PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33626394-0	2021	Short-term standard alcohol consumption enhances platelet response to clopidogrel through inhibition of Nrf2/Ces1 pathway and induction of Cyp2c in mice.	Alcohols	20-27	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	139-144
33626394-5	2021	KEY FINDINGS: Compared with vehicle control, alcohol pretreatment significantly reduced hydrolysis of clopidogrel as a result of significant down-regulation of Nrf2-mediated Ces1 expression (responsible for the formation of clopidogrel carboxylate), increased metabolic activation of clopidogrel due to significant up-regulation of Cyp2c (for the formation of active thiol metabolite H4), and consequently enhanced inhibition of ADP-induced platelet aggregation and activation by clopidogrel.	Alcohols	45-52	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	332-337
33267758-15	2020	CONCLUSION: These data demonstrated the increased transcription of Cyp2c and Cyp2b caused by Cyp3a ablation played a vital role in the metabolic activation of retrorsine, and long-term exposure of retrorsine can reduce the CYP450 activities.	retrorsine	159-169	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	67-72
32587777-6	2020	Overexpression of Cyp2c29 suppressed NF-kappaB activation and proinflammatory cytokine production by increasing the production of 14,15-epoxyeicosatrienoic acid in vitro.	14,15-epoxy-5,8,11-eicosatrienoic acid	130-160	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	18-25
32587777-7	2020	Furthermore, overexpression of Cyp2c29 in vivo protected against liver inflammation in mouse models of liver injury induced by both acetaminophen and CCl4.	Acetaminophen	132-145	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	31-38
31993311-2	2020	Several P450 isoforms, including CYP1A, CYP2B, CYP2C, and CYP3A, were down-regulated, accompanied by decreases in microsomal metabolism of diclofenac and nifedipine, in the liver and small intestine.	Diclofenac	139-149	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	47-52
31993311-2	2020	Several P450 isoforms, including CYP1A, CYP2B, CYP2C, and CYP3A, were down-regulated, accompanied by decreases in microsomal metabolism of diclofenac and nifedipine, in the liver and small intestine.	Nifedipine	154-164	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	47-52
33267758-0	2020	CYP2C and CYP2B mediated metabolic activation of retrorsine in Cyp3a knockout mice.	retrorsine	49-59	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
33267758-1	2020	BACKGROUND: Retrorsine is one of hepatotoxic pyrrolizidine alkaloids, which could be converted into a highly reactive metabolite, dehydroretrorsine, by CYP3A, and a lesser extent by CYP2C and CYP2B.	retrorsine	12-22	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	182-187
33267758-15	2020	CONCLUSION: These data demonstrated the increased transcription of Cyp2c and Cyp2b caused by Cyp3a ablation played a vital role in the metabolic activation of retrorsine, and long-term exposure of retrorsine can reduce the CYP450 activities.	retrorsine	197-207	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	67-72
30943218-11	2019	The WD suppressed the hepatic abundance of reparative oxylipins (19, 20-DiHDPA) as well as the expression of enzymes involved in fatty epoxide metabolism (Cyp2C, Ephx).	fatty epoxide	129-142	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	155-160
33267758-1	2020	BACKGROUND: Retrorsine is one of hepatotoxic pyrrolizidine alkaloids, which could be converted into a highly reactive metabolite, dehydroretrorsine, by CYP3A, and a lesser extent by CYP2C and CYP2B.	PYRROLIZIDINE	45-58	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	182-187
33267758-1	2020	BACKGROUND: Retrorsine is one of hepatotoxic pyrrolizidine alkaloids, which could be converted into a highly reactive metabolite, dehydroretrorsine, by CYP3A, and a lesser extent by CYP2C and CYP2B.	dehydroretrorsine	130-147	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	182-187
33267758-5	2020	The formations of glutathionyl-6,7-dihydro-1- hydroxymethyl-5H-pyrrolizine (GSH-DHP) and the activities of CYP3A, CYP2B and CYP2C were evaluated in the liver microsomes of WT and 3AKO mice before and after treatment.	gsh-dhp	76-83	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	124-129
33267758-10	2020	The chemical inhibitor experiment in liver microsomes indicated the predominant role of CYP3A and CYP2C in GSH-DHP formation in WT and 3AKO mice, respectively.	gsh-dhp	107-114	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	98-103
33267758-13	2020	After a seven-day treatment of retrorsine, the yields of GSH-DHP were lower than the untreated ones in both alleles, accompanied by the decreased mRNA of Cyp3a, Cyp2b and Cyp2c.	retrorsine	31-41	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	171-176
31690125-2	2019	CYP2C and CYP2J subfamily members actively metabolize fatty acids to bioactive eicosanoids, which exhibit potent anti-inflammatory effects.	Fatty Acids	54-65	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
31690125-2	2019	CYP2C and CYP2J subfamily members actively metabolize fatty acids to bioactive eicosanoids, which exhibit potent anti-inflammatory effects.	Eicosanoids	79-90	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
31661783-9	2019	NASH markers of inflammation and fibrosis were inversely associated with hepatic C20-22 omega3 PUFA-derived Cyp2C- and Cyp2J-generated anti-inflammatory oxylipins (false discovery rate adjusted p-value; q <= 0.026).	Fatty Acids, Unsaturated	95-99	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	108-113
29709908-8	2018	These results indicate that oridonin induced the expression and activation of CYP2c and CYP3a family, which might contribute to potential drug-drug interactions and appear to be a risk when co-administered with other clinical drugs.	oridonin	28-36	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	78-83
29130833-9	2017	This study indicated that the presence of UC decreases CYP2C expression levels in the liver, thereby delaying the metabolism of CYP2C substrates, including phenytoin, and increasing blood concentrations of these substrates.	Phenytoin	156-165	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	55-60
29023376-9	2017	These alterations induced by Type II diabetes in the endogenous pathway (CYP450) of arachidonic acid metabolism may increase the risk for cardiovascular disease by disrupting the fine equilibrium between cardioprotective (CYP2J/CYP2C-generated) and cardiotoxic (CYP4A/CYP4F-generated) metabolites of arachidonic acid.	Arachidonic Acid	84-100	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	228-233
29130833-2	2017	In this study, we investigated changes in the pharmacokinetics of phenytoin, a CYP2C substrate drug, in the presence of UC.	Phenytoin	66-75	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	79-84
29130833-5	2017	In DSS-treated animals, both mRNA and protein expression levels of CYP2C in the liver were significantly reduced relative to those in control animals (by 20%-40%).	Dextran Sulfate	3-6	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	67-72
29023376-9	2017	These alterations induced by Type II diabetes in the endogenous pathway (CYP450) of arachidonic acid metabolism may increase the risk for cardiovascular disease by disrupting the fine equilibrium between cardioprotective (CYP2J/CYP2C-generated) and cardiotoxic (CYP4A/CYP4F-generated) metabolites of arachidonic acid.	Arachidonic Acid	300-316	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	228-233
28374976-6	2017	CYP3a, CYP2b and CYP2c were induced in a dose-dependent manner by gemfibrozil.	Gemfibrozil	66-77	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	17-22
28450579-2	2017	CYP2C proteins detoxify xenobiotics and metabolize endogenous lipids such as arachidonic acid to bioactive eicosanoids.	Arachidonic Acid	77-93	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
28450579-2	2017	CYP2C proteins detoxify xenobiotics and metabolize endogenous lipids such as arachidonic acid to bioactive eicosanoids.	Eicosanoids	107-118	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
28514148-5	2017	Therefore, separation of the active principles from the fermented broths was performed, and that has led to the isolation of eight new 5,5,5-tricyclic hirsutane-type sesquiterpenes, namely, chondroterpenes A-H (1-8), together with seven known analogues.	Sesquiterpenes	166-180	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	206-214
28078076-15	2017	In 24 h, DOX exposure caused male-specific induction of Cyp1b1 and female-specific induction of Cyp2c29 and Cyp2e1.	Doxorubicin	9-12	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	96-103
27712037-4	2017	The pharmacokinetics of CYP selective substrates: caffeine, losartan, and omeprazole changed significantly in a diabetic NASH mouse model, indicating attenuation of the activity of Cyp1a2 and Cyp2c29, respectively.	Caffeine	50-58	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	192-199
27712037-4	2017	The pharmacokinetics of CYP selective substrates: caffeine, losartan, and omeprazole changed significantly in a diabetic NASH mouse model, indicating attenuation of the activity of Cyp1a2 and Cyp2c29, respectively.	Omeprazole	74-84	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	192-199
27638959-5	2016	Global bile acid analysis further revealed the absence of MCAs and their conjugated derivatives, and high concentrations of CDCA and UDCA in Cyp2c-null mouse cecum and feces.	Chenodeoxycholic Acid	124-128	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	141-146
27720395-8	2016	Fenofibrate reduced retinal and choroidal neovascularization in PPARalpha-/-mice and augmented omega-3 LCPUFA protection via CYP2C inhibition.	Fenofibrate	0-11	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	125-130
27592832-5	2016	In order to investigate drug efficacy in mice fed the HFHC diet, an intraperitoneal glucose tolerance test was conducted with or without a pretreatment with tolbutamide (a CYP2C substrate) after 4 weeks of feeding.	Tolbutamide	157-168	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	172-177
27417579-2	2016	Increased dietary intake of omega-3 long-chain polyunsaturated fatty acids (LCPUFA) reduces retinal neovascularization and choroidal neovascularization (CNV), but omega-3 LCPUFA metabolites of a major metabolizing pathway, cytochrome P450 oxidase (CYP) 2C, promote ocular pathological angiogenesis.	omega-3 long-chain polyunsaturated fatty acids	28-74	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	223-255
27417579-3	2016	We hypothesized that inhibition of CYP2C activity will add to the protective effects of omega-3 LCPUFA on neovascular eye diseases.	omega-3	88-95	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	35-40
27417579-5	2016	The plasma levels of omega-3 LCPUFA metabolites of CYP2C were determined by mass spectroscopy.	omega-3	21-28	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	51-56
27417579-7	2016	We found that inhibition of CYP2C activity by montelukast added to the protective effects of omega-3 LCPUFA on retinal neovascularization and CNV by 30% and 20%, respectively.	montelukast	46-57	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	28-33
27417579-9	2016	Soluble epoxide hydrolase inhibition, which blocks breakdown and inactivation of CYP2C omega-3 LCPUFA-derived active metabolites, increased oxygen-induced retinopathy and CNV in vivo.	Oxygen	140-146	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	81-86
27417579-10	2016	Exposure to selected omega-3 LCPUFA metabolites of CYP2C significantly reversed the suppression of both angiogenesis ex vivo and endothelial cell functions in vitro by the CYP2C inhibitor montelukast.	omega-3	21-28	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	51-56
27417579-10	2016	Exposure to selected omega-3 LCPUFA metabolites of CYP2C significantly reversed the suppression of both angiogenesis ex vivo and endothelial cell functions in vitro by the CYP2C inhibitor montelukast.	omega-3	21-28	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	172-177
27417579-10	2016	Exposure to selected omega-3 LCPUFA metabolites of CYP2C significantly reversed the suppression of both angiogenesis ex vivo and endothelial cell functions in vitro by the CYP2C inhibitor montelukast.	montelukast	188-199	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	51-56
27417579-10	2016	Exposure to selected omega-3 LCPUFA metabolites of CYP2C significantly reversed the suppression of both angiogenesis ex vivo and endothelial cell functions in vitro by the CYP2C inhibitor montelukast.	montelukast	188-199	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	172-177
26947597-10	2016	When the mice were fed experimental diets for 12 weeks, 0.05% trans-resveratrol increased CYP1A1, CYP2C, and CYP3A activities, whereas 0.5% MSE suppressed CYP3A activity.	Resveratrol	62-79	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	98-103
27683613-1	2016	Epoxyeicosatrienoicacids (EETs), synthesized from arachidonic acid by epoxygenases of the CYP2C and CYP2J gene subfamilies, contribute to hypoxic pulmonary vasoconstriction (HPV) in mice.	epoxyeicosatrienoicacids	0-24	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	90-95
27683613-1	2016	Epoxyeicosatrienoicacids (EETs), synthesized from arachidonic acid by epoxygenases of the CYP2C and CYP2J gene subfamilies, contribute to hypoxic pulmonary vasoconstriction (HPV) in mice.	eets	26-30	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	90-95
27683613-1	2016	Epoxyeicosatrienoicacids (EETs), synthesized from arachidonic acid by epoxygenases of the CYP2C and CYP2J gene subfamilies, contribute to hypoxic pulmonary vasoconstriction (HPV) in mice.	Arachidonic Acid	50-66	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	90-95
27592832-7	2016	The reason for this discrepancy was attributed to the mRNA expression levels of Cyp2c44 being lower and those of Cyp2c29 and Cyp2c66, which are involved in the metabolism of tolbutamide, being higher in the HFHC group than in the Control group.	Tolbutamide	174-185	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	113-120
26102010-8	2015	Continuous consuming of high fat and high fructose for 8weeks significantly increased the expressions of Cyp1a1, Cyp1a2, Cyp1b1, Cyp2c29, and Cyp3a11 while THC ultimately normalized these CYPs profiles.	Fructose	42-50	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	129-136
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	283-288
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	283-288
25867644-5	2015	RESULTS: The mRNA expression levels of CYP (CYP3A11, CYP1A2, CYP2C29, CYP2D9, and CYP2E1) decreased as pathological conditions worsened and reached their lowest levels on day 10 of DSS treatment.	Dextran Sulfate	181-184	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	61-68
24399466-8	2014	We propose that bile acids upregulate expression of hepatic Cyp3a11, Cyp2b10, Cyp2c29 and mEH in Bsep (-/-) mice and that Cyp3a11 and multidrug resistance-1 P-glycoproteins (Mdr1a/1b) are vital components of two distinct pathways utilized by mouse hepatocytes to expel bile acids.	Bile Acids and Salts	16-26	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	78-85
24966089-2	2014	In the present study, we used real-time quantitative PCR techniques to examine the effect of high salt or high K(+) (HK) intake on the expression of Cyp2c44, a major Cyp2c epoxygenase in the mouse kidney.	Salts	98-102	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	149-154
26109562-7	2015	In contrast, Cyp2c KO mice showed a 41% reduction in analgesic responses following systemically (s.c.) administered morphine.	Morphine	116-124	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	13-18
25757928-1	2015	We have previously shown that menthol attenuates the anticoagulant effect of warfarin by increasing the expression levels of CYP3A and CYP2C in the liver.	Menthol	30-37	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	135-140
25757928-1	2015	We have previously shown that menthol attenuates the anticoagulant effect of warfarin by increasing the expression levels of CYP3A and CYP2C in the liver.	Warfarin	77-85	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	135-140
25757928-2	2015	This study evaluated the effects of menthol on the pharmacokinetics of the CYP3A substrate triazolam and the CYP2C substrate phenytoin.	Phenytoin	125-134	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	109-114
25757928-8	2015	Similarly, the AUC of phenytoin was lower and the hepatic CYP2C expression level was higher in the menthol-treated group.	Menthol	99-106	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	58-63
23732297-4	2013	Here a Cyp2c knockout (KO) mouse was investigated for studying DDIs using midazolam (MDZ) a standard human CYP3A4 substrate and troleandomycin (TAO) a potent human CYP3A4 inhibitor.	Midazolam	85-88	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	7-12
24458713-6	2014	We found that CYP2C (localized in wild-type monocytes/macrophages) is upregulated in oxygen-induced retinopathy, whereas sEH is suppressed, resulting in an increased retinal epoxide:diol ratio.	Oxygen	85-91	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	14-19
24458713-6	2014	We found that CYP2C (localized in wild-type monocytes/macrophages) is upregulated in oxygen-induced retinopathy, whereas sEH is suppressed, resulting in an increased retinal epoxide:diol ratio.	Epoxy Compounds	174-181	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	14-19
24458713-6	2014	We found that CYP2C (localized in wild-type monocytes/macrophages) is upregulated in oxygen-induced retinopathy, whereas sEH is suppressed, resulting in an increased retinal epoxide:diol ratio.	diol	182-186	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	14-19
23732297-4	2013	Here a Cyp2c knockout (KO) mouse was investigated for studying DDIs using midazolam (MDZ) a standard human CYP3A4 substrate and troleandomycin (TAO) a potent human CYP3A4 inhibitor.	Troleandomycin	128-142	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	7-12
23732297-6	2013	The noteworthy differences in the metabolism of MDZ in Cyp2c KO compared to wild type mice confirms the important role that Cyp2c enzymes play in the murine metabolism of MDZ in vivo.	Midazolam	48-51	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	55-60
23732297-6	2013	The noteworthy differences in the metabolism of MDZ in Cyp2c KO compared to wild type mice confirms the important role that Cyp2c enzymes play in the murine metabolism of MDZ in vivo.	Midazolam	48-51	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	124-129
23160821-9	2013	The implications of a novel role for alpha-tocopherol in Cyp2c gene regulation are also discussed.	alpha-Tocopherol	37-53	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	57-62
23385081-5	2013	Conversely, activated microglia showed increased protein expression of RA-degrading cytochromes CYP26A1, CYP26B1, CYP3A4 and CYP2C.	Tretinoin	71-73	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	125-130
23146043-4	2012	Direct interaction between CFE and forskolin with CYP2C was evaluated in vitro.	Colforsin	35-44	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-55
22790670-3	2012	Oral administration of 10 mg/kg chalepensin to mice for 7 days significantly decreased hepatic coumarin 7-hydroxylation (Cyp2a) and increased 7-pentoxyresorufin O-dealkylation (Cyp2b) activities, whereas activities of Cyp1a, Cyp2c, Cyp2e1, and Cyp3a were not affected.	3-(alpha,alpha-dimethylallyl)psoralen	32-43	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	225-230
23146043-9	2012	CONCLUSIONS: CFE attenuates the anticoagulant action of warfarin by inducing hepatic CYP2C; thus, caution is required with the combination of warfarin and dietary supplements containing CFE.	Warfarin	56-64	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	85-90
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	epoxyeicosatrienoic	20-39	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
22382835-7	2012	From these experiments, it was suggested that the phenobarbital-induced changes in cyp2c29 and mrp3 are regulated by miR-30a and miR-29b, respectively.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	83-90
22004052-1	2011	Eight new eunicellin-based diterpenoids, klymollins A-H (1-8), were isolated during the chemical investigation of the soft coral Klyxum molle from Taiwan waters.	eunicellin	10-20	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	52-60
22004052-1	2011	Eight new eunicellin-based diterpenoids, klymollins A-H (1-8), were isolated during the chemical investigation of the soft coral Klyxum molle from Taiwan waters.	Diterpenes	27-39	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	52-60
22708815-0	2012	CYP2C29 produces superoxide in response to shear stress.	Superoxides	17-27	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-7
22708815-1	2012	OBJECTIVE: Activation of CYP2C29 releases superoxide during shear stress-induced dilation (SSID).	Superoxides	42-52	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	25-32
22708815-4	2012	RESULTS: Shear stress-induced dilation was significantly attenuated in vessels of eNOS-KO compared with WT mice, which was normalized by tempol and PEG-Catalase, in a PPOH (inhibitor of CYP2C29)-sensitive manner, but remained unaffected by VAS2870 and allopurinol, inhibitors of NADPH oxidase and xanthine oxidase, respectively.	propenylphosphonic acid	167-171	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	186-193
22708815-10	2012	CONCLUSIONS: CYP2C29 synthesizes EETs to mediate SSID, and simultaneously releases superoxide and sequential H(2)O(2), which in turn impair SSID.	Superoxides	83-93	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	13-20
22394353-4	2012	Midazolam is also metabolized by Cyp2c in mice.	Midazolam	0-9	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	33-38
21940400-1	2011	We demonstrated previously that cytochrome P-450 (CYP) 2C29 is the epoxyeicosatrienoic acid (EET) synthase responsible for the EET-mediated flow/shear stress-induced dilation of vessels of female nitric oxide (NO)-deficient mice (Sun D, Yang YM, Jiang H, Wu H, Ojami C, Kaley G, Huang A.	epoxyeicosatrienoic	67-86	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	32-59
21940400-1	2011	We demonstrated previously that cytochrome P-450 (CYP) 2C29 is the epoxyeicosatrienoic acid (EET) synthase responsible for the EET-mediated flow/shear stress-induced dilation of vessels of female nitric oxide (NO)-deficient mice (Sun D, Yang YM, Jiang H, Wu H, Ojami C, Kaley G, Huang A.	Nitric Oxide	196-208	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	32-59
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	dihydroxyeicosatrienoic acids	44-73	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	EET	75-78	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	dhet	79-83	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	20-hydroxy-5,8,11,14-eicosatetraenoic acid	147-178	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
20947618-2	2011	CYP2C/CYP2J-derived epoxyeicosatrienoic and dihydroxyeicosatrienoic acids (EET+DHET) elicit anti-inflammatory effects, whereas CYP4A/CYP4F-derived 20-hydroxyeicosatetraenoic acid (20-HETE) is proinflammatory.	20-hydroxy-5,8,11,14-eicosatetraenoic acid	180-187	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
21319371-4	2011	RESULT: The IC(50) values of both (-)-THP and (+)-THP on isoforms studied were higher than 100 mumol/L except that IC(50) value of (+)-THP on CYP2C was 43.89 mumol/L, indicating weak inhibition of (-)-THP and (+)-THP on CYP1A2, CYP2D22, CYP2E1 and CYP3A11 in vitro.	tetrahydropalmatine	131-138	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	142-147
21319371-4	2011	RESULT: The IC(50) values of both (-)-THP and (+)-THP on isoforms studied were higher than 100 mumol/L except that IC(50) value of (+)-THP on CYP2C was 43.89 mumol/L, indicating weak inhibition of (-)-THP and (+)-THP on CYP1A2, CYP2D22, CYP2E1 and CYP3A11 in vitro.	tetrahydropalmatine	131-138	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	142-147
19109366-12	2009	These data suggest that HS may activate CYP2C29 via A(2A) AR, causing relaxation, whereas NS may contribute to the upregulation of CYP4A causing contraction.	hassio	24-26	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	40-47
20405857-9	2010	In conclusion, these data indicate that nimesulide is bioactivated by CYP2C to a protein-reactive electrophilic intermediate that activates the Nrf2 pathway even at nontoxic exposure levels.	nimesulide	40-50	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	70-75
19903449-7	2010	With the BROD assay, we could clearly dissect CYP3A11 from other P450s induced by phenytoin-like CYP2C29, CYP2B9, CYP1A1, and CYP4A.	Phenytoin	82-91	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	97-104
20056545-1	2010	Eight new lignin derivatives, termed quiquelignan A-H (1-8), comprising three tricin-type flavonolignans (1-3) and five 8-O-4" neolignans (4-8), were isolated from the ethanol extract of Calamus quiquesetinervius stems.	Lignin	10-16	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-58
20056545-1	2010	Eight new lignin derivatives, termed quiquelignan A-H (1-8), comprising three tricin-type flavonolignans (1-3) and five 8-O-4" neolignans (4-8), were isolated from the ethanol extract of Calamus quiquesetinervius stems.	tricin	78-84	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-58
20056545-1	2010	Eight new lignin derivatives, termed quiquelignan A-H (1-8), comprising three tricin-type flavonolignans (1-3) and five 8-O-4" neolignans (4-8), were isolated from the ethanol extract of Calamus quiquesetinervius stems.	Flavonolignans	90-104	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-58
20056545-1	2010	Eight new lignin derivatives, termed quiquelignan A-H (1-8), comprising three tricin-type flavonolignans (1-3) and five 8-O-4" neolignans (4-8), were isolated from the ethanol extract of Calamus quiquesetinervius stems.	8-o-4" neolignans	120-137	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-58
20056545-1	2010	Eight new lignin derivatives, termed quiquelignan A-H (1-8), comprising three tricin-type flavonolignans (1-3) and five 8-O-4" neolignans (4-8), were isolated from the ethanol extract of Calamus quiquesetinervius stems.	Ethanol	168-175	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	50-58
18156313-0	2008	Midazolam metabolism in cytochrome P450 3A knockout mice can be attributed to up-regulated CYP2C enzymes.	Midazolam	0-9	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	91-96
19041682-9	2009	Xenobiotic-treatments with NP and TCPOBOP induced Cyp2b10, Cyp2c29, and Cyp3a11 in a CAR-mediated fashion; however NP only induced these CYPs in females and TCPOBOP induced these CYPs in both males and females.	1,4-bis(2-(3,5-dichloropyridyloxy))benzene	34-41	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	59-66
18156313-10	2008	We provide evidence that CYP2C enzymes, which were found to be up-regulated in Cyp3a knockout mice, are primarily responsible for this metabolism and that several but not all murine CYP2C enzymes are capable of metabolizing midazolam to its 1"-OH and/or 4-OH derivatives.	Midazolam	224-233	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	25-30
18156313-10	2008	We provide evidence that CYP2C enzymes, which were found to be up-regulated in Cyp3a knockout mice, are primarily responsible for this metabolism and that several but not all murine CYP2C enzymes are capable of metabolizing midazolam to its 1"-OH and/or 4-OH derivatives.	Midazolam	224-233	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	182-187
18156313-10	2008	We provide evidence that CYP2C enzymes, which were found to be up-regulated in Cyp3a knockout mice, are primarily responsible for this metabolism and that several but not all murine CYP2C enzymes are capable of metabolizing midazolam to its 1"-OH and/or 4-OH derivatives.	1"-oh	241-246	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	25-30
18156313-10	2008	We provide evidence that CYP2C enzymes, which were found to be up-regulated in Cyp3a knockout mice, are primarily responsible for this metabolism and that several but not all murine CYP2C enzymes are capable of metabolizing midazolam to its 1"-OH and/or 4-OH derivatives.	4-oh	254-258	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	25-30
16280380-9	2006	Both MXC and E2 increased expression of CYP2C29 (DMSO = 0.02 +/- 0.003; MXC = 0.04 +/- 0.008; E2 = 0.46 +/- 0.03 GE, n = 4, p < or = 0.05).	Dimethyl Sulfoxide	49-53	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	40-47
17575466-1	2007	Impaired cytochrome P450 epoxygenase enzyme (Cyp2c) regulation contributes to renal damage in angiotensin salt-sensitive hypertension (ANG/HS).	angiotensin salt	94-110	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	45-50
17575466-5	2007	Renal Cyp2c protein expression significantly decreased with ANG/HS hypertension in WT mice as compared to high salt alone.	Salts	111-115	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	6-11
17575466-6	2007	However, the ability to upregulate Cyp2c expression in response to a high salt diet was restored in the ANG/HS IL6 deficient hypertensive mice.	Salts	74-78	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	35-40
16680137-3	2006	After quantification of warfarin and nine of its metabolites in plasma from 13 inbred mouse strains, we correlated strain-specific differences in 7-hydroxywarfarin accumulation with genetic variation within a chromosomal region encoding cytochrome P450 2C (Cyp2c) enzymes.	Warfarin	24-32	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	237-255
16680137-3	2006	After quantification of warfarin and nine of its metabolites in plasma from 13 inbred mouse strains, we correlated strain-specific differences in 7-hydroxywarfarin accumulation with genetic variation within a chromosomal region encoding cytochrome P450 2C (Cyp2c) enzymes.	7-hydroxywarfarin	146-163	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	237-255
16680137-4	2006	This computational prediction was experimentally confirmed by showing that the rate-limiting step in biotransformation of warfarin to its 7-hydroxylated metabolite was inhibited by tolbutamide, a Cyp2c isoform-specific substrate, and that this transformation was mediated by expressed recombinant Cyp2c29.	Warfarin	122-130	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	196-201
16680137-4	2006	This computational prediction was experimentally confirmed by showing that the rate-limiting step in biotransformation of warfarin to its 7-hydroxylated metabolite was inhibited by tolbutamide, a Cyp2c isoform-specific substrate, and that this transformation was mediated by expressed recombinant Cyp2c29.	Warfarin	122-130	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	297-304
16680137-4	2006	This computational prediction was experimentally confirmed by showing that the rate-limiting step in biotransformation of warfarin to its 7-hydroxylated metabolite was inhibited by tolbutamide, a Cyp2c isoform-specific substrate, and that this transformation was mediated by expressed recombinant Cyp2c29.	Tolbutamide	181-192	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	196-201
16680137-4	2006	This computational prediction was experimentally confirmed by showing that the rate-limiting step in biotransformation of warfarin to its 7-hydroxylated metabolite was inhibited by tolbutamide, a Cyp2c isoform-specific substrate, and that this transformation was mediated by expressed recombinant Cyp2c29.	Tolbutamide	181-192	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	297-304
15155833-4	2004	Herein, we used in vivo and in vitro gene reporter assays of the Cyp2c29 promoter to delineate the phenytoin-response activity to a phenytoin-responsive module located at -1371 kb upstream of the Cyp2c29 translation start site.	Phenytoin	99-108	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	65-72
15205034-5	2004	Chemical inhibitors used to ascertain the contributions made by various cytochromes P450 were imipramine for CYP2C, alpha-methylbenzylaminobenzotriazole (MBA) for CYP2B, alpha-naphthoflavone (ANF) for CYP1A, 5-phenyl-1-pentyne (5P1P) for CYP2F2, and diethyldithiocarbamate (DTTC) for CYP2E1.	Imipramine	94-104	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	109-114
15155833-4	2004	Herein, we used in vivo and in vitro gene reporter assays of the Cyp2c29 promoter to delineate the phenytoin-response activity to a phenytoin-responsive module located at -1371 kb upstream of the Cyp2c29 translation start site.	Phenytoin	99-108	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	196-203
15155833-4	2004	Herein, we used in vivo and in vitro gene reporter assays of the Cyp2c29 promoter to delineate the phenytoin-response activity to a phenytoin-responsive module located at -1371 kb upstream of the Cyp2c29 translation start site.	Phenytoin	132-141	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	65-72
15155833-4	2004	Herein, we used in vivo and in vitro gene reporter assays of the Cyp2c29 promoter to delineate the phenytoin-response activity to a phenytoin-responsive module located at -1371 kb upstream of the Cyp2c29 translation start site.	Phenytoin	132-141	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	196-203
15155833-6	2004	Hepatic CYP2C29 mRNA was induced by phenytoin in wild-type but not in CAR-null mice, indicating that constitutive active or androstane receptor (CAR) regulates phenytoin-induced transcription of the Cyp2c29 gene.	Phenytoin	36-45	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	8-15
15155833-6	2004	Hepatic CYP2C29 mRNA was induced by phenytoin in wild-type but not in CAR-null mice, indicating that constitutive active or androstane receptor (CAR) regulates phenytoin-induced transcription of the Cyp2c29 gene.	Phenytoin	160-169	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	8-15
15155833-6	2004	Hepatic CYP2C29 mRNA was induced by phenytoin in wild-type but not in CAR-null mice, indicating that constitutive active or androstane receptor (CAR) regulates phenytoin-induced transcription of the Cyp2c29 gene.	Phenytoin	160-169	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	199-206
15102943-5	2004	The recombinant CYP2C proteins were expressed in Escherichia coli after N-terminal modification, partially purified, and shown to be active in the metabolism of both arachidonic acid (AA) and linoleic acid, albeit with different catalytic efficiencies and profiles.	Arachidonic Acid	166-182	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	16-21
15102943-10	2004	We conclude that these new CYP2C enzymes are probably involved in AA and linoleic acid metabolism in mouse hepatic and extrahepatic tissues.	Linoleic Acid	73-86	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	27-32
15102943-5	2004	The recombinant CYP2C proteins were expressed in Escherichia coli after N-terminal modification, partially purified, and shown to be active in the metabolism of both arachidonic acid (AA) and linoleic acid, albeit with different catalytic efficiencies and profiles.	Linoleic Acid	192-205	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	16-21
14569871-0	2003	[Activity and induction of CYP2B, CYP2C, and CYP3A in tissues of cyclophosphane-sensitive and resistant neoplasms and the liver of neoplasm-carrying mice].	Cyclophosphamide	65-79	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	34-39
14570766-7	2003	PB also induced CYP2C29 and CYP2C40, but not CYP2C38 mRNA.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	16-23
12746132-8	2003	Chemical inhibitors were used to ascertain the contributions made by various cytochromes P-450: imipramine for CYP2C, alpha -methylbenzylaminobenzotriazole for CYP2B, alpha -naphthoflavone for CYP1A, 5-phenyl-1-pentyne for CYP2F2, and diethyldithiocar-bamate for CYP2E1.	Imipramine	96-106	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	111-116
14569871-1	2003	The activities of three cytochrome P450 families involved in metabolic transformation of cyclophosphamide (CP) (CYP2B and CYP2C responsible for metabolic activation of CP and CYP3A responsible for inactivation of CP) have been investigated in lymphosarcoma and liver microsomes of tumor-bearing CBA mice.	Cyclophosphamide	89-105	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	122-127
14569871-4	2003	CYP2B, CYP2C and CYP3A activities in the CP sensitive tumor were comparable to those in liver, and CYP2B, CYP2C were induced by phenobarbital and dexamethasone.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	106-111
14569871-4	2003	CYP2B, CYP2C and CYP3A activities in the CP sensitive tumor were comparable to those in liver, and CYP2B, CYP2C were induced by phenobarbital and dexamethasone.	Dexamethasone	146-159	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	106-111
14569871-5	2003	CYP2B and CYP2C in the CP resistant tumor were inactive and only slightly induced by dexamethasone.	Dexamethasone	85-98	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	10-15
14569871-9	2003	At the same time, CYP2B and CYP2C activity in liver of RLS-bearing mice were essentially reduced, the activity CYP3A remained unchanged, and inducibility of CYP2B, CYP2C and CYP3A by phenobarbital and dexamethasone was similar to that in liver of mice without tumor.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	164-169
14569871-9	2003	At the same time, CYP2B and CYP2C activity in liver of RLS-bearing mice were essentially reduced, the activity CYP3A remained unchanged, and inducibility of CYP2B, CYP2C and CYP3A by phenobarbital and dexamethasone was similar to that in liver of mice without tumor.	Dexamethasone	201-214	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	164-169
11437368-0	2001	Oxidative hydrolysis of scoparone by cytochrome p450 CYP2C29 reveals a novel metabolite.	scoparone	24-33	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	53-60
11437368-2	2001	After induction with phenobarbital and phenytoin, a new reaction sequence catalyzed by Cyp2c29 was identified in mouse liver microsomes.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	87-94
11437368-2	2001	After induction with phenobarbital and phenytoin, a new reaction sequence catalyzed by Cyp2c29 was identified in mouse liver microsomes.	Phenytoin	39-48	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	87-94
11437368-3	2001	Cyp2c29-dependent 6-demethylation of scoparone resulted in the formation of isoscopoletin, an intermediate which is susceptible to further oxidation.	scoparone	37-46	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-7
11437368-3	2001	Cyp2c29-dependent 6-demethylation of scoparone resulted in the formation of isoscopoletin, an intermediate which is susceptible to further oxidation.	isoscopoletin	76-89	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-7
11437368-4	2001	This subsequent oxidation was also catalyzed by Cyp2c29 with a K(m) of 30,31 microM and a V(max) of 3,41 microM/min x microM P450, and resulted in the formation of the new metabolite 3-[4-methoxy-p-(3,6)-benzoquinone]-2-propenoate.	3-[4-methoxy-p-(3,6)-benzoquinone]-2-propenoate	183-230	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	48-55
7736922-7	1995	In a reconstituted system, P450 MUT-2 (CYP2C29) purified from mouse hepatic microsomes catalyzed the oxidation of o-, m-, and p-tolualdehydes to the carboxylic acids, and the specific activities (nmol/min/nmol P450) were 1.44, 2.81, and 2.32, respectively.	-, and p-tolualdehydes	119-141	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	39-46
9721182-6	1998	Based on coelution with authentic standards on reverse-phase HPLC, themajor metabolites were tentatively identified asfollows: CYP2C29 and CYP2C39 produced 14, 15-cis-epoxyeicosatrienoic acid (EET); CYP2C37 produced 12-hydroxyeicosatetraenoic acid (HETE); CYP2C38 produced 11,12-EET; and CYP2C40 produced an unidentified metabolite that coeluted with 16-,17-, and 18-HETEs.	14, 15-cis-epoxyeicosatrienoic acid	156-191	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	127-134
9721182-6	1998	Based on coelution with authentic standards on reverse-phase HPLC, themajor metabolites were tentatively identified asfollows: CYP2C29 and CYP2C39 produced 14, 15-cis-epoxyeicosatrienoic acid (EET); CYP2C37 produced 12-hydroxyeicosatetraenoic acid (HETE); CYP2C38 produced 11,12-EET; and CYP2C40 produced an unidentified metabolite that coeluted with 16-,17-, and 18-HETEs.	EET	193-196	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	127-134
9721182-6	1998	Based on coelution with authentic standards on reverse-phase HPLC, themajor metabolites were tentatively identified asfollows: CYP2C29 and CYP2C39 produced 14, 15-cis-epoxyeicosatrienoic acid (EET); CYP2C37 produced 12-hydroxyeicosatetraenoic acid (HETE); CYP2C38 produced 11,12-EET; and CYP2C40 produced an unidentified metabolite that coeluted with 16-,17-, and 18-HETEs.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	216-247	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	127-134
9721182-6	1998	Based on coelution with authentic standards on reverse-phase HPLC, themajor metabolites were tentatively identified asfollows: CYP2C29 and CYP2C39 produced 14, 15-cis-epoxyeicosatrienoic acid (EET); CYP2C37 produced 12-hydroxyeicosatetraenoic acid (HETE); CYP2C38 produced 11,12-EET; and CYP2C40 produced an unidentified metabolite that coeluted with 16-,17-, and 18-HETEs.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	249-253	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	127-134
9721182-6	1998	Based on coelution with authentic standards on reverse-phase HPLC, themajor metabolites were tentatively identified asfollows: CYP2C29 and CYP2C39 produced 14, 15-cis-epoxyeicosatrienoic acid (EET); CYP2C37 produced 12-hydroxyeicosatetraenoic acid (HETE); CYP2C38 produced 11,12-EET; and CYP2C40 produced an unidentified metabolite that coeluted with 16-,17-, and 18-HETEs.	11,12-epoxy-5,8,14-eicosatrienoic acid	273-282	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	127-134
9630465-5	1998	In contrast to the marked induction of P450s 3A and 2B, P450 2C was increased only 2.5-fold by PB and to an even lesser extent by Dex or PCP.	Phenobarbital	95-97	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	56-63
9630465-5	1998	In contrast to the marked induction of P450s 3A and 2B, P450 2C was increased only 2.5-fold by PB and to an even lesser extent by Dex or PCP.	Dexamethasone	130-133	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	56-63
9630465-5	1998	In contrast to the marked induction of P450s 3A and 2B, P450 2C was increased only 2.5-fold by PB and to an even lesser extent by Dex or PCP.	Phencyclidine	137-140	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	56-63
8597124-3	1995	We were able to show the expression of P450 species immunorelated to the main phenytoin-induced hepatic isoforms in mice (CYP2C29) and rats (CYP2B1,2) also in the central and peripheral nervous system and primary cultures of cell types from the brain.	Phenytoin	78-87	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	122-129
8597124-5	1995	Contrary, the CYP2C29 related form is inducible by phenytoin at about 1.5-fold starting from an already higher constitutive level.	Phenytoin	51-60	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	14-21
7492985-3	1995	A P450 isozyme in mouse hepatic microsomes, P450 MUT-2 (CYP2C29), catalyzed the reaction (0.96 nmol/min/nmol P450) in which NADPH and NADPH-cytochrome c reductase were essential for the catalytic activity.	NADP	124-129	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	56-63
7492985-5	1995	By addition of antibody against CYP2C29 to the microsomes (3.2 mg/mg microsomal protein) the MALDO activity was inhibited by 35% of the control value with preimmune serum, suggesting that CYP2C29 or an immunologically-related isozyme(s) plays a major role in the NADPH-dependent oxidation of 3,4,5-trimethoxyphenylacetaldehyde to 3,4,5-trimethoxyphenylacetic acid by mouse hepatic microsomes.	NADP	263-268	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	32-39
7492985-5	1995	By addition of antibody against CYP2C29 to the microsomes (3.2 mg/mg microsomal protein) the MALDO activity was inhibited by 35% of the control value with preimmune serum, suggesting that CYP2C29 or an immunologically-related isozyme(s) plays a major role in the NADPH-dependent oxidation of 3,4,5-trimethoxyphenylacetaldehyde to 3,4,5-trimethoxyphenylacetic acid by mouse hepatic microsomes.	3,4,5-trimethoxyphenylacetaldehyde	292-326	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	32-39
7492985-5	1995	By addition of antibody against CYP2C29 to the microsomes (3.2 mg/mg microsomal protein) the MALDO activity was inhibited by 35% of the control value with preimmune serum, suggesting that CYP2C29 or an immunologically-related isozyme(s) plays a major role in the NADPH-dependent oxidation of 3,4,5-trimethoxyphenylacetaldehyde to 3,4,5-trimethoxyphenylacetic acid by mouse hepatic microsomes.	3,4,5-trimethoxyphenylacetic acid	330-363	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	32-39
7736922-7	1995	In a reconstituted system, P450 MUT-2 (CYP2C29) purified from mouse hepatic microsomes catalyzed the oxidation of o-, m-, and p-tolualdehydes to the carboxylic acids, and the specific activities (nmol/min/nmol P450) were 1.44, 2.81, and 2.32, respectively.	Carboxylic Acids	149-165	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	39-46
8466552-5	1993	Immunoprecipitation of microsomal protein with antibodies raised against either P450 2C or 3A revealed that approximately equal amounts of [14C]-CBD were bound to each of these P450s after CBD-mediated inactivation.	14c]-cbd	140-148	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	80-87
8461036-9	1993	The induction data and the greater degree of inhibition of SR 4233 reduction by metyrapone compared to alpha-naphthoflavone suggested a possible involvement of Cyp2b, Cyp2c and Cyp3a cytochrome P450 subfamilies.	Metyrapone	80-90	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	167-172
8461036-13	1993	Immunoinhibition studies with epitope specific monoclonal antibodies were consistent with the major involvement of phenobarbitone- and steroid-inducible products of the Cyp2b and Cyp2c subfamilies.	Phenobarbital	115-129	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	179-184
8461036-13	1993	Immunoinhibition studies with epitope specific monoclonal antibodies were consistent with the major involvement of phenobarbitone- and steroid-inducible products of the Cyp2b and Cyp2c subfamilies.	Steroids	135-142	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	179-184
8466552-5	1993	Immunoprecipitation of microsomal protein with antibodies raised against either P450 2C or 3A revealed that approximately equal amounts of [14C]-CBD were bound to each of these P450s after CBD-mediated inactivation.	Cannabidiol	145-148	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	80-87
8466552-7	1993	Although > 80% of the enzyme activities attributed to P450s 2C and 3A were inactivated by CBD at the anticonvulsant dose of 120 mg/kg, P450 2C was approximately 3-fold more sensitive than P450 3A at the lower CBD doses tested.	Cannabidiol	93-96	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	138-145
1655922-0	1991	[MALDO (microsomal aldehyde oxygenase): a cytochrome P-450 isozyme purified from mouse hepatic microsomes that catalyzes the oxygenation of aldehyde to carboxylic acid].	Carboxylic Acids	152-167	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	19-37
1847130-1	1991	The oxygenation of an aldehyde, 11-oxo-delta 8-tetrahydrocannabinol to a carboxylic acid, delta 8-tetrahydrocannabinol-11-oic acid was catalyzed by cytochrome P-450 MUT-2 purified from hepatic microsomes of male ddN mice.	Aldehydes	22-30	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	148-170
1847130-1	1991	The oxygenation of an aldehyde, 11-oxo-delta 8-tetrahydrocannabinol to a carboxylic acid, delta 8-tetrahydrocannabinol-11-oic acid was catalyzed by cytochrome P-450 MUT-2 purified from hepatic microsomes of male ddN mice.	11-oxo-delta(8)-tetrahydrocannabinol	32-67	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	148-170
1847130-1	1991	The oxygenation of an aldehyde, 11-oxo-delta 8-tetrahydrocannabinol to a carboxylic acid, delta 8-tetrahydrocannabinol-11-oic acid was catalyzed by cytochrome P-450 MUT-2 purified from hepatic microsomes of male ddN mice.	Carboxylic Acids	73-88	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	148-170
1847130-1	1991	The oxygenation of an aldehyde, 11-oxo-delta 8-tetrahydrocannabinol to a carboxylic acid, delta 8-tetrahydrocannabinol-11-oic acid was catalyzed by cytochrome P-450 MUT-2 purified from hepatic microsomes of male ddN mice.	delta(6)-tetrahydrocannabinol-7-oic acid	90-130	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	148-170
1847130-1	1991	The oxygenation of an aldehyde, 11-oxo-delta 8-tetrahydrocannabinol to a carboxylic acid, delta 8-tetrahydrocannabinol-11-oic acid was catalyzed by cytochrome P-450 MUT-2 purified from hepatic microsomes of male ddN mice.	dimethylaminonaphthalene-5-sulfonaminoethylmethylamine	212-215	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	148-170
2004789-3	1991	Comparison of the segregation patterns of these alleles in three sets of recombinant inbred strains with allele segregation patterns of previously characterized loci shows that the Rbp-4 locus is closely linked to the locus for phenobarbital-inducible cytochrome P450-2c (Cyp-2c) that has been shown by in situ hybridization to lie on chromosome 19, bands D1-D2.	Phenobarbital	228-241	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	252-270
2004789-3	1991	Comparison of the segregation patterns of these alleles in three sets of recombinant inbred strains with allele segregation patterns of previously characterized loci shows that the Rbp-4 locus is closely linked to the locus for phenobarbital-inducible cytochrome P450-2c (Cyp-2c) that has been shown by in situ hybridization to lie on chromosome 19, bands D1-D2.	Phenobarbital	228-241	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	272-278
34438105-0	2021	Cyp2c-deficiency depletes muricholic acids and protects against high fat diet-induced obesity in male mice but promotes liver damage.	muricholic acid	26-42	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
34438105-6	2021	RESULTS: Cyp2c deficiency depleted MCAs and caused other changes in BA composition, namely a decrease in the ratio of 12alpha-hydroxylated (12alpha-OH) BAs to non-12alpha-OH BAs, without altering the total BA levels.	Bile Acids and Salts	68-70	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	9-14
34438105-8	2021	Cyp2c-/- male mice also showed reduced intestinal lipid absorption and increased lipid excretion, which was reversed by oral gavage with the 12alpha-OH BA, taurocholic acid.	Bile Acids and Salts	152-154	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
34438105-8	2021	Cyp2c-/- male mice also showed reduced intestinal lipid absorption and increased lipid excretion, which was reversed by oral gavage with the 12alpha-OH BA, taurocholic acid.	Taurocholic Acid	156-172	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-5
35422231-13	2022	In addition, the expression of epoxyeicosatrienoic acid-synthesizing genes, cyp2c29 and cyp2j5, was increased significantly (P < 0.05) in the hearts of high-dose rofecoxib-treated mice by 4- and 16-fold, respectively.	epoxyeicosatrienoic acid	31-55	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	76-83
35422231-13	2022	In addition, the expression of epoxyeicosatrienoic acid-synthesizing genes, cyp2c29 and cyp2j5, was increased significantly (P < 0.05) in the hearts of high-dose rofecoxib-treated mice by 4- and 16-fold, respectively.	rofecoxib	162-171	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	76-83
35401818-3	2022	Methods: By conducting computational modelling to quantitatively fine-tune the twisted intramolecular charge transfer (TICT) tendency of Thioflavin T (ThT) analogues, we developed an ultrasensitive probe AH-2.	thioflavin T	137-149	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	204-208
35401818-3	2022	Methods: By conducting computational modelling to quantitatively fine-tune the twisted intramolecular charge transfer (TICT) tendency of Thioflavin T (ThT) analogues, we developed an ultrasensitive probe AH-2.	thioflavin T	151-154	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	204-208
35401818-4	2022	AH-2 retained the binding affinity and binding mode of ThT towards Abeta deposits, and exhibited ca 10-fold less background fluorescence and 5-10 folds of improved signal-to-background contrast upon binding Abeta deposits.	thioflavin T	55-58	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	0-4
35401818-8	2022	Given this desirable sensitivity and good spatiotemporal resolution, AH-2 was successfully applied in the preclinical evaluation of Abeta-targeted treatment by melatonin.	Melatonin	160-169	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	69-73