 roperoxide-induced lipid peroxidation in rat liver microsomes.
30 of erythromycin with cytochromes P450 in rat liver microsomes.
31  the major cytochrome P-450 enzymes in human liver microsomes.
32 MO3 were comparable to Km values from rabbit liver microsomes.
33 le inhibition of cytochrome P450s from human liver microsomes.
34 ophenol and N,N-dimethylnitrosamine by fetal liver microsomes.
35 hich were 12-27% of those exhibited by adult liver microsomes.
36 glycero-3-phosphocholine (1-acyl-GPC) by rat liver microsomes.
37  is detectable in 90- but not 21-day-old rat liver microsomes.
38 tion favoring (-)-1a was also found in human liver microsomes.
39 of vemurafenib in in vitro assays with human liver microsomes.
40  moderate stability (t1/2 = 44 min) in mouse liver microsomes.
41  to 40-fold increases in half-lives in mouse liver microsomes.
42 g good in vitro metabolic stability in human liver microsomes.
43 d higher metabolic stability than 5 in human liver microsomes.
44 ta(6)-PZQ)Cr(CO)3 (1 and 2), by use of human liver microsomes.
45 te that this compound is stable in serum and liver microsomes.
46 se I metabolism assays performed using human liver microsomes.
47 lyzed (S)-mephenytoin hydroxylation in human liver microsomes.
48 man IMPDH type 2 and good stability in mouse liver microsomes.
49 ediated biotransformation assay based on rat liver microsomes.
50 metabolic stability in the presence of human liver microsomes.
51 he derivatives significantly in pooled human liver microsomes.
52 ism were identified by incubation with human liver microsomes.
53 lectively potent under hypoxia and stable to liver microsomes.
54 s to a complete absence of UGT1A proteins in liver microsomes.
55                                       In rat liver microsomes, 2-(3-mercaptopropyl)pentanedioic acid
56                                     In human liver microsomes, 4-oxo-atRA formation was supported by
57                       Here, we purified from liver microsomes a lumenal, soluble aminopeptidase that
58           P450 3A4 reduction was examined in liver microsomes, a reconstituted system, a fusion prote
59       In the present study, a panel of human liver microsomes activated MMDX with potentiation ratios
60 centration-dependent release of calcium from liver microsomes after a lag period.
61 cy, metabolic stabilities in mouse and human liver microsomes, along with acceptable cytotoxicity pro
62                                              Liver microsomes also preferred 18:0,22:6-PC as the subs
63                 Metabolism of 17AAG by human liver microsomes also required an electron donor, with N
64 sphorylation and good metabolic stability in liver microsome and hepatocyte assays.
65 and quinidine, two prototypic substrates, in liver microsomes and a reconstituted enzyme system with
66 ility in the presence of tumor cells and rat liver microsomes and achieves rapid ingress into cell nu
67 4A enzymes were measured and compared in rat liver microsomes and an artificial membrane system.
68      LOC14 exhibited high stability in mouse liver microsomes and blood plasma, low intrinsic microso
69 UALs and FTUCAs with proteins present in rat liver microsomes and bovine blood plasma.
70        SCD protease is present in normal rat liver microsomes and cleaves purified SCD.
71 phase I metabolic stability studies in mouse liver microsomes and compared to cocaine in locomotor ac
72 ion, concentration, and stoichiometry in rat liver microsomes and cultured cells.
73 e assessment of metabolic stability in human liver microsomes and cytochrome P450 inhibition potentia
74 genic metabolites was not observed in medaka liver microsomes and cytochrome P450 was not induced wit
75                                        Human liver microsomes and cytosol were incubated with 40 micr
76    This compound was metabolically stable in liver microsomes and displayed anti-tumor activity in xe
77 ver lipids, activity of HMG-CoA reductase in liver microsomes and EPA+DHA incorporation in liver, hea
78 of methadone into its main metabolite by rat liver microsomes and for demonstrating the potential of
79 d TBMEHP for deiodinase inhibition using rat liver microsomes and for peroxisome proliferator-activat
80  human liver microsomes, metabolism by human liver microsomes and hepatocytes, and in vivo dispositio
81 d its oligomers was investigated using human liver microsomes and human liver cytosol.
82  Glucuronidation of these retinoids by human liver microsomes and human recombinant UDP-glucuronosylt
83 e were able to profile active enzymes in rat liver microsomes and identify pyrethroid-metabolizing en
84 ism studies were investigated in rat and dog liver microsomes and in the filamentous fungus Cunningha
85 ro metabolic stability of 6a and 6m in mouse liver microsomes and in vivo pharmacokinetic profiles in
86 stereoselective PCB biotransformation by rat liver microsomes and in vivo.
87 tive susceptibility to lipid peroxidation in liver microsomes and mitochondria.
88             Indeed, incubation of 8 with rat liver microsomes and NADPH gave rise to cyanamide as met
89 Incubation of dihydrotestosterone with human liver microsomes and NADPH yielded the 18- and 19-hydrox
90 otentiated up to 100-fold by incubation with liver microsomes and NADPH.
91                             By contrast, the liver microsomes and P450 2B1 enzyme form predominantly
92 ndialdehyde (MDA) synthase activity of human liver microsomes and purified P450s.
93  stability when incubated with rat and human liver microsomes and showed no significant cytochrome P4
94 ere prepared by incubation with female human liver microsomes and subjected to binding experiments wi
95 alogs with low predicted metabolism in human liver microsomes and which showed prolonged exposure in
96 ough in vitro (kinase assay), ex vivo (human liver microsomes) and in vivo (mouse) model systems.
97 l microsomal in vitro assay (Wistar-Han rats liver microsomes), and with concomitant formation of PFC
98 alian models (human liver microsomes, murine liver microsomes, and commercial porcine liver esterase)
99 nM), shows high metabolic stability in human liver microsomes, and displays excellent selectivity in
100 a-hydroxylases (C7alphaH) from human and rat liver microsomes, and from transformed Escherichia coli
101 uman serum, low rates of metabolism in human liver microsomes, and high oral bioavailability in anima
102 ounds are stable in simulated gastric fluid, liver microsomes, and human blood and are largely free f
103 ell culture, enhanced metabolic stability in liver microsomes, and improved tolerability in mice.
104  metabolic stability when incubated with rat liver microsomes, and rate of uptake and subcellular loc
105  of HCY to the same extent observed in human liver microsomes, and the addition of orphenadrine to in
106 droceramide into ceramide in vitro using rat liver microsomes, and the formation of tritiated water a
107 above reactions were carried out using human liver microsomes, and the metabolites were detected by E
108 pidly and selectively degraded when isolated liver microsomes are incubated at 37 degrees C.
109 f tamoxifen (tam) formed by animal and human liver microsomes are mono-N-demethylated tam, 4-hydroxy-
110 was introduced by using stability toward rat liver microsomes as a predictor of bioavailability.
111 re favorably with those obtained using human liver microsomes as well as those of reconstituted in vi
112 g of representative analogues in an in vitro liver microsome assay indicated that the alkyl substitue
113 bility to cytochrome P450 metabolism using a liver microsome assay.
114 e describe the purification of TPST from rat liver microsomes based on its affinity for the N-termina
115                                        Mouse liver microsome bioconversion of the methamidoxime prodr
116 del increased ROS parameters in the isolated liver microsomes, but isoniazid treatment did not.
117 d into two glutathione regioisomers by human liver microsomes, but only the 5-(glutathion-S-yl)-alpha
118 protease was purified some 700-fold from rat liver microsomes by a combination of differential deterg
119  Inhibition of DNA adduct formation in human liver microsomes by alpha-lipoic acid, an inhibitor of N
120            These results indicate that human liver microsomes can catalyze the oxidation of ethanol o
121                                        Human liver microsomes catalyzed HER formation with either NAD
122                                       Rabbit liver microsomes catalyzed the highly stereoselective, N
123 antially improved the metabolic stability in liver microsomes compared to SMART.
124           Data is presented showing that rat liver microsomes contain an enzyme that transfers the pa
125                    Adding TCB to scup or rat liver microsomes containing induced levels of CYP1A, but
126 this, when 8 was incubated in vitro with rat liver microsomes coupled to catalase and yeast A1DH, the
127 ults affirm the hypothesis that, as in human liver microsomes, CYP 1A2 in human lung cells appears to
128 the enzyme is comparable to that observed in liver microsomes, CYP3A4 behaves similarly to that obser
129 petitive intermolecular experiments with rat liver microsomes {(D)V = 12.5; (D)(V/K) = 10.9} but was
130                 Incubation of MDA with human liver microsomes demonstrated that production of both gl
131          Both 23 and 22 were stable in human liver microsomes, did not inhibit the P450 3A4 isozyme,
132                                     In human liver microsomes, difluoro analogue 5b underwent 10,11-e
133 n Km (DK = DKm/HKm), but not on kcat, in rat liver microsomes (e.g. N-nitrosodimethylamine, ethanol,
134          In vitro metabolic studies in mouse liver microsomes established enantiospecific glucuronida
135 on, accounting for 94% of activity for human liver microsome esterase inhibition (p < 0.01).
136           Although previous studies with rat liver microsomes find higher levels of PCP metabolism in
137 e P450 isoform(s) involved in RA metabolism, liver microsomes from AHR-null and wild-type mice were s
138 earance was increased by 20-40% over that by liver microsomes from control animals.
139  Pg-/- mice was markedly diminished, whereas liver microsomes from control mice showed rapid SCD degr
140 rone formation (a minor metabolite formed in liver microsomes from control mice) was increased by app
141 ble-isotope-labeled cortisone to cortisol in liver microsomes from dog, monkey, and human.
142 with pooled human liver microsomes (HLMs) or liver microsomes from male guinea pig, hamster, monkey,
143 bition by these Mabs was also observed using liver microsomes from male mice treated with phenobarbit
144 iphenyl-3'-ol (OH-PCB 102), respectively, by liver microsomes from male rats pretreated with differen
145 as elevated 11.4-fold over control values in liver microsomes from male rats treated with phenobarbit
146                  Incubation of 4-OH-tam with liver microsomes from PCN-treated rat yielded three dete
147 omes from wild-type littermate control mice, liver microsomes from Pg-/- mice had significantly highe
148          In the present study, we found that liver microsomes from phenobarbital pretreated rats (whi
149                                Incubation of liver microsomes from phenobarbital-treated males with m
150 ecies (ROS) formation were examined by using liver microsomes from scup and rat and expressed human C
151 ured as midazolam 1'- and 4-hydroxylation in liver microsomes from these knockout mice revealed a ran
152                                     Isolated liver microsomes from untreated rabbits were treated wit
153                               Finally, human liver microsomes genotyped for rs2108622 demonstrated re
154                                    The human liver microsomes glucuronidated 4-OH-RA and 4-OH-RAc wit
155 ted a long half-life in both human and mouse liver microsomes, good permeability, modest protein bind
156                          We found that human liver microsomes have HHT/MDA synthase activity that is
157                   Recent studies using human liver microsomes have suggested that a single liver enzy
158 ly higher (P < 0.05) number of subjects with liver microsomes having high NNAL-N-Gluc formation activ
159 ly (P < 0.05) higher number of subjects with liver microsomes having low NNAL-O-Gluc formation activi
160 4, resulting in increased stability in human liver microsome (HLM) preparations relative to 2 (T1/2(H
161 inine was similar to that observed for human liver microsomes (HLM) against both substrates.
162  -tetrabromodiphenyl ether (BDE-47) by human liver microsomes (HLM) and recombinant human CYPs, and t
163        The role of CYP was assessed in human liver microsomes (HLM) and tyrosol-to-hydroxytyrosol con
164 , 4-ethylphenol, and 3-methylindole in human liver microsomes (HLM) were analyzed by HPLC coupled wit
165 *2) on SAHA glucuronidation phenotype, human liver microsomes (HLM) were analyzed for glucuronidation
166 ected to in vitro biotransformation by human liver microsomes (HLM).
167 various carbon electrode materials and human liver microsomes (HLM).
168 tection limits (<1 pmol/mg protein) in human liver microsome (HLMs).
169 s a short half-life in the presence of human liver microsomes (HLMs) (T1/2 = 2.91 min).
170 tabolite (AM) from 2-oxoclopidogrel by human liver microsomes (HLMs) is greatly affected by the thiol
171 representative chiral PCB, with pooled human liver microsomes (HLMs) or liver microsomes from male gu
172 For kinetic studies, CYP2B6 and pooled human liver microsomes (HLMs) were incubated with BDE-47 (0-60
173  set of metabolic enzymes from human and rat liver microsomes, human and rat liver cytosol, and mouse
174         In vitro metabolism studies in human liver microsomes identified the production of not only t
175 s, including (i) NADPH- and O2-fortified rat liver microsomes, (ii) cytochrome P450 (P450) 2B1 Suppor
176 penclomedine was also investigated using rat liver microsomes in an attempt to identify the ultimate
177 od involves incubation of cold compound with liver microsomes in the presence of [14C]potassium cyani
178 es of the metabolism of clopidogrel to human liver microsomes in the presence of four reductants, nam
179 -ring hydroxylation of [o-3H]methoxychlor by liver microsomes in the presence of NADPH.
180                                       In rat liver microsomes in vitro, defluorination of 18F-FCWAY w
181 o inhibit defluorination of 18F-FCWAY in rat liver microsomes in vitro.
182 '-hydroxycotinine (3HC)-glucuronide in human liver microsomes in vitro.
183 detected norbuprenorphine formation in human liver microsomes incubated with 5-82 nM buprenorphine, w
184 ha- and beta-adduction was observed in mouse liver microsomes incubated with styrene at various conce
185                The binding of ethanol to rat liver microsomes is shown to be saturable at clinically
186 o design biologically active interfaces with liver microsomes is suggested to have immense significan
187 ETE by hematin (a nonenzymatic reaction), by liver microsomes isolated from control and phenobarbital
188 FMOs, from Schizosaccharomyces pombe and hog liver microsomes) leads to the hypothesis that PvdA cata
189 etabolism in human intestinal microsomes and liver microsomes make phosphoramidate 16 a prospective c
190 ma proteins, metabolic stability using human liver microsomes, metabolism by human liver microsomes a
191 d in three different mammalian models (human liver microsomes, murine liver microsomes, and commercia
192 ndent metabolism of estradiol and estrone by liver microsomes of BHA-treated animals as determined by
193 r the demonstration of the catalysis, by rat liver microsomes, of the conversion of 7-dehydrocholeste
194  ruthenium poly(vinylpyridine), DNA, and rat liver microsomes or bicistronically expressed human cyt
195 s of radioactive 17beta-estradiol with human liver microsomes or recombinant human cytochrome P450 is
196 s, we demonstrated that incubations of human liver microsomes or various human cytochrome P450 isofor
197 ting for 94% of inhibition activity in human liver microsomes (p < 0.01).
198                                           In liver microsomes, peak 1 (BPD-7S-Gluc) was the largest p
199                               Murine and rat liver microsomes prepared from animals that had been tre
200  major components of technical chlordane, by liver microsomes prepared from male rats treated with co
201 Selectivity for CYP2B was demonstrated using liver microsomes prepared from rats and mice treated wit
202 ydrogenases (IC50 = approximately 1 microM), liver microsomes provide 93% of the total retinal synthe
203                                        A rat liver microsome pseudostationary phase has been used for
204 ,3-b]indole (HONH-AalphaC) formed with human liver microsomes, recombinant human UGT isoforms, and hu
205                                           In liver microsomes, reduced RNase-triggered gamma-carboxyl
206 itonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichio
207 eed, incubating LMP400 and LMP776 with human liver microsomes resulted in two major metabolites of ea
208 fluorescent substrates were applied to human liver microsomes, results suggested that there was at le
209 lysis with recombinant CYP4F2 and with human liver microsomes revealed a substrate K(m) of 8 to 10 mi
210  N-(3,3-diphenyl-propyl)-nicotinamide in rat liver microsomes revealed extensive oxidative metabolism
211                 Immunoblot analysis of fetal liver microsomes revealed the presence of a protein immu
212  with rat esophageal microsomes (REM) or rat liver microsomes (RLM) to give [3H]pentaldehyde (depenty
213 rosomal protein were determined for a pooled liver microsome sample, suggesting that this enzyme is a
214                       HER formation by human liver microsomes seems to be catalyzed by an oxidant der
215   One phase I metabolite was formed by human liver microsomes, seven phase I and II metabolites were
216                               Both brain and liver microsomes showed a preference for 18:0 over 16:0
217  exhibited low cytotoxicity and satisfactory liver microsomes stability and plasma protein binding.
218                                          Rat liver microsome studies on a selected number of compound
219                                     Finally, liver microsome studies revealed that (18)F-FTC-146 has
220 nary squirrel monkey imaging and human serum/liver microsome studies were performed to gain informati
221 roxyeicosatetraenoic acid (15S-HPETE) in rat liver microsomes suggested such a specific reaction.
222 ere rapidly metabolized in rodents and human liver microsomes, suggesting the possibility of rapid in
223 at recombinant CYP4F2 (Supersomes) and human liver microsomes supplemented with NADPH converted VK1 t
224 , and metabolic stability in human and mouse liver microsomes, supporting its potential for in vivo u
225 ic metabolites after 1 h incubation in human liver microsomes system.
226 displays a good metabolic stability in human liver microsomes (t1/2 approximately 3 h and CLint = 3.5
227 h more membrane permeable and more stable to liver microsomes than a similar non-statine-containing d
228 h a five times higher conversion rate in dog liver microsomes than in human and monkey liver microsom
229 ously identified proteolytic activity in rat liver microsomes that cleaves an intact tripeptide, VIS,
230                  In an experiment with human liver microsomes, the inclusion of quinidine, a specific
231 tocol, the substrate is incubated with human liver microsomes, the reaction is quenched, and the subs
232 is denitrified to nitrite and acetone by rat liver microsomes; the denitrification rate is increased
233 C after incubation of racemic BPD with human liver microsomes; these were identified as monoglucuroni
234 hylpiperidine (2,2,6,6-TMPi) moiety in human liver microsomes to a ring-contracted 2,2-dimethylpyrrol
235 carried out to evaluate the ability of human liver microsomes to catalyze this reaction, compare the
236 re identified, and the extracts treated with liver microsomes to mimic physiological metabolism, with
237 RA 4-hydroxylase activity of wild-type mouse liver microsomes to the levels of AHR-null mouse liver.
238 ronidation activity of mouse, rat, and human liver microsomes toward the carcinogenic arylamine 4-ami
239 ing enzyme was partially purified from mouse liver microsomes using a fluorescent reporter similar in
240     We examined this process in purified rat liver microsomes using a rapid filtration technique and
241 cularly at low pH, although stability toward liver microsomes was highly variable.
242                        The reaction in human liver microsomes was NADPH-dependent and was nearly comp
243 , and its formation rate in a panel of human liver microsomes was strongly correlated with CYP3A4 con
244                               A set of human liver microsomes was then used to determine the ability
245 etergent-solubilized, desaturase-induced rat liver microsomes we have characterized a protease that d
246           Using wild-type and Cyp3a knockout liver microsomes, we found that 4'-O-deacetylvinorelbine
247                            Solubilized human liver microsomes were incubated with specific antibodies
248 all-trans RA CYP26 mRNA and RA metabolism by liver microsomes were significantly induced.
249                                        Human liver microsomes were the most active in 4-ABP glucuroni
250 lDH or the mixed function oxidase enzymes of liver microsomes, were prepared.
251 rphenadrine inhibition was observed in human liver microsomes (which has been taken to indicate CYP2B
252                                          Rat liver microsomes, which are enriched for enzymes of deto
253 PAP) and (13)C6-APAP were incubated with rat liver microsomes, which are known to bioactivate APAP to
254 ia, but it is efficiently processed in human liver microsomes with a half-life of 2 min.
255  2-ClHA is omega-oxidized in the presence of liver microsomes with initial omega-hydroxylation of 2-C
256 , the activity has been solubilized from rat liver microsomes with n-octyl-beta-D-glucoside and recon
257 one is quickly metabolized in vitro by mouse liver microsomes with NADPH (cytochrome P450) forming 7-
258                          Incubation of human liver microsomes with nicotine gave keto acid by using a
259                             Treatment of rat liver microsomes with S-nitrosoglutathione caused S-nitr
260 oline (PC) vesicles by solubilization of rat liver microsomes with the two substrates lysoPC and acyl
261 nt source of 25OHD(3) hydroxylation by human liver microsomes, with the formation of 4beta,25-dihydro

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