PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
26104860-1	2015	Cytochrome P450 (CYP) enzymes catalyze the metabolism of both, the analgesic and anesthetic drug ketamine and the alpha2 -adrenergic receptor-agonist medetomidine that is used for sedation and analgesia.	Ketamine	97-105	Cytochrome P450 1A1	Canis lupus familiaris	0-15
26679793-7	2015	BaP increased the expression of AhR signaling pathway protein, cytochrome P450 (CYP1A1) in ADMSCs.	Benzo(a)pyrene	0-3	Cytochrome P450 1A1	Canis lupus familiaris	63-86
26104860-1	2015	Cytochrome P450 (CYP) enzymes catalyze the metabolism of both, the analgesic and anesthetic drug ketamine and the alpha2 -adrenergic receptor-agonist medetomidine that is used for sedation and analgesia.	Ketamine	97-105	Cytochrome P450 1A1	Canis lupus familiaris	17-20
26104860-1	2015	Cytochrome P450 (CYP) enzymes catalyze the metabolism of both, the analgesic and anesthetic drug ketamine and the alpha2 -adrenergic receptor-agonist medetomidine that is used for sedation and analgesia.	Medetomidine	150-162	Cytochrome P450 1A1	Canis lupus familiaris	0-15
26104860-1	2015	Cytochrome P450 (CYP) enzymes catalyze the metabolism of both, the analgesic and anesthetic drug ketamine and the alpha2 -adrenergic receptor-agonist medetomidine that is used for sedation and analgesia.	Medetomidine	150-162	Cytochrome P450 1A1	Canis lupus familiaris	17-20
25733012-1	2015	OBJECTIVE: To assess the effects of cytochrome P450 (CYP) inhibitors (ketoconazole, chloramphenicol, trimethoprim, fluoxetine, cimetidine and medetomidine) in various combinations on the pharmacokinetics of oral methadone in Greyhound dogs to determine the specific effects of the different inhibitors and if a clinically relevant interaction occurs.	Medetomidine	142-154	Cytochrome P450 1A1	Canis lupus familiaris	36-51
20020418-0	2010	Metabolic stability and determination of cytochrome P450 isoenzymes" contribution to the metabolism of medetomidine in dog liver microsomes.	Medetomidine	103-115	Cytochrome P450 1A1	Canis lupus familiaris	41-56
21492388-0	2011	The effects of concurrent administration of cytochrome P-450 inhibitors on the pharmacokinetics of oral methadone in healthy dogs.	Methadone	104-113	Cytochrome P450 1A1	Canis lupus familiaris	44-60
20007294-7	2010	The minor caffeine-fluvoxamine interaction (1.78-fold) was slightly higher than predicted values based on determination of a moderate f(m) value for CYP1A1, although CYP1A2 may also be involved in caffeine metabolism.	Caffeine	10-18	Cytochrome P450 1A1	Canis lupus familiaris	149-155
20007294-7	2010	The minor caffeine-fluvoxamine interaction (1.78-fold) was slightly higher than predicted values based on determination of a moderate f(m) value for CYP1A1, although CYP1A2 may also be involved in caffeine metabolism.	Fluvoxamine	19-30	Cytochrome P450 1A1	Canis lupus familiaris	149-155
19303460-2	2009	The associations between in vitro PCB metabolism, activity of oxidative hepatic microsomal cytochrome P450 (CYP) isoenzymes and concentrations of PCBs and hydroxylated metabolites were investigated.	Polychlorinated Biphenyls	146-150	Cytochrome P450 1A1	Canis lupus familiaris	91-106
19406444-0	2009	Long-lasting enhancement of CYP activity after discontinuation of repeated administration of phenobarbital in dogs.	Phenobarbital	93-106	Cytochrome P450 1A1	Canis lupus familiaris	28-31
19406444-1	2009	We investigated how long in vivo hepatic cytochrome P450 (CYP) activity is enhanced even after discontinuation of repeated oral administration of phenobarbital (PB) in dogs using antipyrine clearance, which reflects hepatic CYP activity.	Phenobarbital	146-159	Cytochrome P450 1A1	Canis lupus familiaris	58-61
19406444-4	2009	The result suggests that hepatic CYP activity was enhanced by the repeated administration of PB, and this enhancement may last for at least 4 weeks even after its discontinuation.	Phenobarbital	93-95	Cytochrome P450 1A1	Canis lupus familiaris	33-36
19303460-2	2009	The associations between in vitro PCB metabolism, activity of oxidative hepatic microsomal cytochrome P450 (CYP) isoenzymes and concentrations of PCBs and hydroxylated metabolites were investigated.	Polychlorinated Biphenyls	146-150	Cytochrome P450 1A1	Canis lupus familiaris	108-111
19303460-4	2009	This depletion discrepancy suggests that there exist substrates in liver of the organohalogen-contaminated EXP dogs that can competitively bind and/or interfere with the active sites of CYP isoenzymes, leading to a lower metabolic efficiency for these PCBs.	Polychlorinated Biphenyls	252-256	Cytochrome P450 1A1	Canis lupus familiaris	186-189
19303460-6	2009	Based on documented hepatic microsomal CYP isoenzyme substrate specificities in canines, present associations suggest that primarily CYP2B/2C and CYP3A were inducible in sledge dogs and responsible for the in vitro metabolism of PCB-18 and -33.	Polychlorinated Biphenyls	229-232	Cytochrome P450 1A1	Canis lupus familiaris	39-42
19074522-6	2009	In monitoring the metabolites of common P450 substrates, phenacetin deethylation, temazepam demethylation, and bufuralol 1"-hydroxylation were shown to be relatively selective reactions catalyzed by CYP1A1, 2B11, and 2D15, respectively.	Phenacetin	57-67	Cytochrome P450 1A1	Canis lupus familiaris	199-205
19462483-12	2009	A significant decrease in Salvinorin A concentration ranging from 14.7 +/- 0.80% to 31.1 +/- 1.20% was observed after incubation with CYP2D6, CYP1A1, CYP2C18, and CYP2E1, respectively.	salvinorin A	26-38	Cytochrome P450 1A1	Canis lupus familiaris	142-148
19462483-14	2009	These results suggest that Salvinorin A maybe a substrate of UGT2B7, CYP2D6, CYP1A1, CYP2E1, and CYP2C18.	salvinorin A	27-39	Cytochrome P450 1A1	Canis lupus familiaris	77-83
19074522-6	2009	In monitoring the metabolites of common P450 substrates, phenacetin deethylation, temazepam demethylation, and bufuralol 1"-hydroxylation were shown to be relatively selective reactions catalyzed by CYP1A1, 2B11, and 2D15, respectively.	Temazepam	82-91	Cytochrome P450 1A1	Canis lupus familiaris	199-205
19074522-6	2009	In monitoring the metabolites of common P450 substrates, phenacetin deethylation, temazepam demethylation, and bufuralol 1"-hydroxylation were shown to be relatively selective reactions catalyzed by CYP1A1, 2B11, and 2D15, respectively.	bufuralol	111-120	Cytochrome P450 1A1	Canis lupus familiaris	199-205
15572055-1	2004	Inhibition of 20-hydroxyeicosatrienoic acid (20-HETE), by pretreatment with pharmacological inhibitors of cytochrome P450 (CYP) omega-hydroxylase, has been shown to reduce infarct size in canines when administered prior to ischemia.	20-hydroxyeicosatrieneoic acid	14-43	Cytochrome P450 1A1	Canis lupus familiaris	106-121
19041884-0	2009	Sequencing and characterization of mixed function monooxygenase genes CYP1A1 and CYP1A2 of Mink (Mustela vison) to facilitate study of dioxin-like compounds.	Dioxins	135-141	Cytochrome P450 1A1	Canis lupus familiaris	70-76
19041884-5	2009	Since exposure to both 2,3,7,8-Tetrachlorodibenzofuran (TCDF) and 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) resulted in dose-dependent increases of CYP1A1 mRNA, CYP1A2 mRNA and CYP1A protein levels an underlying AhR-mediated mechanism is suggested.	2,3,7,8-tetrachlorodibenzofuran	23-54	Cytochrome P450 1A1	Canis lupus familiaris	148-154
19041884-5	2009	Since exposure to both 2,3,7,8-Tetrachlorodibenzofuran (TCDF) and 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) resulted in dose-dependent increases of CYP1A1 mRNA, CYP1A2 mRNA and CYP1A protein levels an underlying AhR-mediated mechanism is suggested.	2,3,7,8-tetrachlorodibenzofuran	56-60	Cytochrome P450 1A1	Canis lupus familiaris	148-154
19041884-5	2009	Since exposure to both 2,3,7,8-Tetrachlorodibenzofuran (TCDF) and 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) resulted in dose-dependent increases of CYP1A1 mRNA, CYP1A2 mRNA and CYP1A protein levels an underlying AhR-mediated mechanism is suggested.	2,3,4,7,8-pentachlorodibenzofuran	66-99	Cytochrome P450 1A1	Canis lupus familiaris	148-154
19041884-5	2009	Since exposure to both 2,3,7,8-Tetrachlorodibenzofuran (TCDF) and 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) resulted in dose-dependent increases of CYP1A1 mRNA, CYP1A2 mRNA and CYP1A protein levels an underlying AhR-mediated mechanism is suggested.	2,3,4,7,8-pentachlorodibenzofuran	101-106	Cytochrome P450 1A1	Canis lupus familiaris	148-154
19041884-7	2009	The result suggested that the hepatic-sequestered fraction of PeCDF was biologically inactive to the induction of CYP1A1 and CYP1A2.	2,3,4,7,8-pentachlorodibenzofuran	62-67	Cytochrome P450 1A1	Canis lupus familiaris	114-120
19023539-2	2008	In this study, the two major pyranocoumarin compounds extracted from the Korean Angelica gigas root decursin (DC) and decursinol angelate (DA) were examined in vitro with regard to their abilities to inhibit hepatic CYP1A1/2, CYP2D15, and CYP3A12 catalytic activities in canine liver microsomes.	decursin	118-137	Cytochrome P450 1A1	Canis lupus familiaris	216-222
19023539-4	2008	DC and DA selectively and noncompetitively inhibited CYP1A1/2 activity, with K ( i ) values of 90.176 and 67.560 microM, respectively.	decursin	0-2	Cytochrome P450 1A1	Canis lupus familiaris	53-59
19023539-4	2008	DC and DA selectively and noncompetitively inhibited CYP1A1/2 activity, with K ( i ) values of 90.176 and 67.560 microM, respectively.	decursin	7-9	Cytochrome P450 1A1	Canis lupus familiaris	53-59
15572055-1	2004	Inhibition of 20-hydroxyeicosatrienoic acid (20-HETE), by pretreatment with pharmacological inhibitors of cytochrome P450 (CYP) omega-hydroxylase, has been shown to reduce infarct size in canines when administered prior to ischemia.	20-hydroxyeicosatrieneoic acid	14-43	Cytochrome P450 1A1	Canis lupus familiaris	123-126
15572055-1	2004	Inhibition of 20-hydroxyeicosatrienoic acid (20-HETE), by pretreatment with pharmacological inhibitors of cytochrome P450 (CYP) omega-hydroxylase, has been shown to reduce infarct size in canines when administered prior to ischemia.	20-Hete	45-52	Cytochrome P450 1A1	Canis lupus familiaris	106-121
15572055-1	2004	Inhibition of 20-hydroxyeicosatrienoic acid (20-HETE), by pretreatment with pharmacological inhibitors of cytochrome P450 (CYP) omega-hydroxylase, has been shown to reduce infarct size in canines when administered prior to ischemia.	20-Hete	45-52	Cytochrome P450 1A1	Canis lupus familiaris	123-126
12386126-4	2002	Treatment of male beagle dog hepatocyte cultures (n = 3) with beta-naphthoflavone or 3-methlychloranthrene resulted in up to a 75-fold increase in microsomal 7-ethoxyresorufin O-dealkylase (CYP1A1/2) activity, whereas in vivo treatment of male and female beagle dogs with beta-naphthoflavone followed by ex vivo analysis resulted in up to a 24-fold increase.	beta-Naphthoflavone	62-81	Cytochrome P450 1A1	Canis lupus familiaris	190-198
14769805-7	2004	In contrast, in the presence of E4177+l-NAME, cilazaprilat still caused 8%+/-3% dilation of juxtamedullary Aff, which was completely eliminated by proadifen, a cytochrome-P450 and K(Ca) channel blocker.	cilazaprilat	46-58	Cytochrome P450 1A1	Canis lupus familiaris	160-175
12881219-0	2003	Cytochrome P-450 metabolites but not NO, PGI2, and H2O2 contribute to ACh-induced hyperpolarization of pressurized canine coronary microvessels.	Acetylcholine	70-73	Cytochrome P450 1A1	Canis lupus familiaris	0-16
12881219-4	2003	EDHF has not yet been identified and cytochrome P-450 metabolites and H2O2 are candidates for EDHF.	edhf	94-98	Cytochrome P450 1A1	Canis lupus familiaris	37-53
12881219-12	2003	The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates H2O2 to form water and oxygen, did not.	17-octadecynoic acid	16-36	Cytochrome P450 1A1	Canis lupus familiaris	40-56
12881219-12	2003	The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates H2O2 to form water and oxygen, did not.	Acetylcholine	131-134	Cytochrome P450 1A1	Canis lupus familiaris	40-56
12881219-12	2003	The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates H2O2 to form water and oxygen, did not.	Water	237-242	Cytochrome P450 1A1	Canis lupus familiaris	40-56
12881219-12	2003	The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates H2O2 to form water and oxygen, did not.	Oxygen	61-67	Cytochrome P450 1A1	Canis lupus familiaris	40-56
12881219-14	2003	These results indicate that NO and PGI2 do not contribute to the ACh-induced hyperpolarization and that the cytochrome P-450 metabolites but not H2O2 are involved in EDHF-mediated hyperpolarization in canine coronary arterial microvessels.	edhf	166-170	Cytochrome P450 1A1	Canis lupus familiaris	108-124
13677397-0	2003	Effect of oral administration of low doses of pentobarbital on the induction of cytochrome P450 isoforms and cytochrome P450-mediated reactions in immature Beagles.	Pentobarbital	46-59	Cytochrome P450 1A1	Canis lupus familiaris	80-95
13677397-0	2003	Effect of oral administration of low doses of pentobarbital on the induction of cytochrome P450 isoforms and cytochrome P450-mediated reactions in immature Beagles.	Pentobarbital	46-59	Cytochrome P450 1A1	Canis lupus familiaris	109-124
13677397-1	2003	OBJECTIVE: To determine the effect of oral administration of low doses of pentobarbital on cytochrome P450 (CYP) isoforms and CYP-mediated reactions in immature Beagles.	Pentobarbital	74-87	Cytochrome P450 1A1	Canis lupus familiaris	91-106
13677397-1	2003	OBJECTIVE: To determine the effect of oral administration of low doses of pentobarbital on cytochrome P450 (CYP) isoforms and CYP-mediated reactions in immature Beagles.	Pentobarbital	74-87	Cytochrome P450 1A1	Canis lupus familiaris	108-111
13677397-1	2003	OBJECTIVE: To determine the effect of oral administration of low doses of pentobarbital on cytochrome P450 (CYP) isoforms and CYP-mediated reactions in immature Beagles.	Pentobarbital	74-87	Cytochrome P450 1A1	Canis lupus familiaris	126-129
13677397-11	2003	CONCLUSIONS AND CLINICAL RELEVANCE: Several CYP isoforms and their associated reactions were induced in dogs by oral administration of low amounts of pentobarbital.	Pentobarbital	150-163	Cytochrome P450 1A1	Canis lupus familiaris	44-47
12061540-0	2002	In vitro characterization of the inhibitory effects of ketoconazole on metabolic activities of cytochrome P-450 in canine hepatic microsomes.	Ketoconazole	55-67	Cytochrome P450 1A1	Canis lupus familiaris	95-111
12226743-0	2002	A clinical protocol for treatment of canine mammary tumors using encapsulated, cytochrome P450 synthesizing cells activating cyclophosphamide: a phase I/II study.	Cyclophosphamide	125-141	Cytochrome P450 1A1	Canis lupus familiaris	79-94
12061540-1	2002	OBJECTIVE: To evaluate the inhibitory potency of ketoconazole (KTZ) on the metabolic activities of isozymes of cytochrome P-450 (CYP) in dogs.	Ketoconazole	49-61	Cytochrome P450 1A1	Canis lupus familiaris	111-127
12061540-1	2002	OBJECTIVE: To evaluate the inhibitory potency of ketoconazole (KTZ) on the metabolic activities of isozymes of cytochrome P-450 (CYP) in dogs.	Ketoconazole	49-61	Cytochrome P450 1A1	Canis lupus familiaris	129-132
12061540-1	2002	OBJECTIVE: To evaluate the inhibitory potency of ketoconazole (KTZ) on the metabolic activities of isozymes of cytochrome P-450 (CYP) in dogs.	Ketoconazole	63-66	Cytochrome P450 1A1	Canis lupus familiaris	111-127
12061540-1	2002	OBJECTIVE: To evaluate the inhibitory potency of ketoconazole (KTZ) on the metabolic activities of isozymes of cytochrome P-450 (CYP) in dogs.	Ketoconazole	63-66	Cytochrome P450 1A1	Canis lupus familiaris	129-132
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	Ketoconazole	30-33	Cytochrome P450 1A1	Canis lupus familiaris	37-40
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	Ketoconazole	30-33	Cytochrome P450 1A1	Canis lupus familiaris	171-177
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	ethoxyresorufin	63-80	Cytochrome P450 1A1	Canis lupus familiaris	171-177
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	Tolbutamide	82-93	Cytochrome P450 1A1	Canis lupus familiaris	171-177
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	bufuralol	95-104	Cytochrome P450 1A1	Canis lupus familiaris	171-177
12061540-4	2002	To investigate the effects of KTZ on CYP metabolic activities, 7-ethoxyresorufin, tolbutamide, bufuralol, and midazolam hydrochloride were used as specific substrates for CYP1A1/2, CYP2C21, CYP2D15, and CYP3A12, respectively.	Midazolam	110-133	Cytochrome P450 1A1	Canis lupus familiaris	171-177
12000532-1	2002	In dogs effects of phenobarbital (PB) on hepatic cytochrome P450 (CYP) activities and on concentrations of plasma alpha 1-acid glycoprotein (AGP) were examined.	Phenobarbital	34-36	Cytochrome P450 1A1	Canis lupus familiaris	49-64
12000532-3	2002	Cl(B) of antipyrine, which reflects hepatic CYP activities, gradually increased and was maintained at about threefold concentrations compared with that before treatment, suggesting that PB induced CYP activities at a large extent even in a therapeutic dose, necessary for an antiepileptic effect.	Phenobarbital	186-188	Cytochrome P450 1A1	Canis lupus familiaris	44-47
12000532-3	2002	Cl(B) of antipyrine, which reflects hepatic CYP activities, gradually increased and was maintained at about threefold concentrations compared with that before treatment, suggesting that PB induced CYP activities at a large extent even in a therapeutic dose, necessary for an antiepileptic effect.	Phenobarbital	186-188	Cytochrome P450 1A1	Canis lupus familiaris	197-200
11792681-16	2002	In hepatic microsomes, bergamottin treatment for 10 days reduced the activity of CYP3A12 by 50% and CYP1A1/2 by 75%.	bergamottin	23-34	Cytochrome P450 1A1	Canis lupus familiaris	100-106
11557543-2	2001	EDHF has been proposed to be formed through cytochrome P-450 monooxygenase metabolism of arachidonic acid (AA).	edhf	0-4	Cytochrome P450 1A1	Canis lupus familiaris	44-60
11557543-2	2001	EDHF has been proposed to be formed through cytochrome P-450 monooxygenase metabolism of arachidonic acid (AA).	Arachidonic Acid	89-105	Cytochrome P450 1A1	Canis lupus familiaris	44-60
10561078-0	2000	Metabolism of phenanthrene by house fly CYP6D1 and dog liver cytochrome P450.	phenanthrene	14-26	Cytochrome P450 1A1	Canis lupus familiaris	61-76
10901696-6	2000	The reactions required NADPH as a cofactor and were significantly inhibited by the various inhibitors of cytochrome P450 (i.e., CO, n-octylamine, SKF 525-A, metyrapone, and alpha-naphthoflavone).	NADP	23-28	Cytochrome P450 1A1	Canis lupus familiaris	105-120
10901696-6	2000	The reactions required NADPH as a cofactor and were significantly inhibited by the various inhibitors of cytochrome P450 (i.e., CO, n-octylamine, SKF 525-A, metyrapone, and alpha-naphthoflavone).	co, n-octylamine	128-144	Cytochrome P450 1A1	Canis lupus familiaris	105-120
10901696-6	2000	The reactions required NADPH as a cofactor and were significantly inhibited by the various inhibitors of cytochrome P450 (i.e., CO, n-octylamine, SKF 525-A, metyrapone, and alpha-naphthoflavone).	Proadifen	146-155	Cytochrome P450 1A1	Canis lupus familiaris	105-120
10901696-6	2000	The reactions required NADPH as a cofactor and were significantly inhibited by the various inhibitors of cytochrome P450 (i.e., CO, n-octylamine, SKF 525-A, metyrapone, and alpha-naphthoflavone).	Metyrapone	157-167	Cytochrome P450 1A1	Canis lupus familiaris	105-120
10901696-6	2000	The reactions required NADPH as a cofactor and were significantly inhibited by the various inhibitors of cytochrome P450 (i.e., CO, n-octylamine, SKF 525-A, metyrapone, and alpha-naphthoflavone).	alpha-naphthoflavone	173-193	Cytochrome P450 1A1	Canis lupus familiaris	105-120
10561078-4	2000	The fluorometric assay and direct measurement of [14C]phenanthrene metabolism were used to show that CYP6D1, a house fly cytochrome P450, is the major house fly P450 involved in phenanthrene metabolism.	[14c]phenanthrene	49-66	Cytochrome P450 1A1	Canis lupus familiaris	121-136
10561078-4	2000	The fluorometric assay and direct measurement of [14C]phenanthrene metabolism were used to show that CYP6D1, a house fly cytochrome P450, is the major house fly P450 involved in phenanthrene metabolism.	phenanthrene	54-66	Cytochrome P450 1A1	Canis lupus familiaris	121-136
9128144-1	1997	Previous studies have revealed the functional importance of the negatively charged amino-acid residue Asp-290 of the phenobarbital-inducible dog liver cytochrome P-450 (P-450) 2B11 (Harlow, G.R.	Aspartic Acid	102-105	Cytochrome P450 1A1	Canis lupus familiaris	151-167
10484447-9	1999	The ACh-induced vasodilation remaining after L-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes.	Acetylcholine	4-7	Cytochrome P450 1A1	Canis lupus familiaris	228-244
10484447-9	1999	The ACh-induced vasodilation remaining after L-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes.	iberiotoxin	146-157	Cytochrome P450 1A1	Canis lupus familiaris	228-244
10484447-9	1999	The ACh-induced vasodilation remaining after L-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes.	Miconazole	188-198	Cytochrome P450 1A1	Canis lupus familiaris	228-244
10484447-9	1999	The ACh-induced vasodilation remaining after L-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes.	Metyrapone	202-212	Cytochrome P450 1A1	Canis lupus familiaris	228-244
10484447-10	1999	These observations are consistent with the view that endothelium-derived hyperpolarizing factor (EDHF) is a product of cytochrome P-450 enzymes and produces vasodilation by the opening of large-conductance potassium channels.	hyperpolarizing factor	73-95	Cytochrome P450 1A1	Canis lupus familiaris	119-135
10048153-1	1999	Induction of cytochrome P450 isoforms, specifically CYP1A1, and their catalytic activities are potential biomarkers of environmental contamination by polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	150-175	Cytochrome P450 1A1	Canis lupus familiaris	52-58
10048153-1	1999	Induction of cytochrome P450 isoforms, specifically CYP1A1, and their catalytic activities are potential biomarkers of environmental contamination by polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	177-181	Cytochrome P450 1A1	Canis lupus familiaris	52-58
10048153-3	1999	Relative to controls, hepatic microsomes from dogs dosed with PCBs had higher levels of CYP1A1 detected in immunoblots and higher levels of EROD activity, but low levels of induction for CYP2B and PROD activity.	Polychlorinated Biphenyls	62-66	Cytochrome P450 1A1	Canis lupus familiaris	88-94
10048153-9	1999	The value of CYP1A1 induction as a biomarker of PCB exposure was tenuous because neither CYP1A1 levels nor EROD activity correlated with total PCB body burden.	Polychlorinated Biphenyls	48-51	Cytochrome P450 1A1	Canis lupus familiaris	13-19
9667078-2	1998	Effects of rifampicin (Rif) on the contents of cytochrome P450 (P450) enzymes (CYP1A1/2, 2B11, 2C21 and 3A12) assessed by enzyme-linked immunosorbent assay and catalytic activities (ethoxyresorufin O-deethylase, and testosterone 6 beta-, 16 alpha- and 16 beta-hydroxylase; 6 beta-, 16 alpha- and 16 beta-OHT) in dog liver microsomes were compared between liver lobes of both the male and female dogs.	Rifampin	11-21	Cytochrome P450 1A1	Canis lupus familiaris	79-93
10534314-2	1999	Biotransformation of propofol to 2,6-diisopropyl-1,4-quinol (4-hydroxypropofol) by cytochrome P-450 in the liver is proposed as a critical initial step in the elimination of this drug in dogs.	Propofol	21-29	Cytochrome P450 1A1	Canis lupus familiaris	83-99
10534314-2	1999	Biotransformation of propofol to 2,6-diisopropyl-1,4-quinol (4-hydroxypropofol) by cytochrome P-450 in the liver is proposed as a critical initial step in the elimination of this drug in dogs.	2,6-diisopropyl-1,4-quinol	33-59	Cytochrome P450 1A1	Canis lupus familiaris	83-99
10534314-2	1999	Biotransformation of propofol to 2,6-diisopropyl-1,4-quinol (4-hydroxypropofol) by cytochrome P-450 in the liver is proposed as a critical initial step in the elimination of this drug in dogs.	4-Hydroxy Propofol	61-78	Cytochrome P450 1A1	Canis lupus familiaris	83-99
10534314-9	1999	These results indicate that there are breed differences in propofol hydroxylase activity and that deficient hydroxylation of propofol by one or more hepatic cytochrome P-450 isoforms may contribute to slow pharmacokinetic clearance of propofol by greyhounds.	Propofol	59-67	Cytochrome P450 1A1	Canis lupus familiaris	157-173
10534314-9	1999	These results indicate that there are breed differences in propofol hydroxylase activity and that deficient hydroxylation of propofol by one or more hepatic cytochrome P-450 isoforms may contribute to slow pharmacokinetic clearance of propofol by greyhounds.	Propofol	125-133	Cytochrome P450 1A1	Canis lupus familiaris	157-173
9755108-3	1998	Pretreatment of the lobes with cytochrome P-450 inhibitors clotrimazole (10 microM) or 17-octadecynoic acid (5 microM) abolished the thapsigargin-induced increases in Kf,c.	Clotrimazole	59-71	Cytochrome P450 1A1	Canis lupus familiaris	31-47
9755108-3	1998	Pretreatment of the lobes with cytochrome P-450 inhibitors clotrimazole (10 microM) or 17-octadecynoic acid (5 microM) abolished the thapsigargin-induced increases in Kf,c.	17-octadecynoic acid	87-107	Cytochrome P450 1A1	Canis lupus familiaris	31-47
9755108-3	1998	Pretreatment of the lobes with cytochrome P-450 inhibitors clotrimazole (10 microM) or 17-octadecynoic acid (5 microM) abolished the thapsigargin-induced increases in Kf,c.	Thapsigargin	133-145	Cytochrome P450 1A1	Canis lupus familiaris	31-47
9458878-0	1998	Cytochrome P-450 pathway in acetylcholine-induced canine coronary microvascular vasodilation in vivo.	Acetylcholine	28-41	Cytochrome P450 1A1	Canis lupus familiaris	0-16
9458878-2	1998	We hypothesized that the ACh-induced vasodilation of SmA is mediated by a cytochrome P-450 metabolite of arachidonic acid (AA).	Acetylcholine	25-28	Cytochrome P450 1A1	Canis lupus familiaris	74-90
9458878-2	1998	We hypothesized that the ACh-induced vasodilation of SmA is mediated by a cytochrome P-450 metabolite of arachidonic acid (AA).	Arachidonic Acid	105-121	Cytochrome P450 1A1	Canis lupus familiaris	74-90
9458878-8	1998	These results suggest that the ACh-induced vasodilation of SmA is mediated in part by cytochrome P-450 metabolites of AA and provide the first evidence that the cytochrome P-450 pathway contributes to the regulation of coronary resistance vessels in vivo.	Acetylcholine	31-34	Cytochrome P450 1A1	Canis lupus familiaris	86-102
9458878-8	1998	These results suggest that the ACh-induced vasodilation of SmA is mediated in part by cytochrome P-450 metabolites of AA and provide the first evidence that the cytochrome P-450 pathway contributes to the regulation of coronary resistance vessels in vivo.	Acetylcholine	31-34	Cytochrome P450 1A1	Canis lupus familiaris	161-177
9128144-1	1997	Previous studies have revealed the functional importance of the negatively charged amino-acid residue Asp-290 of the phenobarbital-inducible dog liver cytochrome P-450 (P-450) 2B11 (Harlow, G.R.	Phenobarbital	117-130	Cytochrome P450 1A1	Canis lupus familiaris	151-167
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	37-50	Cytochrome P450 1A1	Canis lupus familiaris	156-162
9034633-8	1996	Similarly, CYP1A1/2 transcripts were induced by 3-MC in both fresh and cryopreserved cells from the three species but also after OPZ treatment for monkey hepatocytes.	Methylcholanthrene	48-52	Cytochrome P450 1A1	Canis lupus familiaris	11-17
9034633-8	1996	Similarly, CYP1A1/2 transcripts were induced by 3-MC in both fresh and cryopreserved cells from the three species but also after OPZ treatment for monkey hepatocytes.	oltipraz	129-132	Cytochrome P450 1A1	Canis lupus familiaris	11-17
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	52-54	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Rifampin	57-67	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	beta-Naphthoflavone	77-96	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	beta-Naphthoflavone	98-105	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	beta-Naphthoflavone	177-184	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Rifampin	256-259	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8652640-13	1996	Thus, arachidonic acid is metabolized in canine PMNs through the cyclooxygenase, lipoxygenases and cytochrome P-450 pathways.	Arachidonic Acid	6-22	Cytochrome P450 1A1	Canis lupus familiaris	99-115
1782403-2	1991	This suggests that SKF-525A is an inhibitor of endothelium-derived relaxing factor (EDRF) and that EDRF may be a product of arachidonic acid metabolism formed via a cytochrome P-450-dependent pathway or that EDRF release is dependent on cytochrome P-450.	Proadifen	19-27	Cytochrome P450 1A1	Canis lupus familiaris	237-253
8967376-2	1996	Pretreatment with the cytochrome P-450 inhibitor 8-methoxypsoralen prevented the ECV-induced increase in venous admixture but not the increased EVLW.	Methoxsalen	49-66	Cytochrome P450 1A1	Canis lupus familiaris	22-38
8967376-3	1996	These findings parallel those reported for cyclooxygenase inhibition in ECV-induced ALI and suggest that an arachidonic acid (AA) metabolite of pulmonary cytochrome P-450 activity may mediate the increase in venous admixture of ALI.	Arachidonic Acid	108-124	Cytochrome P450 1A1	Canis lupus familiaris	154-170
8967376-4	1996	We demonstrate that canine pulmonary microsomes metabolize [1-(14)C]AA to a variety of products, including the cytochrome P-450 metabolites 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid (EET).	,15-epoxyeicosatrienoic acid	166-194	Cytochrome P450 1A1	Canis lupus familiaris	111-127
7506944-4	1993	Renal arteries produce 20-hydroxyeicosatetraenoic acid (20-HETE) via the cytochrome P-450 pathway when incubated with arachidonic acid.	20-hydroxy-5,8,11,14-eicosatetraenoic acid	23-54	Cytochrome P450 1A1	Canis lupus familiaris	73-89
7506944-4	1993	Renal arteries produce 20-hydroxyeicosatetraenoic acid (20-HETE) via the cytochrome P-450 pathway when incubated with arachidonic acid.	20-hydroxy-5,8,11,14-eicosatetraenoic acid	56-63	Cytochrome P450 1A1	Canis lupus familiaris	73-89
7506944-4	1993	Renal arteries produce 20-hydroxyeicosatetraenoic acid (20-HETE) via the cytochrome P-450 pathway when incubated with arachidonic acid.	Arachidonic Acid	118-134	Cytochrome P450 1A1	Canis lupus familiaris	73-89
8335576-10	1993	SKF 525-A and metyrapone, inhibitors of cytochrome P-450 monooxygenases, converted the cooling-induced contractions of preparations with epithelium to relaxations and had no significant effects on the responses of preparations without epithelium.	Proadifen	0-9	Cytochrome P450 1A1	Canis lupus familiaris	40-56
8335576-10	1993	SKF 525-A and metyrapone, inhibitors of cytochrome P-450 monooxygenases, converted the cooling-induced contractions of preparations with epithelium to relaxations and had no significant effects on the responses of preparations without epithelium.	Metyrapone	14-24	Cytochrome P450 1A1	Canis lupus familiaris	40-56
8335576-11	1993	These observations suggest that cooling induces from the epithelium the release of a cytochrome P-450-derived eicosanoid that potentiates contractions of the underlying airway smooth muscle to carbachol.	Eicosanoids	110-120	Cytochrome P450 1A1	Canis lupus familiaris	85-101
8335576-11	1993	These observations suggest that cooling induces from the epithelium the release of a cytochrome P-450-derived eicosanoid that potentiates contractions of the underlying airway smooth muscle to carbachol.	Carbachol	193-202	Cytochrome P450 1A1	Canis lupus familiaris	85-101
1279284-1	1992	We wished to determine whether the metabolism of arachidonic acid, through lipoxygenase and cytochrome P-450 pathways, is involved in production of endothelium-derived relaxing factor(s) (EDRFs) in canine femoral veins.	Arachidonic Acid	49-65	Cytochrome P450 1A1	Canis lupus familiaris	92-108
1381476-3	1992	The carbon monoxide-bound reduced form of P-450(Dah1) showed an absorption peak at 447 nm and specific content of P-450(Dah1) was about 0.1 nmole P-450 per mg of microsomal protein.	Carbon Monoxide	4-19	Cytochrome P450 1A1	Canis lupus familiaris	48-52
1381476-3	1992	The carbon monoxide-bound reduced form of P-450(Dah1) showed an absorption peak at 447 nm and specific content of P-450(Dah1) was about 0.1 nmole P-450 per mg of microsomal protein.	Carbon Monoxide	4-19	Cytochrome P450 1A1	Canis lupus familiaris	120-124
1381476-5	1992	P-450(Dah1) activated 2-amino-3-methyl-imidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) most efficiently in the umu test and exhibited a high activity of aryl hydrocarbon hydroxylase toward benzo[a]pyrene.	2-amino-3-methylimidazo(4,5-f)quinoline	22-62	Cytochrome P450 1A1	Canis lupus familiaris	6-10
1381476-5	1992	P-450(Dah1) activated 2-amino-3-methyl-imidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) most efficiently in the umu test and exhibited a high activity of aryl hydrocarbon hydroxylase toward benzo[a]pyrene.	2-amino-3,4-dimethylimidazo(4,5-f)quinoline	72-115	Cytochrome P450 1A1	Canis lupus familiaris	6-10
1381476-5	1992	P-450(Dah1) activated 2-amino-3-methyl-imidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) most efficiently in the umu test and exhibited a high activity of aryl hydrocarbon hydroxylase toward benzo[a]pyrene.	Benzo(a)pyrene	225-239	Cytochrome P450 1A1	Canis lupus familiaris	6-10
1901255-4	1991	The cytochrome P-450 inhibitors ketoconazole (10 and 100 microM) and beta-diethyl-aminoethyldiphenylpropylacetate (SKF 525A, 10 and 100 microM) also inhibited the myogenic response.	Ketoconazole	32-44	Cytochrome P450 1A1	Canis lupus familiaris	4-20
1901255-4	1991	The cytochrome P-450 inhibitors ketoconazole (10 and 100 microM) and beta-diethyl-aminoethyldiphenylpropylacetate (SKF 525A, 10 and 100 microM) also inhibited the myogenic response.	Proadifen	115-123	Cytochrome P450 1A1	Canis lupus familiaris	4-20
1901255-12	1991	These results are consistent with the involvement of the vasoconstrictor 20-HETE and other cytochrome P-450 metabolites of endogenous fatty acids in the myogenic response.	Fatty Acids	134-145	Cytochrome P450 1A1	Canis lupus familiaris	91-107
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Rifampin	69-72	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8579377-1	1996	Asp-290 of the phenobarbital-inducible dog liver cytochrome P450 (P450) 2B11 was mutated to nine other amino acid residues by site-directed mutagenesis, and the functional significance of the unique negative charge in P450 2B11 at that position was studied.	Aspartic Acid	0-3	Cytochrome P450 1A1	Canis lupus familiaris	49-76
8579377-1	1996	Asp-290 of the phenobarbital-inducible dog liver cytochrome P450 (P450) 2B11 was mutated to nine other amino acid residues by site-directed mutagenesis, and the functional significance of the unique negative charge in P450 2B11 at that position was studied.	Phenobarbital	15-28	Cytochrome P450 1A1	Canis lupus familiaris	49-76
8546869-5	1995	The metabolic inhibitors 2-deoxy-D-glucose (2-DOG; 10 mM) and carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazone (FCCP; 3-5 microM), the reducing agent reduced glutathione and inhibitors of cytochrome P-450, all mimic the effects of hypoxia on IK(V) and Em in PA myocytes.	Deoxyglucose	25-42	Cytochrome P450 1A1	Canis lupus familiaris	191-207
7920427-1	1994	Primary cultures of dog hepatocytes sensitivity responded to various inducers of cytochrome P-450; phenobarbital (PB) significantly elevated the activity of 7-ethoxycoumarin O-deethylase (ECOD) and progesterone 6 beta-hydroxylase (6 beta-OHP).	Phenobarbital	99-112	Cytochrome P450 1A1	Canis lupus familiaris	81-97
7920427-1	1994	Primary cultures of dog hepatocytes sensitivity responded to various inducers of cytochrome P-450; phenobarbital (PB) significantly elevated the activity of 7-ethoxycoumarin O-deethylase (ECOD) and progesterone 6 beta-hydroxylase (6 beta-OHP).	Phenobarbital	114-116	Cytochrome P450 1A1	Canis lupus familiaris	81-97
7920427-4	1994	Pretreatment of the cultures with PB enhanced GSH depletion by bromobenzene, while beta-NF and Rif had little effect, suggesting that the 2B type cytochrome P-450 is responsible for the primary oxidation of bromobenzene to GSH-reactive metabolite(s).	Phenobarbital	34-36	Cytochrome P450 1A1	Canis lupus familiaris	146-162
7920427-4	1994	Pretreatment of the cultures with PB enhanced GSH depletion by bromobenzene, while beta-NF and Rif had little effect, suggesting that the 2B type cytochrome P-450 is responsible for the primary oxidation of bromobenzene to GSH-reactive metabolite(s).	Glutathione	46-49	Cytochrome P450 1A1	Canis lupus familiaris	146-162
7920427-4	1994	Pretreatment of the cultures with PB enhanced GSH depletion by bromobenzene, while beta-NF and Rif had little effect, suggesting that the 2B type cytochrome P-450 is responsible for the primary oxidation of bromobenzene to GSH-reactive metabolite(s).	bromobenzene	207-219	Cytochrome P450 1A1	Canis lupus familiaris	146-162
7920427-4	1994	Pretreatment of the cultures with PB enhanced GSH depletion by bromobenzene, while beta-NF and Rif had little effect, suggesting that the 2B type cytochrome P-450 is responsible for the primary oxidation of bromobenzene to GSH-reactive metabolite(s).	Glutathione	223-226	Cytochrome P450 1A1	Canis lupus familiaris	146-162
1784623-1	1991	Ciclosporin (CsA) is metabolized exclusively by the hepatic cytochrome P-450 mixed function oxidase system.	Cyclosporine	0-11	Cytochrome P450 1A1	Canis lupus familiaris	60-76
1784623-1	1991	Ciclosporin (CsA) is metabolized exclusively by the hepatic cytochrome P-450 mixed function oxidase system.	Cyclosporine	13-16	Cytochrome P450 1A1	Canis lupus familiaris	60-76
35389533-0	2022	Cytochrome P450 reaction phenotyping of itraconazole hydroxylation in the dog.	Itraconazole	40-52	Cytochrome P450 1A1	Canis lupus familiaris	0-15
34886785-6	2021	RESULTS: Enflicoxib was efficiently metabolized by cytochrome P-450 into three main phase I metabolites: M8, E-6132, and M7.	enflicoxib	9-19	Cytochrome P450 1A1	Canis lupus familiaris	51-67
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Fatty Acids, Unsaturated	0-27	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Fatty Acids, Unsaturated	0-27	Cytochrome P450 1A1	Canis lupus familiaris	236-239
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Arachidonic Acid	39-55	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Arachidonic Acid	39-55	Cytochrome P450 1A1	Canis lupus familiaris	236-239
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Docosahexaenoic Acids	62-82	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Docosahexaenoic Acids	62-82	Cytochrome P450 1A1	Canis lupus familiaris	236-239
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Docosahexaenoic Acids	84-87	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Docosahexaenoic Acids	84-87	Cytochrome P450 1A1	Canis lupus familiaris	236-239
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Eicosapentaenoic Acid	94-115	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Eicosapentaenoic Acid	94-115	Cytochrome P450 1A1	Canis lupus familiaris	236-239
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Eicosapentaenoic Acid	117-120	Cytochrome P450 1A1	Canis lupus familiaris	219-234
35321995-1	2022	Polyunsaturated fatty acids, including arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), are converted to hundreds of lipid mediators by cyclooxygenases (COX), lipoxygenases (LOX), and cytochrome P450 (CYP), or through non-enzymatic processes, and they reflect inflammatory states of the body.	Eicosapentaenoic Acid	117-120	Cytochrome P450 1A1	Canis lupus familiaris	236-239
2122230-0	1990	Isolation of cDNAs coding for three different forms of liver microsomal cytochrome P-450 from polychlorinated biphenyl-treated beagle dogs.	Polychlorinated Biphenyls	94-118	Cytochrome P450 1A1	Canis lupus familiaris	72-88
3667808-4	1987	Minimal molecular masses of cytochrome P-450 subpopulations were determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	79-101	Cytochrome P450 1A1	Canis lupus familiaris	28-44
2893713-0	1987	Selective inactivation by chloramphenicol of the major phenobarbital-inducible isozyme of dog liver cytochrome P-450.	Chloramphenicol	26-41	Cytochrome P450 1A1	Canis lupus familiaris	100-116
2893713-0	1987	Selective inactivation by chloramphenicol of the major phenobarbital-inducible isozyme of dog liver cytochrome P-450.	Phenobarbital	55-68	Cytochrome P450 1A1	Canis lupus familiaris	100-116
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Chloramphenicol	0-15	Cytochrome P450 1A1	Canis lupus familiaris	139-162
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Chloramphenicol	17-20	Cytochrome P450 1A1	Canis lupus familiaris	139-162
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Phenobarbital	89-102	Cytochrome P450 1A1	Canis lupus familiaris	139-162
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Phenobarbital	104-106	Cytochrome P450 1A1	Canis lupus familiaris	139-162
2893713-4	1987	CAP binds covalently to PBD-2 with a stoichiometry of 1 nmol of [14C]CAP bound/nmol of cytochrome P-450 inactivated.	Carbon-14	65-68	Cytochrome P450 1A1	Canis lupus familiaris	87-103
3667808-4	1987	Minimal molecular masses of cytochrome P-450 subpopulations were determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	polyacrylamide gels	102-120	Cytochrome P450 1A1	Canis lupus familiaris	28-44
3109323-0	1987	Purification and characterization of the dog hepatic cytochrome P-450 isozyme responsible for the metabolism of 2,2",4,4",5,5"-hexachlorobiphenyl.	2,4,5,2',4',5'-hexachlorobiphenyl	112-145	Cytochrome P450 1A1	Canis lupus familiaris	53-69
3104582-0	1987	Arachidonic acid-induced endothelial-dependent relaxations of canine coronary arteries: contribution of a cytochrome P-450-dependent pathway.	Arachidonic Acid	0-16	Cytochrome P450 1A1	Canis lupus familiaris	106-122
3104582-3	1987	SKF-525A, an inhibitor of cytochrome P-450-dependent enzymes, also attenuated the response to AA although the combination of SKF-525A and indomethacin prevented any relaxant effect.	Proadifen	0-8	Cytochrome P450 1A1	Canis lupus familiaris	26-42
3104582-4	1987	Induction of cytochrome P-450-dependent enzymes in the coronary artery with 3-methylcholanthrene and beta-naphthoflavone given in vivo (40 mg/kg/day for 3 days) or depletion of these enzymes with cobalt chloride (24 mg/kg/day for 2 days) resulted in an enhancement or diminution, respectively, of AA-induced endothelial-dependent relaxations.	Methylcholanthrene	76-96	Cytochrome P450 1A1	Canis lupus familiaris	13-29
3104582-4	1987	Induction of cytochrome P-450-dependent enzymes in the coronary artery with 3-methylcholanthrene and beta-naphthoflavone given in vivo (40 mg/kg/day for 3 days) or depletion of these enzymes with cobalt chloride (24 mg/kg/day for 2 days) resulted in an enhancement or diminution, respectively, of AA-induced endothelial-dependent relaxations.	beta-Naphthoflavone	101-120	Cytochrome P450 1A1	Canis lupus familiaris	13-29
3109323-3	1987	Upon treatment with phenobarbital (PB), at least two cytochrome P-450 isozymes are induced in the dog, and the hepatic microsomal metabolism of 245-HCB is increased on both a per nanomole P-450 basis (twofold) and a per milligram protein basis (fivefold).	Phenobarbital	20-33	Cytochrome P450 1A1	Canis lupus familiaris	53-69
3109323-3	1987	Upon treatment with phenobarbital (PB), at least two cytochrome P-450 isozymes are induced in the dog, and the hepatic microsomal metabolism of 245-HCB is increased on both a per nanomole P-450 basis (twofold) and a per milligram protein basis (fivefold).	Phenobarbital	35-37	Cytochrome P450 1A1	Canis lupus familiaris	53-69
3109323-10	1987	In addition, these results suggest that, in contrast to rats, dogs can readily metabolize 245-HCB as a result of the presence of a cytochrome P-450 isozyme with efficient 245-HCB metabolizing activity.	245-hcb	90-97	Cytochrome P450 1A1	Canis lupus familiaris	131-147
3109323-10	1987	In addition, these results suggest that, in contrast to rats, dogs can readily metabolize 245-HCB as a result of the presence of a cytochrome P-450 isozyme with efficient 245-HCB metabolizing activity.	Hexachlorobenzene	94-97	Cytochrome P450 1A1	Canis lupus familiaris	131-147
3770014-4	1986	These data were used to assess the concentration-response relationship for phenytoin inducing either cytochrome P-450 or the glycoprotein.	Phenytoin	75-84	Cytochrome P450 1A1	Canis lupus familiaris	101-117
6647432-0	1983	[Decrease in the intensity of the EPR cytochrome P-450, adrenodoxine and free radical signals in the adrenal cortex of dogs under the effect of o,p-dichlorodiphenyldichloroethane].	Mitotane	144-178	Cytochrome P450 1A1	Canis lupus familiaris	38-54
6420541-5	1984	Administration of agents that inhibit lipoxygenase and cytochrome P-450 enzymes blocked the constrictor phase, suggesting that this portion of the responses was associated with conversion of the precursor to hydroxylated eicosanoids.	Eicosanoids	221-232	Cytochrome P450 1A1	Canis lupus familiaris	55-71
6647432-1	1983	A study was made of the action of the adrenocorticolytic drug chloditane (o.p"-DDD) on the content of cytochrome P-450 adrenodoxine and free radicals in the dog adrenal cortex.	chloditane	62-72	Cytochrome P450 1A1	Canis lupus familiaris	102-118
6647432-1	1983	A study was made of the action of the adrenocorticolytic drug chloditane (o.p"-DDD) on the content of cytochrome P-450 adrenodoxine and free radicals in the dog adrenal cortex.	Mitotane	74-82	Cytochrome P450 1A1	Canis lupus familiaris	102-118
6647432-1	1983	A study was made of the action of the adrenocorticolytic drug chloditane (o.p"-DDD) on the content of cytochrome P-450 adrenodoxine and free radicals in the dog adrenal cortex.	adrenodoxine	119-131	Cytochrome P450 1A1	Canis lupus familiaris	102-118
457876-2	1979	Cytochrome P-450 (C-P450) is found in the lung and may modify pulmonary vascular tone via its sensitivity to changes in oxygen tension or by affecting metabolism of a chemical mediator.	Oxygen	120-126	Cytochrome P450 1A1	Canis lupus familiaris	0-24
959670-3	1976	In-vitro hepatic microsomal metabolism of warfarin and cytochrome P-450 content were greater for hepatic microsomes derived from phenylbutazone pretreated animals.	Phenylbutazone	129-143	Cytochrome P450 1A1	Canis lupus familiaris	55-71
1257603-0	1976	Treatment with o,p"-DDD (mitotane) decreased cytochrome P-450, heme, and microsomal protein content in the dog adrenal cortex in vivo.	Mitotane	15-23	Cytochrome P450 1A1	Canis lupus familiaris	45-61
1257603-0	1976	Treatment with o,p"-DDD (mitotane) decreased cytochrome P-450, heme, and microsomal protein content in the dog adrenal cortex in vivo.	Mitotane	25-33	Cytochrome P450 1A1	Canis lupus familiaris	45-61
1257603-2	1976	The reduction of cytochrome P-450 content was accompanied by decrease in heme content, which explains the apparent loss of cytochrome P-450.	Heme	73-77	Cytochrome P450 1A1	Canis lupus familiaris	17-33
1257603-2	1976	The reduction of cytochrome P-450 content was accompanied by decrease in heme content, which explains the apparent loss of cytochrome P-450.	Heme	73-77	Cytochrome P450 1A1	Canis lupus familiaris	123-139
28652520-9	2017	Taken together, these findings suggest that the Trp50Leu substitution leads to an enhancement of holo-CYP1A1 formation, but diminishes the enzyme activity because of the small size of Leu compared with Trp.	Leucine	53-56	Cytochrome P450 1A1	Canis lupus familiaris	102-108
28652520-9	2017	Taken together, these findings suggest that the Trp50Leu substitution leads to an enhancement of holo-CYP1A1 formation, but diminishes the enzyme activity because of the small size of Leu compared with Trp.	Tryptophan	48-51	Cytochrome P450 1A1	Canis lupus familiaris	102-108
33674269-3	2021	In vitro metabolism of midazolam (MDZ) and DCA in recombinant canine CYP1A1, 1A2, 2B11, 2C21, 2C41, 2D15, 3A12, 3A26 enzymes clarified that CYP3A12 was primarily responsible for either the oxidation elimination of MDZ or the regioselective oxidation metabolism of DCA into DCA-1beta-ol and DCA-5beta-ol in dog liver microsomes.	Midazolam	23-32	Cytochrome P450 1A1	Canis lupus familiaris	69-75
33674269-3	2021	In vitro metabolism of midazolam (MDZ) and DCA in recombinant canine CYP1A1, 1A2, 2B11, 2C21, 2C41, 2D15, 3A12, 3A26 enzymes clarified that CYP3A12 was primarily responsible for either the oxidation elimination of MDZ or the regioselective oxidation metabolism of DCA into DCA-1beta-ol and DCA-5beta-ol in dog liver microsomes.	Midazolam	34-37	Cytochrome P450 1A1	Canis lupus familiaris	69-75
33674269-3	2021	In vitro metabolism of midazolam (MDZ) and DCA in recombinant canine CYP1A1, 1A2, 2B11, 2C21, 2C41, 2D15, 3A12, 3A26 enzymes clarified that CYP3A12 was primarily responsible for either the oxidation elimination of MDZ or the regioselective oxidation metabolism of DCA into DCA-1beta-ol and DCA-5beta-ol in dog liver microsomes.	Deoxycholic Acid	43-46	Cytochrome P450 1A1	Canis lupus familiaris	69-75