PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34088742-9	2021	1G4 transgenic mice suppressed growth of syngeneic methylcholanthrene (MCA) induced HHD tumor cells expressing the full-length human NY-ESO-1 protein but not MCA HHD tumor cells lacking NY-ESO-1.	Methylcholanthrene	51-69	cancer/testis antigen 1A	Homo sapiens	133-141
34088742-9	2021	1G4 transgenic mice suppressed growth of syngeneic methylcholanthrene (MCA) induced HHD tumor cells expressing the full-length human NY-ESO-1 protein but not MCA HHD tumor cells lacking NY-ESO-1.	Methylcholanthrene	71-74	cancer/testis antigen 1A	Homo sapiens	133-141
34505065-3	2021	C3 -/-, MBL1/2 -/- and C4 -/- mice showed reduced susceptibility to 3-methylcholanthrene sarcomagenesis and transplanted sarcomas, whereas C1q and factor B deficiency had marginal effects.	Methylcholanthrene	68-88	mannose-binding lectin (protein A) 1	Mus musculus	8-14
35538380-9	2022	MC interacted with critical residues of NSP3 macro-domain and NSP10-NSP16 complex and occupied their active sites.	Methylcholanthrene	0-2	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	40-44
35538380-9	2022	MC interacted with critical residues of NSP3 macro-domain and NSP10-NSP16 complex and occupied their active sites.	Methylcholanthrene	0-2	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	62-67
35195769-7	2022	E-FABP-immunopositive septoclasts were detected for the first time at the beginning of MC resorption and localized along the resorption surface.	Methylcholanthrene	87-89	fatty acid binding protein 5, epidermal	Mus musculus	0-6
35472854-2	2022	To fully exploit the information given by the probe, we carefully re-investigated the thG spectroscopic properties in 12-bp duplexes, when the Set and Ring Associated (SRA) domain of UHRF1 flips its 5" flanking methylcytosine (mC).	Methylcholanthrene	227-229	macrophage scavenger receptor 1	Homo sapiens	168-171
35472854-2	2022	To fully exploit the information given by the probe, we carefully re-investigated the thG spectroscopic properties in 12-bp duplexes, when the Set and Ring Associated (SRA) domain of UHRF1 flips its 5" flanking methylcytosine (mC).	Methylcholanthrene	227-229	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	183-188
35472854-3	2022	The SRA-induced flipping of mC was found to strongly increase the fluorescence intensity of thG, but this increase was much larger when thG was flanked in 3" by a C residue as compared to an A residue.	Methylcholanthrene	28-30	macrophage scavenger receptor 1	Homo sapiens	4-7
35195769-11	2022	The present study showed that E-FABP-immunopositive septoclasts participated in the disappearance of MC through the resorption of the uncalcified cartilage matrix and that they have different roles from osteoclasts/chondroclasts.	Methylcholanthrene	101-103	fatty acid binding protein 5, epidermal	Mus musculus	30-36
2632253-7	1989	This difference was primarily related to the fact that patients with MC had a significantly higher CK-BB activity than patients without CNS metastases or patients with parenchymal brain metastases only (P less than 0.01 and P less than 0.05, respectively).	Methylcholanthrene	69-71	creatine kinase B	Homo sapiens	99-104
35267370-6	2022	The presence and stage of CMC and MC incorporation affected the rate and extent of lipolysis, with SPC/MC-seq presenting an inferior concentration of free fatty acids.	Methylcholanthrene	34-36	surfactant protein C	Homo sapiens	99-102
35172159-6	2022	Furthermore, inactivation of VIP interneurons leads to increased MC firing and impaired olfactory detection and odor discrimination.	Methylcholanthrene	65-67	vasoactive intestinal polypeptide	Mus musculus	29-32
2512292-2	1989	The Gunn rat is also deficient in a 3-methylcholanthrene (MC)-inducible UDPGT isoenzyme that has high activity toward phenolic substrates.	Methylcholanthrene	36-56	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	72-77
2512292-2	1989	The Gunn rat is also deficient in a 3-methylcholanthrene (MC)-inducible UDPGT isoenzyme that has high activity toward phenolic substrates.	Methylcholanthrene	58-60	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	72-77
2512292-3	1989	We have isolated and sequenced a cDNA, designated 4-NP UDPGT, which encodes an MC-inducible UDPGT from normal Wistar rat livers (Iyanagi, T., Haniu, M., Sogawa, F., Fujii-Kuriyama, Y., Watanabe, S., Shively, J.E., and Anan, K.F.	Methylcholanthrene	79-81	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	55-60
2512292-3	1989	We have isolated and sequenced a cDNA, designated 4-NP UDPGT, which encodes an MC-inducible UDPGT from normal Wistar rat livers (Iyanagi, T., Haniu, M., Sogawa, F., Fujii-Kuriyama, Y., Watanabe, S., Shively, J.E., and Anan, K.F.	Methylcholanthrene	79-81	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	92-97
2512292-7	1989	In the present study, we found that this cDNA detected MC-inducible UDPGT mRNA in the MC-treated homozygous Gunn rat liver.	Methylcholanthrene	55-57	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	68-73
2512292-7	1989	In the present study, we found that this cDNA detected MC-inducible UDPGT mRNA in the MC-treated homozygous Gunn rat liver.	Methylcholanthrene	86-88	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	68-73
2512292-9	1989	The size of mRNA in Gunn rats was identical to that of the functionally mature UDPGT mRNA in Wistar rats, but the MC-inducible UDPGT protein was absent from homozygous Gunn rat microsomes.	Methylcholanthrene	114-116	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	127-132
2512292-10	1989	We therefore made a cDNA library from MC-treated Gunn rat liver mRNA and isolated cDNA clones, using the 4-NP UDPGT cDNA as a probe.	Methylcholanthrene	38-40	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	110-115
35149128-4	2022	Among 164 kinase inhibitors listed in these kits, tyrphostin AG1024, commonly used as an inhibitor of insulin-like growth factor receptor (IGF1R) and insulin receptor (IR), was identified as a potent inhibitor of 3-methylcholanthrene (MC)-mediated AhR activation.	Methylcholanthrene	213-233	insulin	Homo sapiens	102-109
35149128-4	2022	Among 164 kinase inhibitors listed in these kits, tyrphostin AG1024, commonly used as an inhibitor of insulin-like growth factor receptor (IGF1R) and insulin receptor (IR), was identified as a potent inhibitor of 3-methylcholanthrene (MC)-mediated AhR activation.	Methylcholanthrene	213-233	insulin like growth factor 1 receptor	Homo sapiens	139-144
35149128-4	2022	Among 164 kinase inhibitors listed in these kits, tyrphostin AG1024, commonly used as an inhibitor of insulin-like growth factor receptor (IGF1R) and insulin receptor (IR), was identified as a potent inhibitor of 3-methylcholanthrene (MC)-mediated AhR activation.	Methylcholanthrene	213-233	insulin receptor	Homo sapiens	150-166
35149128-4	2022	Among 164 kinase inhibitors listed in these kits, tyrphostin AG1024, commonly used as an inhibitor of insulin-like growth factor receptor (IGF1R) and insulin receptor (IR), was identified as a potent inhibitor of 3-methylcholanthrene (MC)-mediated AhR activation.	Methylcholanthrene	213-233	insulin receptor	Homo sapiens	168-170
35149128-4	2022	Among 164 kinase inhibitors listed in these kits, tyrphostin AG1024, commonly used as an inhibitor of insulin-like growth factor receptor (IGF1R) and insulin receptor (IR), was identified as a potent inhibitor of 3-methylcholanthrene (MC)-mediated AhR activation.	Methylcholanthrene	213-233	aryl hydrocarbon receptor	Homo sapiens	248-251
35149128-5	2022	We further investigated the mechanism by which AG1024 suppresses MC-mediated AhR activation.	Methylcholanthrene	65-67	aryl hydrocarbon receptor	Homo sapiens	77-80
35548339-3	2022	Our study challenges the PI3K/Akt axis in a cisplatin-resistant cervical cancer scenario with phenethylisothiocyanate (PEITC) for chemosensitization of SiHaR, a cisplatin-resistant sub-line of SiHa and 3-methylcholanthrene-induced cervical cancer mice models.	Methylcholanthrene	202-222	thymoma viral proto-oncogene 1	Mus musculus	30-33
35176999-11	2022	The therapeutic effect of MC on sarcopenia may associate with PI3K-Akt signaling pathway, EGFR tyrosine kinase inhibitor resistance, longevity regulating pathway, and other cellular and innate immune signaling pathways.	Methylcholanthrene	26-28	AKT serine/threonine kinase 1	Homo sapiens	67-70
34997082-10	2022	MiR-29b inhibits TGF-beta1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC.	Methylcholanthrene	169-171	transforming growth factor beta 1	Homo sapiens	17-26
34997082-10	2022	MiR-29b inhibits TGF-beta1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC.	Methylcholanthrene	169-171	microRNA 29b-1	Homo sapiens	58-65
2632253-12	1989	The CSF activity of CK-BB appears to be a contribution in the diagnosis of MC secondary to breast cancer and seems superior to protein and LDH.	Methylcholanthrene	75-77	creatine kinase B	Homo sapiens	20-25
2805235-7	1989	On the other hand, microsomes from uninduced LEC rat liver had more 3-methylcholanthrene (MC) inducible P450MC, mainly P450c and P450d, than microsomes from LEA rat liver and these isozymes in the LEC were markedly induced by 3-methylcholanthrene treatment.	Methylcholanthrene	68-88	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	104-110
2583111-7	1989	Individual myogenic colonies derived from MCA C115 cells (10T1/2 fibroblast transformed by methylcholanthrene) express various levels of endogenous MyoD1 mRNA ranging from nearly zero to high levels.	Methylcholanthrene	91-109	myogenic differentiation 1	Mus musculus	148-153
2805235-7	1989	On the other hand, microsomes from uninduced LEC rat liver had more 3-methylcholanthrene (MC) inducible P450MC, mainly P450c and P450d, than microsomes from LEA rat liver and these isozymes in the LEC were markedly induced by 3-methylcholanthrene treatment.	Methylcholanthrene	90-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	104-110
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Methylcholanthrene	281-301	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Methylcholanthrene	303-307	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2554926-2	1989	The aromatic hydrocarbon responsiveness (Ah) locus encodes the Ah receptor, which regulates the induction of certain drug-metabolizing enzymes by polycyclic aromatic compounds such as 3-methylcholanthrene and tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	184-204	aryl-hydrocarbon receptor	Mus musculus	63-74
2509008-2	1989	The current studies demonstrate increased cell proliferation (i.e., [3H]-thymidine incorporation into DNA and tetrazolium salt reduction/deposition) in the osteoblastic murine cell line MC-3T3-E1 in response to salmon calcitonin (P less than 0.005) and to human calcitonin (P less than 0.005), but not to human calcitonin gene-related peptide.	Methylcholanthrene	186-188	calcitonin related polypeptide alpha	Homo sapiens	218-228
2509008-2	1989	The current studies demonstrate increased cell proliferation (i.e., [3H]-thymidine incorporation into DNA and tetrazolium salt reduction/deposition) in the osteoblastic murine cell line MC-3T3-E1 in response to salmon calcitonin (P less than 0.005) and to human calcitonin (P less than 0.005), but not to human calcitonin gene-related peptide.	Methylcholanthrene	186-188	calcitonin related polypeptide alpha	Homo sapiens	262-272
2509008-2	1989	The current studies demonstrate increased cell proliferation (i.e., [3H]-thymidine incorporation into DNA and tetrazolium salt reduction/deposition) in the osteoblastic murine cell line MC-3T3-E1 in response to salmon calcitonin (P less than 0.005) and to human calcitonin (P less than 0.005), but not to human calcitonin gene-related peptide.	Methylcholanthrene	186-188	calcitonin related polypeptide alpha	Homo sapiens	262-272
2548720-5	1989	Further experiments revealed that this decreased activation of the carcinogens in resistant rat livers is due to a low inducibility of 3-methylcholanthrene-inducible forms of cytochrome P-450 mRNA.	Methylcholanthrene	135-155	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	175-191
2775885-0	1989	Strain- and organ-dependent differences in induction of aryl hydrocarbon hydroxylase activity by 3-methylcholanthrene.	Methylcholanthrene	97-117	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	56-84
2509440-5	1989	Activation of aflatoxin B1 by hepatic microsomes of 3-methylcholanthrene-treated hamsters was inhibited almost completely by the antibody against P-450-AFB but not by the antibody against P-450-II, indicating that P-450-AFB is the major component responsible for the activation of aflatoxin B1 by hamster liver.	Methylcholanthrene	52-72	cytochrome P450 2A8	Mesocricetus auratus	152-155
2509440-5	1989	Activation of aflatoxin B1 by hepatic microsomes of 3-methylcholanthrene-treated hamsters was inhibited almost completely by the antibody against P-450-AFB but not by the antibody against P-450-II, indicating that P-450-AFB is the major component responsible for the activation of aflatoxin B1 by hamster liver.	Methylcholanthrene	52-72	cytochrome P450 2A8	Mesocricetus auratus	220-223
2639905-1	1989	We have used the 3-Methylcholanthrene induced T-10 fibrosarcoma tumour cell system (H-2b xH-2k)F1 to elucidate the possible correlation between metastatic potential, expression of individual H-2 antigens and susceptibility to NK cells.	Methylcholanthrene	17-37	relaxin 2	Homo sapiens	84-87
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	204-224	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-68
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	204-224	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-89
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	204-224	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
2787638-5	1989	However, there was anomalous expression and induction by phenobarbital of the major 3-methylcholanthrene-inducible isozyme, cytochrome P-450c, in cultured hepatocytes in each of the three media tested, but this response was more pronounced in T1 medium.	Methylcholanthrene	84-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	124-141
2502109-1	1989	Cytochrome P-450AFB is major isozyme inducible by 3-methylcholanthrene in Syrian golden hamsters and shows high potency toward aflatoxin B1 activation.	Methylcholanthrene	50-70	cytochrome P450 2A8	Mesocricetus auratus	0-19
2512389-1	1989	The involvement of cytochrome P-450 isozymes in the activation of benzo[a]pyrene (BP) by human placental and liver microsomes was studied in vitro using monoclonal antibodies (Mab) toward the major 3-methylcholanthrene (MC)-inducible and phenobarbital-inductible rat liver P-450 isozymes (Mab 1-7-1 and Mab 2-66-3, respectively).	Methylcholanthrene	198-218	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	19-35
2480220-2	1989	With MC stimulation, the TCR consisted of an initially positive wave with an onset latency of 8.8-12.2 msec, a duration of 7-15 msec, and an amplitude which reached up to 20 microV, sometimes followed by a broad low amplitude negative wave.	Methylcholanthrene	5-7	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	25-28
2480220-6	1989	Unlike with anodic stimulation, the MC evoked TCR was usually not preceded by a prominent EMG potential from temporalis muscle and was not associated with subject discomfort.	Methylcholanthrene	36-38	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	46-49
2804169-3	1989	The properties of cytochrome P-450d were compared to those of cytochrome P-450c isolated from 3-methylcholanthrene-induced rats.	Methylcholanthrene	94-114	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	62-79
2804169-4	1989	The yield of these cytochromes under the conditions used (10% P-450d from isosafrol-induced microsomes and 15% P-450c from 3-methylcholanthrene-induced microsomes) was relatively high.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	111-117
2731175-0	1989	Characterization of 3-methylcholanthrene effects on the rat glucocorticoid receptor in vivo.	Methylcholanthrene	20-40	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	60-83
2747632-0	1989	The human cytochrome Cyp1A2 gene contains regulatory elements responsive to 3-methylcholanthrene.	Methylcholanthrene	76-96	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	21-27
2747632-3	1989	Transfection of this construct into HepG2 cells generated a 2-3-fold increase in Cyp1A2-directed chloramphenicol acetyltransferase activity when the cells were treated with 3-methylcholanthrene.	Methylcholanthrene	173-193	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	81-87
2747632-7	1989	When this Cyp1A2 responsive element was transfected into human breast carcinoma MCF-7 cells, 3-methylcholanthrene did not stimulate chloramphenicol acetyltransferase activity.	Methylcholanthrene	93-113	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	10-16
2747632-8	1989	In comparison, when a DNA fragment that contained a copy of the human Cyp1A1 xenobiotic-responsive element was analyzed for enhancer activity, 3-methylcholanthrene initiated chloramphenicol acetyltransferase activity in both HepG2 cells and MCF-7 cells.	Methylcholanthrene	143-163	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	70-76
2747632-9	1989	These results suggest that the 3-methylcholanthrene-responsive Cyp1A2 element may be regulated in a tissue-specific manner.	Methylcholanthrene	31-51	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	63-69
2815336-2	1989	PB-treatment leads to localization of P-450b in the centrilobular region, whereas homogeneous distribution of P-450c in the lobule is observed after MC-treatment.	Methylcholanthrene	149-151	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-116
2815336-3	1989	The consecutive treatment with PB and MC is accompanied by the localization of P-450c only in cells of the periportal region of the lobule.	Methylcholanthrene	38-40	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	79-85
2789150-0	1989	Chemoimmunotherapy of MC-induced mouse sarcomas with human recombinant interleukin 2 and cyclophosphamide: age-dependent decline of the therapeutic efficacy.	Methylcholanthrene	22-24	interleukin 2	Homo sapiens	71-84
2543914-0	1989	Detection and characterization of a low affinity form of cytosolic Ah receptor in livers of mice nonresponsive to induction of cytochrome P1-450 by 3-methylcholanthrene.	Methylcholanthrene	148-168	aryl-hydrocarbon receptor	Mus musculus	67-78
2501188-6	1989	(3) The AHH activity of TCDD-microsomes seemed to be more greatly reduced with either 3-MSF-TCB or ANF than that of MC-microsomes.	Methylcholanthrene	116-118	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	8-11
2919889-16	1989	These findings demonstrate that a major portion of the omega-2 hydroxylation of PGs in MC-microsomes is catalyzed by P450c; however, the possibility that some omega-2 hydroxylating activity is due to P450d was not ruled out.	Methylcholanthrene	87-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	117-122
2919889-16	1989	These findings demonstrate that a major portion of the omega-2 hydroxylation of PGs in MC-microsomes is catalyzed by P450c; however, the possibility that some omega-2 hydroxylating activity is due to P450d was not ruled out.	Methylcholanthrene	87-89	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	200-205
2752066-0	1989	[Identification of molecular forms of cytochrome P-450 isolated from liver microsomes of rats induced with phenobarbital and 3-methylcholanthrene].	Methylcholanthrene	125-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
2752066-1	1989	Eight electrophoretically homogeneous forms of cytochrome P-450 were isolated from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced male Wistar rats, using chromatography on 1.8-diaminooctyl-Sepharose, SEAE-Sephacel and hydroxylapatite.	Methylcholanthrene	127-147	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
2752066-1	1989	Eight electrophoretically homogeneous forms of cytochrome P-450 were isolated from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced male Wistar rats, using chromatography on 1.8-diaminooctyl-Sepharose, SEAE-Sephacel and hydroxylapatite.	Methylcholanthrene	149-151	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
2752066-5	1989	Cytochrome P-450c possessing a high 7-ER-O-deethylase activity, and a high spin cytochrome P-450d as well as cytochrome P-450a specifically catalyzing the 7 alpha-oxidation of AD were isolated from MC-microsomes.	Methylcholanthrene	198-200	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-17
2752066-5	1989	Cytochrome P-450c possessing a high 7-ER-O-deethylase activity, and a high spin cytochrome P-450d as well as cytochrome P-450a specifically catalyzing the 7 alpha-oxidation of AD were isolated from MC-microsomes.	Methylcholanthrene	198-200	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	80-97
2752066-5	1989	Cytochrome P-450c possessing a high 7-ER-O-deethylase activity, and a high spin cytochrome P-450d as well as cytochrome P-450a specifically catalyzing the 7 alpha-oxidation of AD were isolated from MC-microsomes.	Methylcholanthrene	198-200	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
2703963-6	1989	Of the cytochrome P-450 inducers, 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin, increased the biliary excretion of AA-GS (2.9- and 3.2-fold, respectively) whereas ethanol and isoniazid did not affect it, and pregnenolone-16 alpha-carbonitrile tended to decrease it (43%).	Methylcholanthrene	34-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	7-23
2646640-0	1989	Tumorigenic methylcholanthrene transformants of C3H/10T1/2 cells have a common nucleotide alteration in the c-Ki-ras gene.	Methylcholanthrene	12-30	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	108-116
2917017-5	1989	In phenobarbital- and 3-methylcholanthrene-induced microsomes, 73% and 64%, respectively, of cytochrome P-450 are converted to P-420 in presence of 200 microM ebselen.	Methylcholanthrene	22-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
2930512-10	1989	Treatment of rats with methylcholanthrene, hexachlorobenzene and o-aminoazotoluene increased uroporphyrinogen oxidation and P-450d, whereas phenobarbital did not increase either.	Methylcholanthrene	23-41	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	124-130
2930512-11	1989	The contribution of hepatic P-450c and P-450d to uroporphyrinogen oxidation and ethoxyresorufin O-de-ethylation in methylcholanthrene-induced microsomes was assessed by using specific antibodies to P-450c and P-450d.	Methylcholanthrene	115-133	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	28-34
2930512-12	1989	Uroporphyrinogen oxidation by methylcholanthrene-induced rat liver microsomes was inhibited up to 75% by specific antibodies to P-450d, but not by specific antibodies to P-450c.	Methylcholanthrene	30-48	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	128-134
2930512-14	1989	Methylcholanthrene-induced kidney microsomes which contain P-450c but non P-450d did not oxidize uroporphyrinogen.	Methylcholanthrene	0-18	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	59-65
2930512-14	1989	Methylcholanthrene-induced kidney microsomes which contain P-450c but non P-450d did not oxidize uroporphyrinogen.	Methylcholanthrene	0-18	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	74-80
2536534-1	1989	Antibody-inhibition experiments established that the induction of cytochrome P450c is largely responsible for the marked increase in liver microsomal 7-ethoxyresorufin O-dealkylation in rats treated with 3-methylcholanthrene, whereas the induction of cytochrome P450b and/or P450e is largely responsible for the marked increase in 7-pentoxy- and 7-benzyloxyresorufin O-dealkylation in rats treated with phenobarbital.	Methylcholanthrene	204-224	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	66-82
2536534-1	1989	Antibody-inhibition experiments established that the induction of cytochrome P450c is largely responsible for the marked increase in liver microsomal 7-ethoxyresorufin O-dealkylation in rats treated with 3-methylcholanthrene, whereas the induction of cytochrome P450b and/or P450e is largely responsible for the marked increase in 7-pentoxy- and 7-benzyloxyresorufin O-dealkylation in rats treated with phenobarbital.	Methylcholanthrene	204-224	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	251-267
2920375-2	1989	TCDD and 3-MC, which are comparatively poor inducers of GSTs in rats, were most effective in enhancing GST activities in hamster liver.	Methylcholanthrene	9-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	56-59
2498299-5	1989	Immunochemical analysis of P-450/B[a]P indicated that P-450/B[a]P is immunologically distinct from P-450b (a major phenobarbital-inducible form of P-450) and P-450c (a major 3-methylcholanthrene-inducible form of P-450, which highly catalyzes the hydroxylation of B[a]P).	Methylcholanthrene	174-194	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	54-61
2498302-1	1989	Two forms of cytochrome P-450 (P-450MC1 and P-450MC2) were purified from liver microsomes of crab-eating monkeys (Macaca irus) treated with 3-methylcholanthrene (MC).	Methylcholanthrene	140-160	cytochrome P450 family 1 subfamily A member 1	Macaca fascicularis	13-29
2498302-1	1989	Two forms of cytochrome P-450 (P-450MC1 and P-450MC2) were purified from liver microsomes of crab-eating monkeys (Macaca irus) treated with 3-methylcholanthrene (MC).	Methylcholanthrene	36-38	cytochrome P450 family 1 subfamily A member 1	Macaca fascicularis	13-29
2498302-7	1989	Monkey P-450MC1 and P-450MC2 were detected by immunoblotting using an antibody prepared against rat cytochrome P-450c, which is a major form of cytochrome P-450 in liver microsomes of MC-treated rats.	Methylcholanthrene	12-14	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	100-117
2498302-7	1989	Monkey P-450MC1 and P-450MC2 were detected by immunoblotting using an antibody prepared against rat cytochrome P-450c, which is a major form of cytochrome P-450 in liver microsomes of MC-treated rats.	Methylcholanthrene	12-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
2498302-8	1989	These results suggested that the molecular properties of cytochrome P-450 in liver microsomes of crab-eating monkeys treated with MC are similar to those in rats.	Methylcholanthrene	130-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
2542235-3	1989	Experiments with various microsomal preparations induced by phenobarbital (PB), polychlorinated biphenyls (PCB), or 3-methylcholanthrene (3-MC) revealed that the reduction rate was correlated to the concentration of cytochrome P-450 but not to that of NADPH reductase.	Methylcholanthrene	116-136	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
2783733-8	1989	An overrepresentation of the uncommon variant phenotypes of alpha 1-antitrypsin was found in first-degree relatives of affected patients (four had the MZ phenotype, and one each the MS or MC phenotype, of 19 relatives studied).	Methylcholanthrene	188-190	serpin family A member 1	Homo sapiens	60-79
2498247-2	1989	The results of enzyme-linked immunosorbent assay using monoclonal antibodies against rat P-450 isozymes revealed that the amount of cytochrome P-450d induced by 3-MeO-AAB or MC declined rapidly during culture and fell to 10 to 15% of the initial value after 24 h. A similar tendency was observed with PB-induced cytochrome P-450b/e.	Methylcholanthrene	174-176	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	132-149
2498247-2	1989	The results of enzyme-linked immunosorbent assay using monoclonal antibodies against rat P-450 isozymes revealed that the amount of cytochrome P-450d induced by 3-MeO-AAB or MC declined rapidly during culture and fell to 10 to 15% of the initial value after 24 h. A similar tendency was observed with PB-induced cytochrome P-450b/e.	Methylcholanthrene	174-176	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	323-329
2498247-3	1989	By contrast, cytochrome P-450c in MC-induced hepatocytes declined more slowly than cytochrome P-450d and remained at 45 to 60% of the initial value after 24 h. Similar quantitative changes of the individual cytochrome P-450 isozymes in culture were also observed by immunoblotting using the anti-cytochrome P-450 monoclonal antibodies.	Methylcholanthrene	34-36	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-30
2498247-3	1989	By contrast, cytochrome P-450c in MC-induced hepatocytes declined more slowly than cytochrome P-450d and remained at 45 to 60% of the initial value after 24 h. Similar quantitative changes of the individual cytochrome P-450 isozymes in culture were also observed by immunoblotting using the anti-cytochrome P-450 monoclonal antibodies.	Methylcholanthrene	34-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2783379-1	1989	The growth of 3-methylcholanthrene-induced fibrosarcomas, Meth 1 and Meth A, was strongly suppressed by a combination of recombinant human interleukin 2 (rIL-2) with proteose-peptone (PP) administered i.p.	Methylcholanthrene	14-34	ADAM metallopeptidase with thrombospondin type 1 motif 1	Homo sapiens	58-64
2783379-1	1989	The growth of 3-methylcholanthrene-induced fibrosarcomas, Meth 1 and Meth A, was strongly suppressed by a combination of recombinant human interleukin 2 (rIL-2) with proteose-peptone (PP) administered i.p.	Methylcholanthrene	14-34	interleukin 2	Homo sapiens	139-152
2783379-1	1989	The growth of 3-methylcholanthrene-induced fibrosarcomas, Meth 1 and Meth A, was strongly suppressed by a combination of recombinant human interleukin 2 (rIL-2) with proteose-peptone (PP) administered i.p.	Methylcholanthrene	14-34	interleukin 2	Rattus norvegicus	154-159
2505482-1	1989	Methylcholanthrene-induced murine rhabdomyosarcomas and skeletal muscle of 10 and 18 d old murine embryos were investigated by lectin histochemistry (WGA, RCA-I, LCA, Con-A, PSA, UEA-I, PNA) and by immunohistochemistry (vimentin, desmin, myoglobulin).	Methylcholanthrene	0-18	vimentin	Mus musculus	220-228
2505482-1	1989	Methylcholanthrene-induced murine rhabdomyosarcomas and skeletal muscle of 10 and 18 d old murine embryos were investigated by lectin histochemistry (WGA, RCA-I, LCA, Con-A, PSA, UEA-I, PNA) and by immunohistochemistry (vimentin, desmin, myoglobulin).	Methylcholanthrene	0-18	desmin	Mus musculus	230-236
2572101-6	1989	During therapy with MC 903 a decline in the staining intensity for IL-6, but not for TNF alpha, was observed in both lesional and unaffected skin.	Methylcholanthrene	20-22	interleukin 6	Homo sapiens	67-71
2665407-9	1989	The level of serum proinsulin-binding IgG decreased in the MC group only (from 9.3 +/- 2.2 to 1.9 +/- 0.6 ng/ml after 12 months), and even showed a slight increase in the Conv.	Methylcholanthrene	59-61	insulin	Homo sapiens	19-29
2742497-6	1989	3-Methylcholanthrene treatment resulted in a significant increase of cytochrome P-450 content and 7-ethoxyresorufin O-deethylase activity in all five fractions: both parameters were slightly higher in fractions 4 and 5 than in fractions 1 and 2.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	69-85
2764709-2	1989	3-Methylcholanthrene (MC) was given as a model inducer of ALDH (100 mg/kg, i.p., as a single dose) and the animals were killed after 3 days.	Methylcholanthrene	0-20	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	58-62
2764709-2	1989	3-Methylcholanthrene (MC) was given as a model inducer of ALDH (100 mg/kg, i.p., as a single dose) and the animals were killed after 3 days.	Methylcholanthrene	22-24	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	58-62
2764709-11	1989	Our findings show that substances affecting microsomal drug metabolism can interfere with the process of ALDH induction by MC.	Methylcholanthrene	123-125	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	105-109
2499361-1	1989	Cytochrome P-450 forms appearing in the liver after injection of methylcholanthrene, polychlorinated biphenyls and perfluorochemical emulsion to rats were studied.	Methylcholanthrene	65-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
2541801-3	1989	It was shown that RIII and RIV bind as type I substrates to cytochrome P-450 from rat microsomes induced with phenobarbital or 3-methylcholanthrene as well as to those from control rats.	Methylcholanthrene	127-147	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Methylcholanthrene	130-132	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	46-52
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Methylcholanthrene	130-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-63
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Methylcholanthrene	130-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	34-54	C-C motif chemokine ligand 4	Rattus norvegicus	100-104
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	34-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	192-208
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	34-54	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	210-216
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	34-54	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	221-227
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	56-58	C-C motif chemokine ligand 4	Rattus norvegicus	100-104
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	56-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	192-208
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	56-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	210-216
2773513-2	1989	The effects of acute treatment of 3-methylcholanthrene (MC)-induced rats with carbon tetrachloride (CCl4) on the content and activity of the polycyclic aromatic hydrocarbon-inducible forms of cytochrome P-450 (P-450c and P-450d) in liver and kidney have been determined.	Methylcholanthrene	56-58	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	221-227
2773513-4	1989	Post-treatment of MC-induced rats with CCl4 in vivo decreased the specific content of total, spectrally determined, P-450 in both hepatic and renal microsomes, by 60% and 40%, respectively.	Methylcholanthrene	18-20	C-C motif chemokine ligand 4	Rattus norvegicus	39-43
2773513-4	1989	Post-treatment of MC-induced rats with CCl4 in vivo decreased the specific content of total, spectrally determined, P-450 in both hepatic and renal microsomes, by 60% and 40%, respectively.	Methylcholanthrene	18-20	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	116-121
2773513-9	1989	Hepatic phenacetin O-deethylase, an activity catalysed specifically by P-450d in this tissue, was dramatically decreased following administration of CCl4 to MC-induced rats.	Methylcholanthrene	157-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	71-77
2773513-9	1989	Hepatic phenacetin O-deethylase, an activity catalysed specifically by P-450d in this tissue, was dramatically decreased following administration of CCl4 to MC-induced rats.	Methylcholanthrene	157-159	C-C motif chemokine ligand 4	Rattus norvegicus	149-153
2773513-13	1989	Treatment of MC-induced rats with CCl4 causes a selective loss of hepatic P-450d and associated monooxygenase activities.	Methylcholanthrene	13-15	C-C motif chemokine ligand 4	Rattus norvegicus	34-38
2773513-13	1989	Treatment of MC-induced rats with CCl4 causes a selective loss of hepatic P-450d and associated monooxygenase activities.	Methylcholanthrene	13-15	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	74-80
2732953-0	1989	Epidermal cytochrome P-450: immunochemical characterization of isoform induced by topical application of 3-methylcholanthrene to neonatal rat.	Methylcholanthrene	105-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	10-26
2732953-3	1989	After a single topical application of 3-MC to rats aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin-O-deethylase and 7-ethoxyresorufin-O-deethylase activities in epidermal microsomes were induced significantly.	Methylcholanthrene	38-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	51-79
2732953-3	1989	After a single topical application of 3-MC to rats aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin-O-deethylase and 7-ethoxyresorufin-O-deethylase activities in epidermal microsomes were induced significantly.	Methylcholanthrene	38-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-84
2468428-2	1989	In order to delineate further the biochemical and molecular processes underlying the observed biological effects, the inductive effect of MC and beta-naphthoflavone (beta NF) on cytochrome P-450 was determined at the biochemical and molecular levels.	Methylcholanthrene	138-140	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	178-194
2468428-6	1989	MC caused maximal induction of aryl hydrocarbon hydroxylase (AHH) activity by 8 h in both the liver and lung.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	31-59
2468428-6	1989	MC caused maximal induction of aryl hydrocarbon hydroxylase (AHH) activity by 8 h in both the liver and lung.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	61-64
2468428-9	1989	Addition of monoclonal antibody 1-7-1, specific for the MC-inducible forms of cytochrome P-450 (P-450IA1 and A2), to the incubation mixtures resulted in a 55-70% inhibition of AHH activity in both lung and liver assays, regardless of the inducing agent used, while having no effect on AHH activity from oil-treated mice.	Methylcholanthrene	56-58	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	78-94
2468428-9	1989	Addition of monoclonal antibody 1-7-1, specific for the MC-inducible forms of cytochrome P-450 (P-450IA1 and A2), to the incubation mixtures resulted in a 55-70% inhibition of AHH activity in both lung and liver assays, regardless of the inducing agent used, while having no effect on AHH activity from oil-treated mice.	Methylcholanthrene	56-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	176-179
2468428-9	1989	Addition of monoclonal antibody 1-7-1, specific for the MC-inducible forms of cytochrome P-450 (P-450IA1 and A2), to the incubation mixtures resulted in a 55-70% inhibition of AHH activity in both lung and liver assays, regardless of the inducing agent used, while having no effect on AHH activity from oil-treated mice.	Methylcholanthrene	56-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	285-288
2787328-2	1989	EGF was iodinated using one of three oxidative reagents: chloramine T (CT), lactoperoxidase (LP), or monochloride (MC).	Methylcholanthrene	115-117	epidermal growth factor like 1	Rattus norvegicus	0-3
2631798-0	1989	H-2 antigens and tumour-associated transplantation antigens in clones derived from a methylcholanthrene-induced BALB/c tumour: their influence on the generation in vitro and in vivo of the specific anti-tumour immune response.	Methylcholanthrene	85-103	histocompatibility-2, MHC	Mus musculus	0-3
2789150-2	1989	Repeated peritumoral injections of rIL-2 substantially inhibited growth of transplantable MC-induced sarcomas in syngeneic young adult mice whereas no effect was observed in the aged mice.	Methylcholanthrene	90-92	interleukin 2	Rattus norvegicus	35-40
2789150-3	1989	Chemoimmunotherapy of the MC-induced sarcomas in the young adult and in the aged mice treated with cyclophosphamide plus rIL-2 revealed that subthreshold doses of CY were capable of significantly potentiating the immunotherapeutic effect of rIL-2 in young adult mice but not in the aged mice.	Methylcholanthrene	26-28	interleukin 2	Rattus norvegicus	121-126
2502445-7	1989	Pretreatment with phenobarbitone and 3-methylcholanthrene stimulated both the glutathione S-transferase and organic nitrate reductase activities.	Methylcholanthrene	37-57	glutathione S-transferase kappa 1	Homo sapiens	78-103
2539339-5	1989	MC administered at 40 mg/kg impaired the ability of C3 and B10.Q mice to eliminate adult worms.	Methylcholanthrene	0-2	complement component 3	Mus musculus	52-54
2502444-12	1989	The content of P-450 and the activity of NADPH-cytochrome P-450 reductase were high in PB-, MC- and BNF-microsomes, whereas NADH-cytochrome b5 reductase activity was high in two flavonoid-microsomes and the content of cytochrome b5 was not changed except the PB-treated rats.	Methylcholanthrene	92-94	cytochrome p450 oxidoreductase	Rattus norvegicus	41-73
2807635-0	1989	Effect of endotoxin to differentially affect cytochrome P-450 monooxygenase activities of untreated rats and animals induced with phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	147-167	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	45-75
2807635-1	1989	The effect of endotoxin in decreasing the cytochrome P-450-dependent metabolism of aniline, aminopyrine and ethoxycoumarin was examined in untreated rats, and in rats pretreated with either phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	207-227	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
2539339-8	1989	Muscle larvae burdens of MC-treated B10 and C3 mice were elevated, while those of AK strain mice were unaffected.	Methylcholanthrene	25-27	complement component 3	Mus musculus	44-46
3264498-0	1988	Appearance of hybridoma growth factor/interleukin-6 in the serum of mice bearing a methylcholanthrene-induced sarcoma.	Methylcholanthrene	83-101	interleukin 6	Mus musculus	38-51
2508589-2	1989	First, we established a tumor specific CTL clone (E-4) against 203-glioma cells (a 20-methylcholanthrene induced mouse ependymoblastoma line of C57BL/6 mouse origin), and then transferred murine IFN-gamma cDNA into E-4 by using retroviral vector (pSVX(Mu gamma delta A].	Methylcholanthrene	83-104	skull morphology 6	Mus musculus	50-53
2755909-0	1989	Tissue distribution of inducible aldehyde dehydrogenase activity in the rat after treatment with phenobarbital or methylcholanthrene.	Methylcholanthrene	114-132	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	33-55
2755909-3	1989	Both substrains, however, respond to treatment with methylcholanthrene (MC), exhibiting a uniform increase of the ALDH activity in the liver.	Methylcholanthrene	52-70	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	114-118
2755909-3	1989	Both substrains, however, respond to treatment with methylcholanthrene (MC), exhibiting a uniform increase of the ALDH activity in the liver.	Methylcholanthrene	72-74	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	114-118
2755909-10	1989	The effect of MC on various tissues was less distinct, when ALDH was measured as P/NAD or Ph/NAD activity.	Methylcholanthrene	14-16	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	60-64
2755909-11	1989	It is concluded, that PB and MC not only induce different types of ALDH activity, but they also reveal differences in the tissue distribution of the inducibility of ALDH.	Methylcholanthrene	29-31	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	67-71
2755909-11	1989	It is concluded, that PB and MC not only induce different types of ALDH activity, but they also reveal differences in the tissue distribution of the inducibility of ALDH.	Methylcholanthrene	29-31	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	165-169
20702290-2	1989	The b and e forms of cytochrome P-450 were found to be non-inducible by either in vitro co-incubation for 5 days or by transplacental maternal induction with phenobarbitone (PB), 3-methylcholanthrene (3MC) or beta-naphthoflavone (betaNF) in either cell type.	Methylcholanthrene	179-199	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
20702290-2	1989	The b and e forms of cytochrome P-450 were found to be non-inducible by either in vitro co-incubation for 5 days or by transplacental maternal induction with phenobarbitone (PB), 3-methylcholanthrene (3MC) or beta-naphthoflavone (betaNF) in either cell type.	Methylcholanthrene	201-204	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
20702290-8	1989	The b and e forms of cytochrome P-450 were non-inducible but it is highly likely that the c form was both inducible (by 3MC and betaNF) and functional, the latter being assessed by modulation of DPH toxicity and CPA activation.	Methylcholanthrene	120-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
3145631-5	1988	When the para" substituent was a halogen (F, Cl, Br or I), the derivative induced both cytochromes P-450b and P-450e, and cytochromes P-450c and P-450d, which are the major phenobarbital- and 3-methylcholanthrene-inducible isozymes, respectively.	Methylcholanthrene	192-212	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	99-105
3145631-5	1988	When the para" substituent was a halogen (F, Cl, Br or I), the derivative induced both cytochromes P-450b and P-450e, and cytochromes P-450c and P-450d, which are the major phenobarbital- and 3-methylcholanthrene-inducible isozymes, respectively.	Methylcholanthrene	192-212	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	134-151
3264498-1	1988	Serum concentrations of hybridoma growth factor/interleukin-6 progressively increased in mice bearing a transplantable methylcholanthrene-induced sarcoma with tumor growth.	Methylcholanthrene	119-137	interleukin 6	Mus musculus	48-61
2461286-7	1988	Amplitude and latency of the CMAP were both altered, but not identically, by changing the intensity of MC and cathodal stimuli.	Methylcholanthrene	103-105	cystatin F	Homo sapiens	29-33
3264502-1	1988	Monoclonal antibodies (MAbs) raised to rat liver cytochrome P-450s induced by phenobarbital, 3-methylcholanthrene, and pregnenolone-16 alpha-carbonitrile were used to detect these epitope specific P-450s in human abortion fetuses 14-24 weeks of age.	Methylcholanthrene	93-113	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
2462160-3	1988	Treatment with either 3-methylcholanthrene or beta-naphthoflavone produced striking increases of 3-methylcholanthrene-specific cytochromes P-450 in hepatocytes from all regions of the hepatic lobule in CD-1 and C57BL/6 mice, but not in DBA/2 mice.	Methylcholanthrene	22-42	CD1 antigen complex	Mus musculus	202-206
2462160-3	1988	Treatment with either 3-methylcholanthrene or beta-naphthoflavone produced striking increases of 3-methylcholanthrene-specific cytochromes P-450 in hepatocytes from all regions of the hepatic lobule in CD-1 and C57BL/6 mice, but not in DBA/2 mice.	Methylcholanthrene	97-117	CD1 antigen complex	Mus musculus	202-206
2849781-2	1988	We have studied the activity of SOD up to 24 h after intratumoral administration of 50, 100, 150, and 300 mg/kg DDC in 3-methylcholanthrene-induced tumors in BALB/c mice.	Methylcholanthrene	119-139	superoxide dismutase 1	Homo sapiens	32-35
3264607-8	1988	Although the decreased production of TNF by neonatal MC was statistically significant, these cells did produce substantial amounts of this cytokine.	Methylcholanthrene	53-55	tumor necrosis factor	Homo sapiens	37-40
3049217-4	1988	Dot blot analysis using a panel of 10 electrophoretically homogeneous rat liver cytochrome P-450 forms under nondenaturing conditions established that the two methylcholanthrene-inducible forms, P-450 BNF-B and P-450 ISF-G (P-450 gene subfamily IA), are selectively recognized by the anti-liver/kidney microsome1 antibodies.	Methylcholanthrene	159-177	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
2846197-5	1988	Pretreatment of fetuses with phenobarbital potentiated the inducing effect of MC upon P-450c and P-450d mRNA accumulation in relation to the duration of pretreatment, as well as increasing the hepatic content in TCDD-binding protein.	Methylcholanthrene	78-80	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	86-103
2846197-6	1988	Data strongly suggest that the hepatic TCDD-binding protein level is the rate-limiting step in MC induction of P-450c and P-450d in fetal but not in adult rat liver.	Methylcholanthrene	95-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	111-128
3225481-8	1988	These results suggest that EGF-R may play an important role in the early stage of carcinogenesis of the mouse uterine cervix induced by 20-MC.	Methylcholanthrene	136-141	epidermal growth factor receptor	Mus musculus	27-32
3181265-5	1988	For binding to cytochrome P-450 in 3-MC-induced microsomes conclusions (a) and (d) appeared to hold true.	Methylcholanthrene	35-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-31
3131144-8	1988	In this regard it was interesting that 3-methylcholanthrene was an effective inducer of a wide variety of acute-phase proteins including metallothionein, serum amyloid A, fibrinogen and hemopexin.	Methylcholanthrene	39-59	hemopexin	Mus musculus	186-195
3403555-2	1988	Primary cultures of adult rat hepatocytes grown in serum-free hormonally defined medium were shown, for the first time, to be capable of supporting the 3-methylcholanthrene-inducible expression of cytochrome P-450d.	Methylcholanthrene	152-172	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	197-214
3403555-4	1988	After 1 day of growth in culture, P-450c and P-450d mRNAs were induced 33- and 28-fold, respectively, by 3-methylcholanthrene treatment.	Methylcholanthrene	105-125	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	34-51
3403555-11	1988	Thus, the 3-methylcholanthrene induction of P-450c and P-450d mRNAs in the hepatocyte cultures appeared to be mediated primarily at the post-transcriptional level.	Methylcholanthrene	10-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	44-61
3415241-11	1988	The 3-methylcholanthrene-inducible forms P-450 MC-1 (P-450d) and MC-5 (P-450c) had aminopyrine N-demethylation activity but no hydroxylation activity.	Methylcholanthrene	4-24	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	53-60
3415241-11	1988	The 3-methylcholanthrene-inducible forms P-450 MC-1 (P-450d) and MC-5 (P-450c) had aminopyrine N-demethylation activity but no hydroxylation activity.	Methylcholanthrene	4-24	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	71-77
3402044-3	1988	The dose-response curves for the induction of hepatic microsomal AHH by 3-methylcholanthrene (MC) were indistinguishable in both +4S and -4S rats and comparable results were observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as an inducer.	Methylcholanthrene	72-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	65-68
3402044-3	1988	The dose-response curves for the induction of hepatic microsomal AHH by 3-methylcholanthrene (MC) were indistinguishable in both +4S and -4S rats and comparable results were observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as an inducer.	Methylcholanthrene	94-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	65-68
3402044-8	1988	These results show that there was a correlation between the Ah receptor binding affinities of MC, B[a]P and perylene and their potencies as AHH inducers in Sprague-Dawley rats, and this corresponds to previous correlations for the induction of AHH in rat hepatoma H-4-II E cells in culture.	Methylcholanthrene	94-96	aryl hydrocarbon receptor	Rattus norvegicus	60-71
3402044-8	1988	These results show that there was a correlation between the Ah receptor binding affinities of MC, B[a]P and perylene and their potencies as AHH inducers in Sprague-Dawley rats, and this corresponds to previous correlations for the induction of AHH in rat hepatoma H-4-II E cells in culture.	Methylcholanthrene	94-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	140-143
3402044-8	1988	These results show that there was a correlation between the Ah receptor binding affinities of MC, B[a]P and perylene and their potencies as AHH inducers in Sprague-Dawley rats, and this corresponds to previous correlations for the induction of AHH in rat hepatoma H-4-II E cells in culture.	Methylcholanthrene	94-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	244-247
3402050-0	1988	Activated c-K-ras and c-N-ras oncogenes in 3-methylcholanthrene-induced BALB/c fibrosarcomas.	Methylcholanthrene	43-63	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	10-17
2968871-5	1988	Based on reports that interleukin 2 receptor (IL2R) expression correlates well with proliferative responses in HIV infection, we used dual-color cytofluorometry to measure IL2R expression by CD4 and CD8 cells following PHA activation of MC from HIV-seropositive blood donors.	Methylcholanthrene	237-239	interleukin 2 receptor subunit alpha	Homo sapiens	172-176
2968871-7	1988	When compared to the seronegative control and sero + NML groups, the sero + LOW group exhibited significant reductions in the percentage of MC expressing IL2R, the proportion of CD4 cells expressing IL2R, and the proportion of CD8 cells expressing IL2R.	Methylcholanthrene	140-142	interleukin 2 receptor subunit alpha	Homo sapiens	154-158
2968871-9	1988	These findings show that reduced PHA-induced proliferative responses by MC from HIV-infected persons are associated with decreased IL2R expression by both CD4 and CD8 lymphocyte subsets.	Methylcholanthrene	72-74	interleukin 2 receptor subunit alpha	Homo sapiens	131-135
2968871-9	1988	These findings show that reduced PHA-induced proliferative responses by MC from HIV-infected persons are associated with decreased IL2R expression by both CD4 and CD8 lymphocyte subsets.	Methylcholanthrene	72-74	CD4 molecule	Homo sapiens	155-158
2968871-9	1988	These findings show that reduced PHA-induced proliferative responses by MC from HIV-infected persons are associated with decreased IL2R expression by both CD4 and CD8 lymphocyte subsets.	Methylcholanthrene	72-74	CD8a molecule	Homo sapiens	163-166
22148771-1	1988	Analytical computation of the MC-SCF Hessians for transition states of ethylene with ethylene, singlet oxygen, and ketene.	Methylcholanthrene	30-32	KIT ligand	Homo sapiens	33-36
3404457-7	1988	Purified and reconstituted cytochrome P-450c from 3-methylcholanthrene or ABZ-treated rat liver were able to produce SO2-ABZ (2.01 and 1.70 nmol/mg/15 min, respectively, whereas cytochrome P-450b produced 10 times less SO2-ABZ).	Methylcholanthrene	50-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	27-44
3404457-7	1988	Purified and reconstituted cytochrome P-450c from 3-methylcholanthrene or ABZ-treated rat liver were able to produce SO2-ABZ (2.01 and 1.70 nmol/mg/15 min, respectively, whereas cytochrome P-450b produced 10 times less SO2-ABZ).	Methylcholanthrene	50-70	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	178-195
3404457-8	1988	Immunological assays, as well as activity measurements showed a relationship between cytochrome P-450c-3-methylcholanthrene and cytochrome P-450c-ABZ.	Methylcholanthrene	103-123	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	85-102
3404457-8	1988	Immunological assays, as well as activity measurements showed a relationship between cytochrome P-450c-3-methylcholanthrene and cytochrome P-450c-ABZ.	Methylcholanthrene	103-123	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	128-145
3141331-6	1988	The cytotoxic activity of regional lymph node lymphocytes from rIL2-treated mice was demonstrated against primary culture of M-MSV-induced sarcoma but not against syngeneic tumor induced by methylcholanthrene (Meth A).	Methylcholanthrene	210-216	interleukin 2	Rattus norvegicus	63-67
2842891-3	1988	MC administration resulted in a dose-dependent suppression of ear swelling and a concomitant dose-dependent induction of hepatic AHH activity.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	129-132
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Methylcholanthrene	35-55	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Methylcholanthrene	35-55	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	160-170
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Methylcholanthrene	57-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Methylcholanthrene	183-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
3220829-2	1988	Whereas P-450(PB-1) and P-450(MC-1) in liver microsomes were markedly induced in both sexes by treatment with PB and MC, respectively, the contents of P-450(M-1) and P-450(F-1) were significantly decreased by the treatments.	Methylcholanthrene	117-119	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	8-18
2455834-3	1988	C56BL/6 mice bearing established pulmonary metastases induced by the iv injection of the methylcholanthrene-induced fibrosarcoma MCA 106 were treated for 12 days with intraperitoneal injections of (1) Hanks" balanced salt solution, (2) recombinant IL-2, (3) rHuIFN-alpha-A/D, and (4) a combination of IL-2 and HuIFN-alpha-A/D.	Methylcholanthrene	89-107	complement component 6	Mus musculus	0-7
3261011-6	1988	Only the monoclonal antibody against the 3-methylcholanthrene induced cytochrome P-450 inhibited the O-deethylation of 7-ethoxyresorufin to 64 to 79 percent of control values.	Methylcholanthrene	41-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3261011-8	1988	Thus, the 7-ethoxyresorufin O-deethylase is partly catalyzed in human adult liver by a cytochrome with an epitope that is recognized by the monoclonal antibody against 3-methylcholanthrene induced rat liver cytochrome P-450.	Methylcholanthrene	168-188	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	207-223
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	108-128	purine nucleoside phosphorylase	Rattus norvegicus	19-23
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	108-128	calsyntenin 2	Rattus norvegicus	38-41
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	130-134	purine nucleoside phosphorylase	Rattus norvegicus	19-23
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	130-134	calsyntenin 2	Rattus norvegicus	38-41
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	189-193	purine nucleoside phosphorylase	Rattus norvegicus	19-23
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Methylcholanthrene	189-193	calsyntenin 2	Rattus norvegicus	38-41
2455523-2	1988	Sudan III [1-[[4-(phenylazo)phenyl]azo]-2-naphthalenol] and 3-methylcholanthrene (MCA), but not butylated hydroxyanisole (BHA), induced DT-diaphorase in a concentration-dependent manner.	Methylcholanthrene	60-80	NAD(P)H dehydrogenase, quinone 1	Mus musculus	136-149
3390203-0	1988	Loss of 3-methylcholanthrene-inducible form of cytochrome P-450 in liver microsomes following administration of carbon disulfide in C57BL/6 Cr mice.	Methylcholanthrene	8-28	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	47-63
3390203-2	1988	These results indicate that the 3-MC-inducible form of cytochrome P-450 was more susceptible to CS2 than the PB-inducible form.	Methylcholanthrene	32-36	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	55-71
3390203-2	1988	These results indicate that the 3-MC-inducible form of cytochrome P-450 was more susceptible to CS2 than the PB-inducible form.	Methylcholanthrene	32-36	calsyntenin 2	Mus musculus	96-99
3179354-0	1988	[Relation between the 7-ethoxyresorufin-O-deethylase activity of the liver microsomal monooxygenase system and the level of methylcholanthrene-induced form of cytochrome P-450].	Methylcholanthrene	124-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	159-175
3179354-1	1988	Changes in the metabolic activity of 7-ethoxyresorufin in rat liver microsomes containing different amounts of cytochrome P-450 induced by 3-methylcholanthrene and other polycyclic hydrocarbons (P-450c) were studied.	Methylcholanthrene	139-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
3130800-1	1988	The expression and activity of the phenobarbital (PB)-inducible P-450 isozymes, P-450b and P-450e, and the major 3-methylcholanthrene (MC)-inducible form, P-450c, were studied in primary cultures of adult rat hepatocytes in T1, Leibovitz L-15 (L-15), and a modification of Waymouth 752/1 (Way) media.	Methylcholanthrene	135-137	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	155-161
3258789-2	1988	After initiation of BALB/c 3T3 cells with 3-methylchol-anthrene, treatment with TGF beta at 1 ng/ml alone or in combination with epidermal growth factor (EGF) for 4 weeks enhanced the number of transformed foci by 5- to 6-fold in comparison with uninitiated cells.	Methylcholanthrene	42-63	transforming growth factor, beta 1	Mus musculus	80-88
3372997-1	1988	The experiments presented were designed first to determine the effects of rTNF on the methylcholanthrene-induced fibrosarcoma (FSA-1) in C3H/JSed mice and second to determine whether the observed effects are the result of direct action by rTNF on the tumor or whether rTNF acts as a mediator of other effector mechanisms.	Methylcholanthrene	86-104	tumor necrosis factor	Rattus norvegicus	74-78
3372997-1	1988	The experiments presented were designed first to determine the effects of rTNF on the methylcholanthrene-induced fibrosarcoma (FSA-1) in C3H/JSed mice and second to determine whether the observed effects are the result of direct action by rTNF on the tumor or whether rTNF acts as a mediator of other effector mechanisms.	Methylcholanthrene	86-104	sperm associated antigen 7	Mus musculus	127-132
3143703-0	1988	Effects of a combination of cyclophosphamide and human recombinant interleukin 2 on pulmonary metastasis after the surgical removal of a 3-methylcholanthrene-induced primary tumor in autochthonous mice.	Methylcholanthrene	137-157	interleukin 2	Homo sapiens	67-80
3259880-2	1988	This study was undertaken into liver microsomal fractions prepared from untreated rabbits or animals treated with drugs known to specifically induce various cytochrome P-450 isozymes such as form LM2 by phenobarbital, LM4 and LM6 by 3-methylcholanthrene and beta-naphthoflavone, LM3a by ethyl alcohol and acetone, and LM3c by macrolide antibiotics (rifampicin, erythromycin and triacetyloleandomycin).	Methylcholanthrene	233-253	cytochrome P-450	Oryctolagus cuniculus	157-173
3260135-0	1988	Localization of cytochrome P-450 in the colonic mucosa of 3-methylcholanthrene-pretreated and untreated rats.	Methylcholanthrene	58-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
3260135-2	1988	Immunohistochemical localization of cytochrome P-450 in the colonic mucosa of 3-methylcholanthrene-pretreated and untreated rats was studied by indirect fluorescent antibody staining technique.	Methylcholanthrene	78-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	36-52
2834735-1	1988	The first constant region of the Tcrb gene was completely deleted from the DNA of 8/10 mouse cell lines established from 3-methylcholanthrene-induced RF/J thymic lymphomas, but 6/7 primary lymphomas contained the first constant region sequences.	Methylcholanthrene	121-141	T cell receptor beta chain	Mus musculus	33-37
3413034-2	1988	A panel of nine inhibitors displaying some P-450 isozyme specificity was used to characterize aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (ERDE) activities in human liver and placenta in vitro in comparison with liver enzymes from control, phenobarbital (PB) and 3-methylcholanthrene (MC) treated rats.	Methylcholanthrene	289-309	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-127
3050970-7	1988	These results demonstrate that maternal cigarette smoking induces in the trophoblastic layer of the placenta a cytochrome P-450 form which is detectable immunohistochemically with the monoclonal antibody to 3-methylcholanthrene-inducible P-450 in rat liver.	Methylcholanthrene	207-227	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
3413034-2	1988	A panel of nine inhibitors displaying some P-450 isozyme specificity was used to characterize aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (ERDE) activities in human liver and placenta in vitro in comparison with liver enzymes from control, phenobarbital (PB) and 3-methylcholanthrene (MC) treated rats.	Methylcholanthrene	311-313	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-127
3050970-7	1988	These results demonstrate that maternal cigarette smoking induces in the trophoblastic layer of the placenta a cytochrome P-450 form which is detectable immunohistochemically with the monoclonal antibody to 3-methylcholanthrene-inducible P-450 in rat liver.	Methylcholanthrene	207-227	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	122-127
3349488-1	1988	Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter.	Methylcholanthrene	83-101	tumor necrosis factor	Mus musculus	166-187
3135673-2	1988	Five isozymes of cytochrome P-450 were purified from liver microsomes of phenobarbital-pretreated (P-450-SD-I and -II), 3-methylcholanthrene-pretreated (P-450-SD-III) and untreated rats (P-450-SD-IV and -V) to determine their catalytic activities in metabolic reactions of methamphetamine.	Methylcholanthrene	120-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3349488-1	1988	Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter.	Methylcholanthrene	83-101	tumor necrosis factor	Mus musculus	189-192
3349488-1	1988	Stereoscopic observation via an implanted sight glass in mice bearing transplanted methylcholanthrene-induced A-cells showed tumorivascular hemorrhage at 1-2 h after tumor necrosis factor (TNF) administration, congestion at 4-6 h, and hemorrhage, congestion, and blood circulation blockage at 24 h. Histological examination after TNF administration to mice bearing similar methylcholanthrene-induced A-cell transplants showed thrombus formation in the tumor vasculature at 4 h and thereafter.	Methylcholanthrene	83-101	tumor necrosis factor	Mus musculus	330-333
3258905-4	1988	Our results using recombinant human interleukin-2 (IL-2) and recombinant human tumor necrosis factor (TNF) against established methylcholanthrene-induced fibrosarcoma (MCA sarcoma) pulmonary metastases showed that TNF and IL-2 therapy at low nontoxic dosages alone did not produce significant tumor regression, but when combined at the same dosage synergize producing significant antitumor effects in mice induced with MCA sarcoma.	Methylcholanthrene	127-145	interleukin 2	Homo sapiens	36-49
3293833-1	1988	A model has been proposed for the induction of cytochrome P450c in liver by polycyclic hydrocarbons such as benzo(a)pyrene (BaP) and 3-methylcholanthrene (3MC).	Methylcholanthrene	133-153	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	47-63
3293833-1	1988	A model has been proposed for the induction of cytochrome P450c in liver by polycyclic hydrocarbons such as benzo(a)pyrene (BaP) and 3-methylcholanthrene (3MC).	Methylcholanthrene	155-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	47-63
3258905-4	1988	Our results using recombinant human interleukin-2 (IL-2) and recombinant human tumor necrosis factor (TNF) against established methylcholanthrene-induced fibrosarcoma (MCA sarcoma) pulmonary metastases showed that TNF and IL-2 therapy at low nontoxic dosages alone did not produce significant tumor regression, but when combined at the same dosage synergize producing significant antitumor effects in mice induced with MCA sarcoma.	Methylcholanthrene	127-145	tumor necrosis factor	Homo sapiens	79-100
3258905-4	1988	Our results using recombinant human interleukin-2 (IL-2) and recombinant human tumor necrosis factor (TNF) against established methylcholanthrene-induced fibrosarcoma (MCA sarcoma) pulmonary metastases showed that TNF and IL-2 therapy at low nontoxic dosages alone did not produce significant tumor regression, but when combined at the same dosage synergize producing significant antitumor effects in mice induced with MCA sarcoma.	Methylcholanthrene	127-145	tumor necrosis factor	Homo sapiens	102-105
3346217-3	1988	Liver microsomes from untreated (control), phenobarbital-treated, and 3-methylcholanthrene-treated rats metabolized 6-FB[c]Ph at rates of 3.5, 1.5, and 7.7 nmol of products/nmol of cytochrome P-450/min, respectively.	Methylcholanthrene	70-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-201
3346217-7	1988	Substitution with fluorine at C-6 caused an almost 2.5-fold increase in the percentages of the putative proximate carcinogens, i.e. benzo-ring dihydrodiols with bay-region double bonds, when liver microsomes from 3-methylcholanthrene-treated rats were used.	Methylcholanthrene	213-233	complement C6	Rattus norvegicus	30-33
3355579-5	1988	This polypeptide co-migrated with protein bands which were correspondingly intensified after pretreatment with known inducers of cytochrome P-450d (3-methylcholanthrene and isosafrole).	Methylcholanthrene	148-168	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	129-146
3355583-5	1988	GST activity toward 1-chloro-2,4-dinitrobenzene, 1,2-dichloro-4-nitrobenzene and ethacrynic acid was enhanced by all compounds, hexachlorobenzene and 3-methylcholanthrene causing the largest and the smallest increase respectively.	Methylcholanthrene	150-170	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-3
3278056-3	1988	It was found in liver sections from phenobarbital-treated rats incubated with anti-P-450b and anti-epoxide hydrolase and from 3-methylcholanthrene-treated rats incubated with anti-P-450c.	Methylcholanthrene	126-146	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	180-186
3348807-1	1988	Administration of 3-methylcholanthrene (MC) to rats results in a striking increase in the transcription of cytochrome P-450 (c + d) messenger RNA with isolated nuclei, which is blocked by the simultaneous administration of cobalt chloride, an inhibitor of heme biosynthesis.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	107-126
3348807-1	1988	Administration of 3-methylcholanthrene (MC) to rats results in a striking increase in the transcription of cytochrome P-450 (c + d) messenger RNA with isolated nuclei, which is blocked by the simultaneous administration of cobalt chloride, an inhibitor of heme biosynthesis.	Methylcholanthrene	40-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	107-126
3348807-2	1988	Transcription of cytochrome P-450 (c + d) mRNAs with nuclei isolated from MC treated rats shows a linear increase with time of incubation, whereas it shows a progressive decrease with incubation time in the case of nuclei isolated from MC+CoCl2 treated rats.	Methylcholanthrene	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	17-36
3348807-2	1988	Transcription of cytochrome P-450 (c + d) mRNAs with nuclei isolated from MC treated rats shows a linear increase with time of incubation, whereas it shows a progressive decrease with incubation time in the case of nuclei isolated from MC+CoCl2 treated rats.	Methylcholanthrene	236-238	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	17-36
3350857-5	1988	Likewise, the use of matrigel greatly enhanced the induction of mRNA and protein for P-450c by 3-methylcholanthrene and for P-450p by steroidal and nonsteroidal inducers.	Methylcholanthrene	95-115	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	85-91
3258422-8	1988	The MAb were raised against 3-methylcholanthrene (MAb 1-7-1) or phenobarbital (MAB 2-66-3) induced rat liver microsomal cytochrome P-450.	Methylcholanthrene	28-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-136
3337745-1	1988	Role of cytochrome P-450 homologous to a 3-methylcholanthrene-inducible isozyme in rat liver.	Methylcholanthrene	41-61	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	19-24
2901335-14	1988	Untransformed 3T3 cells carry abundant 1.9 kb Hox 1.3 RNA, whereas the methylcholanthrene-transformed MB66 and LTK- cells or 3T3 cells transformed by the oncogenes src, fos or SV40 T antigen express only low levels.	Methylcholanthrene	71-89	Rous sarcoma oncogene	Mus musculus	164-167
2901335-14	1988	Untransformed 3T3 cells carry abundant 1.9 kb Hox 1.3 RNA, whereas the methylcholanthrene-transformed MB66 and LTK- cells or 3T3 cells transformed by the oncogenes src, fos or SV40 T antigen express only low levels.	Methylcholanthrene	71-89	FBJ osteosarcoma oncogene	Mus musculus	169-172
3335509-1	1988	Identification and characterization of a precursor form of mitochondrial cytochrome P-450 induced by 3-methylcholanthrene.	Methylcholanthrene	101-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
3335509-2	1988	Hepatic mitoplasts from 3-methylcholanthrene-treated rats contain cytochrome P-450 which can metabolize polycyclic aromatic hydrocarbons like benzo(a)pyrene.	Methylcholanthrene	24-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	66-82
3335509-4	1988	A polyclonal antibody to purified microsomal P-450c (a major 3-methylcholanthrene-inducible form) inhibited the activity of mitochondrial enzyme in a concentration-dependent manner and also reacted with a 54-kDa protein on the immunoblots.	Methylcholanthrene	61-81	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	45-51
3335509-8	1988	These results present evidence for the true intramitochondrial location of the P-450c-antibody reactive isoform detected in 3-methylcholanthrene-induced rat liver mitochondria.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	79-85
3358961-0	1988	[Isolation and comparative analysis of multiple isoenzymes of glutathione-S-transferase from the liver of intact rats and rats administered phenobarbital, 3-methylcholanthrene and butylhydroxytoluene].	Methylcholanthrene	155-175	hematopoietic prostaglandin D synthase	Rattus norvegicus	62-87
3276319-3	1988	In general, cytochrome P-450c, the major cytochrome P-450 isozyme contained in liver microsomes from 3-methylcholanthrene-treated rats, has the highest degree of stereoselectivity.	Methylcholanthrene	101-121	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	12-29
3276319-3	1988	In general, cytochrome P-450c, the major cytochrome P-450 isozyme contained in liver microsomes from 3-methylcholanthrene-treated rats, has the highest degree of stereoselectivity.	Methylcholanthrene	101-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Methylcholanthrene	262-280	interleukin 2	Homo sapiens	28-41
3257697-6	1988	3-Methylcholanthrene (3-MC), given to rats 24 hr previously, induced increases in AHH activity of 4- to 7-fold in the villus and of 19- to 26-fold in the crypt cells.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	82-85
3257697-6	1988	3-Methylcholanthrene (3-MC), given to rats 24 hr previously, induced increases in AHH activity of 4- to 7-fold in the villus and of 19- to 26-fold in the crypt cells.	Methylcholanthrene	22-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	82-85
3121205-10	1988	These results indicate that the metabolic activation of MeIQx is catalyzed mainly by two forms of cytochrome P-450, P-448-H and P-488-L, in the livers of PCB- or 3-MC-treated rats, but also that P-450-male may play an important role in the activation in livers of intact male rats.	Methylcholanthrene	162-166	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Methylcholanthrene	262-280	interleukin 2	Homo sapiens	43-47
3259499-1	1988	The ability of lymph node and spleen cells to secrete and sorb interleukin-2 (IL-2) during the growth of sarcomas induced by 20-methylcholanthrene is studied.	Methylcholanthrene	125-146	interleukin 2	Homo sapiens	63-76
3259499-1	1988	The ability of lymph node and spleen cells to secrete and sorb interleukin-2 (IL-2) during the growth of sarcomas induced by 20-methylcholanthrene is studied.	Methylcholanthrene	125-146	interleukin 2	Homo sapiens	78-82
3350839-6	1988	A series of MC derivatives substituted at C-1 or C-2 was tested.	Methylcholanthrene	12-14	complement C2	Rattus norvegicus	49-52
3142693-14	1988	Furthermore, MC, an inducer of certain cytochrome P-450 species ("aryl hydrocarbon hydroxylase"), potentiates the effect of BP.	Methylcholanthrene	13-15	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
2455035-8	1988	In mc-IgG1-mediated 1.5-h PCA, the delay was significant.	Methylcholanthrene	3-5	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	6-10
2469089-0	1988	Influence of protein and RNA synthesis inhibitors on methylcholanthrene-mediated induction of aryl hydrocarbon hydroxylase activity in intestinal mucosa.	Methylcholanthrene	53-71	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	94-122
2469089-1	1988	The sensitivity of the 3-methylcholanthrene (MC)-mediated induction of aryl hydrocarbon hydroxylase (AHH) activity to pretreatment with inhibitors of protein and RNA synthesis was studied.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	71-99
2469089-1	1988	The sensitivity of the 3-methylcholanthrene (MC)-mediated induction of aryl hydrocarbon hydroxylase (AHH) activity to pretreatment with inhibitors of protein and RNA synthesis was studied.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-104
2469089-1	1988	The sensitivity of the 3-methylcholanthrene (MC)-mediated induction of aryl hydrocarbon hydroxylase (AHH) activity to pretreatment with inhibitors of protein and RNA synthesis was studied.	Methylcholanthrene	45-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	71-99
2469089-1	1988	The sensitivity of the 3-methylcholanthrene (MC)-mediated induction of aryl hydrocarbon hydroxylase (AHH) activity to pretreatment with inhibitors of protein and RNA synthesis was studied.	Methylcholanthrene	45-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-104
2469089-11	1988	In addition, the methods used may lack sufficient sensitivity to detect the small net change in protein necessary to account for the increase in AHH activity seen after MC induction.	Methylcholanthrene	169-171	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	145-148
2894946-3	1988	The treatment of Suncus murinus with phenobarbital and 3-methylcholanthrene elevated the level of cytochrome P-450 and the activity of drug-metabolizing enzymes, but not the level of cytochrome b5.	Methylcholanthrene	55-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
2894946-4	1988	Two distinct forms of cytochrome P-450 have been purified from hepatic microsomes of 3-methylcholanthrene-treated Suncus murinus.	Methylcholanthrene	85-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
2455035-9	1988	Both 1.5-h PCA"s mediated by heated antiserum and mc-IgG1, and the 48-h PCA"s mediated by antiserum and mc-IgE were not observed in WBB6 F1-W/Wv mice, which lack mast cells.	Methylcholanthrene	50-52	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	53-57
3677310-10	1987	The preponderance of the potentially mutagenic BfQ-7,8-dihydrodiol amongst the metabolites generated by liver microsomes from 3-MC-pretreated rats suggests a possible role for cytochrome P-450c, the major form of rat hepatic cytochrome P-450 induced by 3-MC, in the metabolic activation of BfQ.	Methylcholanthrene	126-130	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	176-193
3120735-3	1987	Treatment of rats with 3-methylcholanthrene resulted in a 2.7-fold increase in liver cytosolic DT-diaphorase activity and a 1.5-fold increase in liver microsomal vitamin K-dependent carboxylase activity.	Methylcholanthrene	23-43	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	95-108
2825716-7	1987	(3) A human hepatoma cell line (Hep G2) was studied to obtain information on the inducibility of human UDP-GT activities by 3-methylcholanthrene-type inducers.	Methylcholanthrene	124-144	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	103-109
2825716-8	1987	UDP-GT activities towards benzo(a)pyrene-3,6-quinol and 1-naphthol were moderately but significantly induced by 3-methylcholanthrene-treatment of the cells (2-fold), whereas 7-ethoxyresorufin O-deethylase and 7-ethoxycoumarin O-deethylase were increased over 100- and 10-fold, respectively.	Methylcholanthrene	114-132	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	0-6
2829388-7	1988	In contrast, Mab 2-66-3 (against phenobarbital-inducible P-450) did not recognize any proteins in either strain, confirming the conclusion that TCDD elicits a MC-type induction of hepatic cytochrome P-450 in both strains of rats.	Methylcholanthrene	159-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	188-204
3500726-1	1987	The imidazole N-substituted antifungal agents ketoconazole, miconazole and clotrimazole have been shown to be potent inhibitors of oxidative metabolism by both a phenobarbital-induced cytochrome P-450 (P-450b) and a 3-methylcholanthrene-induced cytochrome P-448-protein (P-450c) in reconstituted systems.	Methylcholanthrene	216-236	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	195-200
3677314-7	1987	The induced hepatic enzymes in mice and rats were suggested to be 3-methylcholanthrene-inducible cytochrome P-448 isozymes as determined by mutation tests with Trp P-1, Trp P-2 and two other substrates and by immunochemical analyses of rat hepatic cytochrome P-450 using monoclonal antibodies against rat cytochrome P-448 isozymes.	Methylcholanthrene	66-86	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	97-113
3677314-7	1987	The induced hepatic enzymes in mice and rats were suggested to be 3-methylcholanthrene-inducible cytochrome P-448 isozymes as determined by mutation tests with Trp P-1, Trp P-2 and two other substrates and by immunochemical analyses of rat hepatic cytochrome P-450 using monoclonal antibodies against rat cytochrome P-448 isozymes.	Methylcholanthrene	66-86	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	160-176
3677314-7	1987	The induced hepatic enzymes in mice and rats were suggested to be 3-methylcholanthrene-inducible cytochrome P-448 isozymes as determined by mutation tests with Trp P-1, Trp P-2 and two other substrates and by immunochemical analyses of rat hepatic cytochrome P-450 using monoclonal antibodies against rat cytochrome P-448 isozymes.	Methylcholanthrene	66-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	248-264
3677314-7	1987	The induced hepatic enzymes in mice and rats were suggested to be 3-methylcholanthrene-inducible cytochrome P-448 isozymes as determined by mutation tests with Trp P-1, Trp P-2 and two other substrates and by immunochemical analyses of rat hepatic cytochrome P-450 using monoclonal antibodies against rat cytochrome P-448 isozymes.	Methylcholanthrene	66-86	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	305-321
3129417-2	1987	Treatments with PenCB and MC resulted in about 8- and 7-fold increases of cytosolic DT-diaphorase activity, respectively.	Methylcholanthrene	26-28	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	84-97
3130250-1	1987	Cytochrome P450 from rat brain mitochondrial and microsomal fractions was found to be inducible by 3-methylcholanthrene, both in quantity of enzyme and in activity towards 7-ethoxyresorufin, which is a model substrate for the cytochrome P450 isoform specifically induced by 3-methylcholanthrene.	Methylcholanthrene	99-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
2445468-2	1987	When cells were grown in complete medium with 10% fetal bovine serum, GRP78 mRNA was increased 4- to 9-fold in 3-methylcholanthrene (MCA; Clones 15 and 16)-, bleomycin (Bleo 1)-, and ultraviolet light (UV-C3)-transformed cell lines compared to nontransformed 10T1/2 clone 8 cells (Cl 8) at similar cell number and growth phase.	Methylcholanthrene	111-131	heat shock protein 5	Mus musculus	70-75
2445468-2	1987	When cells were grown in complete medium with 10% fetal bovine serum, GRP78 mRNA was increased 4- to 9-fold in 3-methylcholanthrene (MCA; Clones 15 and 16)-, bleomycin (Bleo 1)-, and ultraviolet light (UV-C3)-transformed cell lines compared to nontransformed 10T1/2 clone 8 cells (Cl 8) at similar cell number and growth phase.	Methylcholanthrene	133-136	heat shock protein 5	Mus musculus	70-75
3500724-0	1987	Monoclonal antibody characterization of hepatic and extrahepatic cytochrome P-450 activities in rats treated with phenobarbital or methylcholanthrene and fed various cholesterol diets.	Methylcholanthrene	131-149	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
3500724-1	1987	Monoclonal antibodies (MAb) against 3-methylcholanthrene (MC)- and phenobarbital (PB)-inducible forms of cytochrome P-450 isozyme were used to characterize changes in aryl hydrocarbon hydroxylase (AHH) and ethoxycoumarin O-deethylase (ECDE) activities modulated by dietary cholesterol.	Methylcholanthrene	36-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
3689389-1	1987	The induction of cytochrome P-450 (c+d) messenger RNAs in rat liver by 3-methyl cholanthrene follows a biphasic pattern.	Methylcholanthrene	71-92	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3689389-2	1987	Administration of cycloheximide blocks the induction of cytochrome P-450 (c+d) messenger RNAs by 3-methylcholanthrene as well as cytochrome P-450 (b+e) messenger RNAs by Phenobarbitone.	Methylcholanthrene	97-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-72
3663241-2	1987	The inhibitory effectiveness of these agents was increased in microsomes isolated from rats treated chronically with ethanol as compared to microsomes from pair-fed controls or from rats treated with other cytochrome P-450 inducers such as phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	257-277	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	206-222
3663244-0	1987	In vivo selection of a low spin form of cytochrome P-448 from 3-methylcholanthrene-induced rat cytochrome P-450 isozymes by carbon tetrachloride.	Methylcholanthrene	62-82	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	40-56
3663244-0	1987	In vivo selection of a low spin form of cytochrome P-448 from 3-methylcholanthrene-induced rat cytochrome P-450 isozymes by carbon tetrachloride.	Methylcholanthrene	62-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
3318837-1	1987	Effect of 2-methoxy-4-aminoazobenzene (2-MeO-AAB) and 3-methylcholanthrene (MC) on the induction of microsomal cytochrome P-448 isozymes in primary cultured rat hepatocytes was examined by means of immunochemical methods such as protein A-enzyme-linked immonosorbent assay and immuno-blots using anti-rat cytochrome P-448 monoclonal antibodies and by means of bacterial mutation tests.	Methylcholanthrene	54-74	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-127
3318837-1	1987	Effect of 2-methoxy-4-aminoazobenzene (2-MeO-AAB) and 3-methylcholanthrene (MC) on the induction of microsomal cytochrome P-448 isozymes in primary cultured rat hepatocytes was examined by means of immunochemical methods such as protein A-enzyme-linked immonosorbent assay and immuno-blots using anti-rat cytochrome P-448 monoclonal antibodies and by means of bacterial mutation tests.	Methylcholanthrene	76-78	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-127
3318837-1	1987	Effect of 2-methoxy-4-aminoazobenzene (2-MeO-AAB) and 3-methylcholanthrene (MC) on the induction of microsomal cytochrome P-448 isozymes in primary cultured rat hepatocytes was examined by means of immunochemical methods such as protein A-enzyme-linked immonosorbent assay and immuno-blots using anti-rat cytochrome P-448 monoclonal antibodies and by means of bacterial mutation tests.	Methylcholanthrene	76-78	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	305-321
3674890-5	1987	262, 2787-2793) who recently reported that an antibody prepared against cytochrome P-450a completely inhibited testosterone 7 alpha-hydroxylase activity in microsomes from untreated or 3-methylcholanthrene-treated rats but only inhibited 50% of the activity in microsomes from dexamethasone-treated rats.	Methylcholanthrene	185-205	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	111-143
3664959-1	1987	In prior studies with neonatal rats we have suggested that nitrated polycyclic aromatic hydrocarbons (NPAH) are 3-methylcholanthrene (3-MC) type of inducers of cytochrome P-450.	Methylcholanthrene	112-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	160-176
3664959-1	1987	In prior studies with neonatal rats we have suggested that nitrated polycyclic aromatic hydrocarbons (NPAH) are 3-methylcholanthrene (3-MC) type of inducers of cytochrome P-450.	Methylcholanthrene	134-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	160-176
3433801-2	1987	The imidazole antifungal agents, ketoconazole, miconazole and clotrimazole have been shown to be potent inhibitors of the phenobarbital-induced cytochromes P-450 and the 3-methylcholanthrene-induced cytochromes P-448-dependent rat hepatic microsomal mixed-function oxidases.	Methylcholanthrene	171-190	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	211-216
3445541-2	1987	Phenobarbital-induced cytochrome P-450 was especially sensitive to the influence of all the agents studied, while cytochrome P-450 from untreated animals was the least sensitive; the 3-methyl-cholanthrene-induced cytochrome P-448 exhibited the least sensitivity to guanidine.	Methylcholanthrene	183-204	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	22-38
3130250-1	1987	Cytochrome P450 from rat brain mitochondrial and microsomal fractions was found to be inducible by 3-methylcholanthrene, both in quantity of enzyme and in activity towards 7-ethoxyresorufin, which is a model substrate for the cytochrome P450 isoform specifically induced by 3-methylcholanthrene.	Methylcholanthrene	99-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-241
3130250-1	1987	Cytochrome P450 from rat brain mitochondrial and microsomal fractions was found to be inducible by 3-methylcholanthrene, both in quantity of enzyme and in activity towards 7-ethoxyresorufin, which is a model substrate for the cytochrome P450 isoform specifically induced by 3-methylcholanthrene.	Methylcholanthrene	274-294	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
3130250-1	1987	Cytochrome P450 from rat brain mitochondrial and microsomal fractions was found to be inducible by 3-methylcholanthrene, both in quantity of enzyme and in activity towards 7-ethoxyresorufin, which is a model substrate for the cytochrome P450 isoform specifically induced by 3-methylcholanthrene.	Methylcholanthrene	274-294	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-241
3118178-4	1987	Treatment of adult male rats with 3-methylcholanthrene (3-MC) or 3,4,5,3",4",5"-hexachlorobiphenyl (HCB) (two compounds known to induce P-450c and P-450d as a consequence of their interaction with the aromatic hydrocarbon receptor) decreased hepatic content of P-450 2c and its associated steroid hormone 2 alpha- and 16 alpha-hydroxylase activities.	Methylcholanthrene	34-54	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	136-153
3675602-0	1987	Synergy of phenobarbital and 3-methylcholanthrene in "superinduction" of cytochrome P-450c mRNA but not enzyme activity.	Methylcholanthrene	29-49	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	73-90
3675602-1	1987	The combination of phenobarbital and 3-methylcholanthrene in the inductive process of the rat hepatic cytochrome P-450c gene was evaluated.	Methylcholanthrene	37-57	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	102-119
3675602-5	1987	Four daily injections of phenobarbital followed by a single dose of 3-methylcholanthrene produced 5-24 times more poly (A)+ RNA coding for P-450c than 3-methylcholanthrene treatment alone.	Methylcholanthrene	68-88	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-145
3675602-5	1987	Four daily injections of phenobarbital followed by a single dose of 3-methylcholanthrene produced 5-24 times more poly (A)+ RNA coding for P-450c than 3-methylcholanthrene treatment alone.	Methylcholanthrene	151-171	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-145
3675602-6	1987	This superinduction of RNA transcripts was also observed for a species coding for cytochrome P-450d, which was increased 3-6 times over 3-methylcholanthrene treatment alone.	Methylcholanthrene	136-156	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	82-99
3321438-3	1987	A metastatic subline (ESb) of the methylcholanthrene-induced DBA/2 T-lymphoma invaded the vascular endothelium at a higher rate than its parental nonmetastatic (Eb) subline.	Methylcholanthrene	34-52	DBA2	Homo sapiens	61-66
3040233-0	1987	Ah receptor in human placenta: stabilization by molybdate and characterization of binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin, 3-methylcholanthrene, and benzo(a)pyrene.	Methylcholanthrene	130-150	aryl hydrocarbon receptor	Homo sapiens	0-11
3040233-1	1987	Aryl hydrocarbon hydroxylase (AHH, cytochrome P1-450) is highly inducible in several human cells and tissues exposed to specific halogenated and nonhalogenated aromatic chemicals of the "3-methylcholanthrene-type."	Methylcholanthrene	187-207	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	0-28
3040233-1	1987	Aryl hydrocarbon hydroxylase (AHH, cytochrome P1-450) is highly inducible in several human cells and tissues exposed to specific halogenated and nonhalogenated aromatic chemicals of the "3-methylcholanthrene-type."	Methylcholanthrene	187-207	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	30-33
3496953-2	1987	While only the s.c. methylcholanthrene-induced tumor exhibited regression and/or cures in response to immunomodulatory therapy with either agent alone, the simultaneous administration of a maximally tolerated dose of TNF and IL-2 given daily from within 1 day (B16 melanoma), 3 days (L1210 leukemia and P815 mastocytoma) or 5 and 10 days (EL-4 lymphoma and methylcholanthrene-induced sarcoma) after tumor cell implant resulted in no tumor takes (growth).	Methylcholanthrene	20-38	tumor necrosis factor	Homo sapiens	217-220
3684951-1	1987	The oxidative metabolism of 2,5-diphenyloxazole (PPO) is associated with 3-methylcholanthrene inducible cytochrome P-450.	Methylcholanthrene	73-93	protoporphyrinogen oxidase	Homo sapiens	49-52
3684951-6	1987	PPO metabolism is readily catalyzed by 3-methylcholanthrene-induced rat liver microsomes and strongly inhibited by alpha-naphthoflavone, but poorly inhibited by metyrapone or SKF 525A, indicating the involvement of cytochrome P-448 or P1-450 in the metabolism of PPO.	Methylcholanthrene	39-59	protoporphyrinogen oxidase	Homo sapiens	0-3
3684951-6	1987	PPO metabolism is readily catalyzed by 3-methylcholanthrene-induced rat liver microsomes and strongly inhibited by alpha-naphthoflavone, but poorly inhibited by metyrapone or SKF 525A, indicating the involvement of cytochrome P-448 or P1-450 in the metabolism of PPO.	Methylcholanthrene	39-59	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	235-241
3684951-6	1987	PPO metabolism is readily catalyzed by 3-methylcholanthrene-induced rat liver microsomes and strongly inhibited by alpha-naphthoflavone, but poorly inhibited by metyrapone or SKF 525A, indicating the involvement of cytochrome P-448 or P1-450 in the metabolism of PPO.	Methylcholanthrene	39-59	protoporphyrinogen oxidase	Homo sapiens	263-266
3111484-5	1987	On the other hand, the binding of dantrolene on microsomal cytochrome P-450 produced a type I difference spectrum, these data were obtained with liver microsomal cytochrome P-450c induced by 3-methylcholanthrene.	Methylcholanthrene	191-211	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	162-179
3301048-0	1987	Activation of H-ras oncogene in 3-methylcholanthrene-transformed human cell line.	Methylcholanthrene	32-52	HRas proto-oncogene, GTPase	Homo sapiens	14-19
2960636-1	1987	We have developed a simple culture assay system for measuring the in vitro effects of a chemical carcinogen, 3-methylcholanthrene (MCA), on certain activities of human peripheral blood lymphocytes: blastogenesis, cell-mediated cytotoxicity by natural killer cells, interleukin-2 production, lymphotoxin release and percent T-cell subpopulations.	Methylcholanthrene	109-129	interleukin 2	Homo sapiens	265-278
2960636-1	1987	We have developed a simple culture assay system for measuring the in vitro effects of a chemical carcinogen, 3-methylcholanthrene (MCA), on certain activities of human peripheral blood lymphocytes: blastogenesis, cell-mediated cytotoxicity by natural killer cells, interleukin-2 production, lymphotoxin release and percent T-cell subpopulations.	Methylcholanthrene	131-134	interleukin 2	Homo sapiens	265-278
3496953-2	1987	While only the s.c. methylcholanthrene-induced tumor exhibited regression and/or cures in response to immunomodulatory therapy with either agent alone, the simultaneous administration of a maximally tolerated dose of TNF and IL-2 given daily from within 1 day (B16 melanoma), 3 days (L1210 leukemia and P815 mastocytoma) or 5 and 10 days (EL-4 lymphoma and methylcholanthrene-induced sarcoma) after tumor cell implant resulted in no tumor takes (growth).	Methylcholanthrene	20-38	interleukin 2	Homo sapiens	225-229
3495587-1	1987	Peritoneal macrophages from mice bearing a transplantable methylcholanthrene-induced sarcoma produced progressively less IL 1 as tumor burden increased.	Methylcholanthrene	58-76	interleukin 1 complex	Mus musculus	121-125
3298908-6	1987	The activities of liver microsomes from untreated male and female rats and rats treated with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyl were expressed dependent on the activities of forms of cytochrome P-450 examined.	Methylcholanthrene	108-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	212-228
3110162-9	1987	Neither enzyme was active towards estrone, androsterone and substrates typical of 3-methylcholanthrene-inducible forms of UDP-glucuronosyltransferase.	Methylcholanthrene	82-102	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	122-149
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Methylcholanthrene	255-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Methylcholanthrene	255-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Methylcholanthrene	255-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Methylcholanthrene	255-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
3040651-1	1987	Repeated topical application of 3-methylcholanthrene to the backs of BALB/c mice lowered the tissue levels of lathosterol and provitamin D3, intermediates in one of the cholesterol biosynthetic pathways (the delta 7 pathway), though the activities of lathosterol 5-desaturase and provitamin D3 7-reductase were similar to those of control animals.	Methylcholanthrene	32-52	sterol-C5-desaturase	Mus musculus	251-275
3110592-5	1987	Glucuronidation was also determined with purified phenol UDP-glucuronosyltransferase from 3-methylcholanthrene-treated rats.	Methylcholanthrene	90-110	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	57-84
3581059-0	1987	Correlation of thyroid hormone dose-dependent regulation of K-ras protooncogene expression with oncogene activation by 3-methylcholanthrene: loss of thyroidal regulation in the transformed mouse cell.	Methylcholanthrene	119-139	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	60-65
3581059-3	1987	It has previously been shown that 3-methylcholanthrene transformation of C3H/10T1/2 mouse embryo cells in culture is the result of activation of the k-ras oncogene.	Methylcholanthrene	34-54	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	149-154
3581059-7	1987	It was of further interest to find that 3-methylcholanthrene-transformed C3H/10T1/2 cells have lost the sensitivity to thyroid hormone regulation of "activated" K-ras oncogene transcription and subsequent K-ras-specific RNA levels.	Methylcholanthrene	40-60	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	161-166
3581059-7	1987	It was of further interest to find that 3-methylcholanthrene-transformed C3H/10T1/2 cells have lost the sensitivity to thyroid hormone regulation of "activated" K-ras oncogene transcription and subsequent K-ras-specific RNA levels.	Methylcholanthrene	40-60	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	205-210
2953796-1	1987	Daily local administration at the tumor challenge site of 10 injections of 10 U of recombinant interleukin 2 (IL 2) obtained from different factories induces a consistent, though limited inhibition of the growth of CE-2, a poorly immunogenic methylcholanthrene-induced tumor.	Methylcholanthrene	242-260	interleukin 2	Mus musculus	95-108
3312182-0	1987	Organ selective induction of cytochrome P-448 isozymes in the rat by 2-methoxy-4-aminoazobenzene and 3-methylcholanthrene.	Methylcholanthrene	101-121	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	29-45
3312182-2	1987	The results of protein A-enzyme-linked immunosorbent assaying and immunoblotting using anti-rat cytochrome P-448 monoclonal antibodies showed that MC induced at least two microsomal cytochrome P-448 isozymes, a high spin form (cytochrome P-448H) and a low spin form (cytochrome P-448L), in liver, but that it induced only cytochrome P-448L in extrahepatic tissues such as lung, kidney, small intestine, and colon.	Methylcholanthrene	147-149	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	96-112
3312182-2	1987	The results of protein A-enzyme-linked immunosorbent assaying and immunoblotting using anti-rat cytochrome P-448 monoclonal antibodies showed that MC induced at least two microsomal cytochrome P-448 isozymes, a high spin form (cytochrome P-448H) and a low spin form (cytochrome P-448L), in liver, but that it induced only cytochrome P-448L in extrahepatic tissues such as lung, kidney, small intestine, and colon.	Methylcholanthrene	147-149	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	182-198
2953796-1	1987	Daily local administration at the tumor challenge site of 10 injections of 10 U of recombinant interleukin 2 (IL 2) obtained from different factories induces a consistent, though limited inhibition of the growth of CE-2, a poorly immunogenic methylcholanthrene-induced tumor.	Methylcholanthrene	242-260	interleukin 2	Mus musculus	110-114
3110589-4	1987	Results obtained from enzyme activity measurements and immunoblot analysis of microsomes isolated from xenobiotic-treated Wistar and Gunn rat liver are consistent with the 3-methylcholanthrene/UDPGT induction deficiency in the Gunn rat being due to the absence of this phenol UDPGT isoenzyme.	Methylcholanthrene	172-192	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	193-198
3574292-9	1987	The levels of 3-MC-inducible P-450c and P-450d mRNAs increased with age and peaked approximately 3 weeks after birth.	Methylcholanthrene	14-18	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-46
3552201-1	1987	The metastatic properties of the methylcholanthrene-induced T-10 sarcoma tumor variants which originated in C3H x C57Bl/6 F1 mice are correlated with the relative expression of class I major histocompatibility complex antigens.	Methylcholanthrene	33-51	ATPase, aminophospholipid transporter (APLT), class I, type 8A, member 1	Mus musculus	177-184
3579981-4	1987	The fluorographic pattern of the protein labeling was cytochrome P-450-dependent, as was demonstrated by CO and metyrapone inhibition as well as by pretreatment of rats with inducing drugs such as 3-methylcholanthrene, benzo(a)pyrene, phenobarbitone and Aroclor 1254.	Methylcholanthrene	197-217	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
3574292-10	1987	Hepatic P-450d mRNA levels in 3-MC-treated or control rats was consistently higher than P-450c mRNA levels at all ages studied.	Methylcholanthrene	30-34	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	8-14
3113478-4	1987	Several xenobiotics, such as Aroclor 1254, mirex, and 3-methylcholanthrene, repressed cytochrome P-450j levels when administered to male rats.	Methylcholanthrene	54-74	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	86-103
3109500-1	1987	Studies with monospecific antibodies to individual forms of monooxygenases P-450b (phenobarbital-induced) and P-450c (3-methylcholanthrene-induced) by immunochemical, kinetic and spectral methods revealed differences in the dynamics of xenobiotic-induced changes in the content and monooxygenase activity of the total microsomal CO-binding hemoprotein and of its molecular forms.	Methylcholanthrene	118-138	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-116
3545456-1	1987	Rabbit antibodies to the phenobarbital (PB) inducible rat liver microsomal cytochrome P-450s b and e and to 3-methylcholanthrene (MC) inducible P-450c were used to examine the expression of these isozymes in rat lungs.	Methylcholanthrene	130-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	144-150
3545456-8	1987	An increase in type II alveolar cell and Clara cell immunoreactivity to P-450c was observed after MC induction.	Methylcholanthrene	98-100	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	72-78
3545456-10	1987	In conclusion, P-450c is highly inducible by MC in rat lung (detected in microsomes by Western blot), specifically in endothelial cells, Clara cells, and alveolar type II cells (as visualized by immunocytochemistry); and P-450b is present in rat lung microsomes, and immunoreactivity to this isozyme is localized in alveolar type II and Clara cells.	Methylcholanthrene	45-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	15-21
3567888-1	1987	The induction of ornithine decarboxylase (ODC) in rat liver by the carcinogen 2-acetylaminofluorene (2AAF), the strong liver tumor initiator trans-4-acetylaminostilbene (AAS), the non-carcinogen 4-acetylaminofluorene (4AAF) and, as a control, 3-methylcholanthrene (MC) has been examined.	Methylcholanthrene	243-263	ornithine decarboxylase 1	Rattus norvegicus	17-40
3567888-1	1987	The induction of ornithine decarboxylase (ODC) in rat liver by the carcinogen 2-acetylaminofluorene (2AAF), the strong liver tumor initiator trans-4-acetylaminostilbene (AAS), the non-carcinogen 4-acetylaminofluorene (4AAF) and, as a control, 3-methylcholanthrene (MC) has been examined.	Methylcholanthrene	243-263	ornithine decarboxylase 1	Rattus norvegicus	42-45
3567888-1	1987	The induction of ornithine decarboxylase (ODC) in rat liver by the carcinogen 2-acetylaminofluorene (2AAF), the strong liver tumor initiator trans-4-acetylaminostilbene (AAS), the non-carcinogen 4-acetylaminofluorene (4AAF) and, as a control, 3-methylcholanthrene (MC) has been examined.	Methylcholanthrene	265-267	ornithine decarboxylase 1	Rattus norvegicus	17-40
3567888-1	1987	The induction of ornithine decarboxylase (ODC) in rat liver by the carcinogen 2-acetylaminofluorene (2AAF), the strong liver tumor initiator trans-4-acetylaminostilbene (AAS), the non-carcinogen 4-acetylaminofluorene (4AAF) and, as a control, 3-methylcholanthrene (MC) has been examined.	Methylcholanthrene	265-267	ornithine decarboxylase 1	Rattus norvegicus	42-45
3567888-2	1987	MC and all aromatic amines increased the ODC activity of rat liver from 3.6-fold (MC) to maximal 5.7-fold (AAS).	Methylcholanthrene	0-2	ornithine decarboxylase 1	Rattus norvegicus	41-44
3567888-2	1987	MC and all aromatic amines increased the ODC activity of rat liver from 3.6-fold (MC) to maximal 5.7-fold (AAS).	Methylcholanthrene	82-84	ornithine decarboxylase 1	Rattus norvegicus	41-44
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Methylcholanthrene	210-231	RT1 class II, locus Db1	Rattus norvegicus	4-7
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Methylcholanthrene	210-231	RT1 class II, locus Db2	Rattus norvegicus	12-15
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Methylcholanthrene	210-231	RT1 class II, locus Db2	Rattus norvegicus	74-77
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Methylcholanthrene	210-231	RT1 class II, locus Db2	Rattus norvegicus	74-77
3108693-2	1987	Activated microsomes from the brain of the rat conjugated 1-naphthol with an apparent Km of 95 microM and a Vmax of 5.47 nmol/hr mg protein at 30 degrees C. Microsomal uridine diphosphate (UDP)-glucuronosyltransferase activity in brain towards 1-naphthol was not significantly induced by pretreatment of animals with 3-methylcholanthrene or phenobarbital.	Methylcholanthrene	317-337	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	168-217
3589155-4	1987	Addition of 3-MC to erythropoietin dependent CFU-E was found to induce AHH activity above controls in a dose dependent manner, with 75 micrograms generating a maximal effect.	Methylcholanthrene	12-16	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	71-74
3589155-6	1987	In contrast, maximal AHH activity was obtained from 6-7 day CFU-GM and 40 micrograms of 3-MC stimulated the activity by 88%.	Methylcholanthrene	88-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	21-24
2882982-0	1987	In vivo and in vitro biotransformation of theobromine by phenobarbital- and 3-methylcholanthrene-inducible cytochrome P-450 monooxygenases in rat liver.	Methylcholanthrene	76-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
2882982-2	1987	A new in vitro method was developed and applied to establish the role of the hepatic cytochrome P-450 monooxygenases in theobromine biotransformation by control and phenobarbital (PB)- and 3-methylcholanthrene (3MC)-induced Sprague-Dawley rats.	Methylcholanthrene	189-209	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
2882982-2	1987	A new in vitro method was developed and applied to establish the role of the hepatic cytochrome P-450 monooxygenases in theobromine biotransformation by control and phenobarbital (PB)- and 3-methylcholanthrene (3MC)-induced Sprague-Dawley rats.	Methylcholanthrene	211-214	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
2882982-5	1987	Following induction with 3MC, but not PB, selective increases occurred in the urinary excretion of 3,7DAU, indicating that a 3MC-inducible cytochrome P-450 isozyme plays a significant role in this metabolic pathway.	Methylcholanthrene	25-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
2882982-5	1987	Following induction with 3MC, but not PB, selective increases occurred in the urinary excretion of 3,7DAU, indicating that a 3MC-inducible cytochrome P-450 isozyme plays a significant role in this metabolic pathway.	Methylcholanthrene	125-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
3299136-1	1987	The presence of cytochrome P-450 in rat brain was studied by immunohistochemistry, using antibodies to cytochrome P-450 purified from livers of phenobarbital- or 3-methylcholanthrene-treated rats.	Methylcholanthrene	162-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
3299136-2	1987	Immunoreactive nerves were observed only in brain sections incubated with immunoglobulin-G to 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	94-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	123-139
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	165-185	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	100-117
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	165-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	165-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	129-145
3299136-9	1987	The present results indicate that rat brain contains a form of cytochrome P-450 with antigenic relatedness to the hepatic 3-methylcholanthrene-inducible cytochrome P-450c.	Methylcholanthrene	122-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
3299136-9	1987	The present results indicate that rat brain contains a form of cytochrome P-450 with antigenic relatedness to the hepatic 3-methylcholanthrene-inducible cytochrome P-450c.	Methylcholanthrene	122-142	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	153-170
3818621-13	1987	These results establish testosterone 7 alpha-hydroxylase as a member of the P-450e gene family that is developmentally regulated, sex-dependent, and markedly inducible by 3-methylcholanthrene.	Methylcholanthrene	171-191	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	24-56
3492267-7	1987	In vitro addition of these plant phenols (240 microM) to the incubation mixture prepared from control and 3-methylcholanthrene-treated animals resulted in varying degrees of inhibition of epidermal microsomal AHH (57-92%), ethoxycoumarin O-deethylase (19-58%), and ethoxyresorufin O-deethylase (33-85%) activities.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	209-212
3622636-2	1987	The addition of phenobarbital, 3-methylcholanthrene, or nafenopin from Day 3 to Day 6 increased the contents of cytochrome P-450 to 128, 239, and 251%, respectively, compared to untreated controls at Day 3.	Methylcholanthrene	31-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	112-128
3599463-1	1987	To investigate life environmental factors which affect aryl hydrocarbon hydroxylase (AHH) activity, basal and 3-methylcholanthrene(3-MC)-induced AHH activities were determined by the formation of 3-hydroxybenzo(a)pyrene in cultured lymphocytes obtained from 111 healthy male subjects who lived in Fukuoka Prefecture, Japan.	Methylcholanthrene	110-130	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	85-88
3599463-1	1987	To investigate life environmental factors which affect aryl hydrocarbon hydroxylase (AHH) activity, basal and 3-methylcholanthrene(3-MC)-induced AHH activities were determined by the formation of 3-hydroxybenzo(a)pyrene in cultured lymphocytes obtained from 111 healthy male subjects who lived in Fukuoka Prefecture, Japan.	Methylcholanthrene	110-130	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	145-148
3599463-1	1987	To investigate life environmental factors which affect aryl hydrocarbon hydroxylase (AHH) activity, basal and 3-methylcholanthrene(3-MC)-induced AHH activities were determined by the formation of 3-hydroxybenzo(a)pyrene in cultured lymphocytes obtained from 111 healthy male subjects who lived in Fukuoka Prefecture, Japan.	Methylcholanthrene	131-135	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	85-88
3599463-1	1987	To investigate life environmental factors which affect aryl hydrocarbon hydroxylase (AHH) activity, basal and 3-methylcholanthrene(3-MC)-induced AHH activities were determined by the formation of 3-hydroxybenzo(a)pyrene in cultured lymphocytes obtained from 111 healthy male subjects who lived in Fukuoka Prefecture, Japan.	Methylcholanthrene	131-135	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	145-148
3495296-6	1987	In 3-methylcholanthrene-induced microsomes the sensitivity of O-deethylation of 7-ethoxycumarin to the inhibiting effect of phospholipase A2 or lysolecithine is lower than that in non-induced or phenobarbital-induced microsomes.	Methylcholanthrene	3-23	phospholipase A2 group IB	Rattus norvegicus	124-140
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
3545085-10	1987	MAb 1-12-3 and anti-P-450E PAb recognized a second band of lower molecular weight than P-450c in BNF rat microsomes which may correspond to P-450d, the MC- and isosafrole-inducible rat isozyme.	Methylcholanthrene	152-154	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	87-93
3805049-14	1987	(1984) Biochemistry 23, 4598-4603) (71%), while its sequence similarity with 3-methylcholanthrene-inducible P-450c and P-450d is rather low.	Methylcholanthrene	77-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	108-125
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Methylcholanthrene	49-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	204-210
3107519-3	1987	The amount of in vitro covalent binding of TCB to proteins by liver microsomes was increased markedly by pretreatment of AHH-responsive C57BL/6N mice with either 3-methylcholanthrene (MC) or TCB itself, although these two inducers were not effective in AHH-nonresponsive DBA/2N mice.	Methylcholanthrene	162-182	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	121-124
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Methylcholanthrene	49-69	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	215-221
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Methylcholanthrene	49-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	243-259
3107519-3	1987	The amount of in vitro covalent binding of TCB to proteins by liver microsomes was increased markedly by pretreatment of AHH-responsive C57BL/6N mice with either 3-methylcholanthrene (MC) or TCB itself, although these two inducers were not effective in AHH-nonresponsive DBA/2N mice.	Methylcholanthrene	184-186	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	121-124
3104258-3	1987	High-spin forms of cytochrome P-450 purified from 3-methylcholanthrene-pretreated rats (MC-P-448-H) or hamsters (P-488 ham-II) showed higher catalytic activity for N-hydroxylation of phenetidine than three other low-spin forms of cytochrome P-450 purified from the same animals or from phenobarbital-pretreated rats.	Methylcholanthrene	50-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
3104258-3	1987	High-spin forms of cytochrome P-450 purified from 3-methylcholanthrene-pretreated rats (MC-P-448-H) or hamsters (P-488 ham-II) showed higher catalytic activity for N-hydroxylation of phenetidine than three other low-spin forms of cytochrome P-450 purified from the same animals or from phenobarbital-pretreated rats.	Methylcholanthrene	50-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	230-246
3100897-5	1987	CsA had inhibitory effects on MC-26 colon cancer growth which were similar to DFMO; these effects were blocked by the addition of the polyamine, putrescine.	Methylcholanthrene	30-33	excision repaiross-complementing rodent repair deficiency, complementation group 8	Mus musculus	0-3
3105185-0	1987	Difference in the effects of phenobarbital and 3-methylcholanthrene treatment on subunit composition of hepatic glutathione S-transferase in male and female rats.	Methylcholanthrene	47-67	hematopoietic prostaglandin D synthase	Rattus norvegicus	112-137
3105187-0	1987	Induction of liver microsomal epoxide hydrolase, UDP-glucuronyl transferase and cytosolic glutathione transferase in different rodent species by 2-acetylaminofluorene or 3-methylcholanthrene.	Methylcholanthrene	170-190	epoxide hydrolase 1	Rattus norvegicus	19-47
3105187-4	1987	Treatment with 3-methylcholanthrene also produces the largest effects on these three enzyme activities in rat liver; exceptions are its failure to induce microsomal epoxide hydrolase in female rat and the large induction of cytosolic GSH transferase in hamster liver.	Methylcholanthrene	15-35	epoxide hydrolase 1	Rattus norvegicus	154-182
3304211-9	1987	Mechanistically best known is the program turned on by 3-methylcholanthrene-type inducers which includes enhanced synthesis of certain isoenzymes of cytochrome P-450, GT and probably GSH-transferase.	Methylcholanthrene	55-75	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-165
3496154-2	1987	Experiments were designed to test what percentage of experimental MC-induced murine sarcomas were sensitive to the local tumour inhibitory effect of IL-2 and whether any correlation existed between the sensitivity of these sarcomas to the immunotherapeutic effect of IL-2 and their susceptibility to the cytolytic effect of IL-2-activated killer cells.	Methylcholanthrene	66-68	interleukin 2	Mus musculus	149-153
3566772-9	1987	Inducibility of AHH by 3-methylcholanthrene (MCA) or phenobarbital (PB) was largely reduced due to AA feeding.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-19
3496154-3	1987	It was found that the sensitivity of MC-induced sarcomas to local IL-2 immunotherapy was a general phenomenon.	Methylcholanthrene	37-39	interleukin 2	Mus musculus	66-70
2954636-1	1987	BALB/c mice were immunized with the syngeneic 3-methylcholanthrene-induced fibrosarcoma CA-2 by the growth and excision method.	Methylcholanthrene	46-66	carbonic anhydrase 2	Mus musculus	88-92
3621371-4	1987	Cytosolic epoxide hydrolase activity was induced by chlorinated paraffins, di(2-ethylhexyl)phthalate and clofibrate and depressed by alpha-naphthylisothiocyanate, 3-methylcholanthrene, benzil and quercitin.	Methylcholanthrene	163-183	epoxide hydrolase 2, cytoplasmic	Mus musculus	0-27
3621371-12	1987	The most potent inducers of DT-diaphorase activity were 3-methylcholanthrene, polychlorinated biphenyls and dinitrotoluene.	Methylcholanthrene	56-76	NAD(P)H dehydrogenase, quinone 1	Mus musculus	28-41
3106031-2	1987	After chronic ethanol consumption, microsomal ethanol-oxidizing system (MEOS) activity increases with an associated rise in microsomal cytochrome P-450, including a form different from that induced by phenobarbital and methylcholanthrene and which has a high affinity for ethanol, as shown in reconstituted systems.	Methylcholanthrene	219-237	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	135-151
3816655-2	1987	The changes occur mainly in iron-sulphur centres and cytochrome P-450 under chemical and viral blastomogenesis in the muscular tissue induced by 3-methyl cholanthrene and Moloney oncornavirus.	Methylcholanthrene	145-166	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	53-69
2446997-1	1987	With the use of 3H-arginine labelled cationic proteins derived from fibrosarcoma induced by methylcholanthrene it has been shown in studies in vitro that these proteins interact with fibrinogen under the influence of thrombin.	Methylcholanthrene	92-110	coagulation factor II, thrombin	Homo sapiens	217-225
3559914-6	1987	The administration of 3-MC increased cytochrome P-448 content of microsomes from all rats, regardless of diet, however highest content was present in microsomes from rats fed the 20% corn oil diet.	Methylcholanthrene	22-26	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	48-53
3609441-6	1987	ODC induction by TPA was lower in C3H/10T1/2 CL8 cells initiated with 3-methyl-cholanthrene (MCA).	Methylcholanthrene	70-91	ornithine decarboxylase, structural 1	Mus musculus	0-3
3609441-6	1987	ODC induction by TPA was lower in C3H/10T1/2 CL8 cells initiated with 3-methyl-cholanthrene (MCA).	Methylcholanthrene	93-96	ornithine decarboxylase, structural 1	Mus musculus	0-3
3550106-11	1987	AHH activity is mediated by a form of cytochrome P-450 that is inducible by 3-methylcholanthrene/beta-naphthoflavone.	Methylcholanthrene	76-96	cytochrome P-450	Oryctolagus cuniculus	38-54
3500321-6	1987	Thus it appears that the NGF receptors on rat splenic MC are physiologically relevant and that NGF can modulate proliferation of T- and B- cells.	Methylcholanthrene	54-56	nerve growth factor	Rattus norvegicus	25-28
2884771-0	1987	Effects of tumor necrosis factor (TNF) on transplanted tumors induced by methylcholanthrene in mice.	Methylcholanthrene	73-91	tumor necrosis factor	Mus musculus	11-32
3576079-2	1987	Further experiments with these cells on the expression of different forms of cytochrome P-450, inducible not only by phenobarbital (PB) and 3-methylcholanthrene (MC), but also by metyrapone (MP), ethanol (E), and beta-naphthoflavone (BNF) are reported here.	Methylcholanthrene	140-160	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
3576079-2	1987	Further experiments with these cells on the expression of different forms of cytochrome P-450, inducible not only by phenobarbital (PB) and 3-methylcholanthrene (MC), but also by metyrapone (MP), ethanol (E), and beta-naphthoflavone (BNF) are reported here.	Methylcholanthrene	162-164	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
2884771-0	1987	Effects of tumor necrosis factor (TNF) on transplanted tumors induced by methylcholanthrene in mice.	Methylcholanthrene	73-91	tumor necrosis factor	Mus musculus	34-37
2884771-2	1987	The effects of a highly purified tumor necrosis factor (TNF) on transplanted methylcholanthrene (Meth A)-induced murine tumors were compared with those of lipopolysaccharide (LPS).	Methylcholanthrene	77-95	tumor necrosis factor	Mus musculus	33-54
2884771-2	1987	The effects of a highly purified tumor necrosis factor (TNF) on transplanted methylcholanthrene (Meth A)-induced murine tumors were compared with those of lipopolysaccharide (LPS).	Methylcholanthrene	77-95	tumor necrosis factor	Mus musculus	56-59
2884771-2	1987	The effects of a highly purified tumor necrosis factor (TNF) on transplanted methylcholanthrene (Meth A)-induced murine tumors were compared with those of lipopolysaccharide (LPS).	Methylcholanthrene	97-103	tumor necrosis factor	Mus musculus	56-59
3792550-0	1986	Restoration of hydroperoxide-dependent lipid peroxidation by 3-methylcholanthrene induction of cytochrome P-448 in hepatoma microsomes.	Methylcholanthrene	61-81	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	95-111
3825173-1	1987	From the hepatic cytochrome P-450 isozymes b and c isolated from rats treated with phenobarbital and 3-methylcholanthrene respectively, only cytochrome P-450c was found to be active in the oxidation of paracetamol, in the presence of glutathione ultimately leading to the formation of the 3-glutathionyl conjugate.	Methylcholanthrene	101-121	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	141-158
3099430-1	1986	Both 4,4"-dichlorobiphenyl (4,4"-DCB) and 3-methylcholanthrene (3-MC) caused a substantial increase of phenacetin-induced hepatic glutathione (GSH) depletion, whereas phenobarbital (PB) had no effect, suggesting that 4,4"-DCB possesses cytochrome P-448 inducing activity.	Methylcholanthrene	42-62	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	236-252
3099430-1	1986	Both 4,4"-dichlorobiphenyl (4,4"-DCB) and 3-methylcholanthrene (3-MC) caused a substantial increase of phenacetin-induced hepatic glutathione (GSH) depletion, whereas phenobarbital (PB) had no effect, suggesting that 4,4"-DCB possesses cytochrome P-448 inducing activity.	Methylcholanthrene	64-68	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	236-252
3792550-6	1986	Treatment of the tumor-bearing rats with 3-methylcholanthrene increases the hepatoma cytochrome P-450 to values comparable to those of control membranes, although the hemoprotein has a peak in the CO-reduced difference absorption spectrum at 448 nm.	Methylcholanthrene	41-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
3096993-0	1986	Cloning and characterization of cDNA encoding 3-methylcholanthrene inducible rat mRNA for UDP-glucuronosyltransferase.	Methylcholanthrene	46-66	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	90-117
3096339-2	1986	UDPGT activities tested could be divided in four groups on the basis of their tissue distribution and induction by PB or 3MC in liver microsomes.	Methylcholanthrene	121-124	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	0-5
3536915-5	1986	On Western (immuno) blot analysis, large increases in this hepatic menadione reductase protein (NMOR1) of 3-methylcholanthrene-treated C57BL/6N but not DBA/2N mice confirmed that induction of this enzyme by 3-methyl-cholanthrene is regulated by the Ah receptor.	Methylcholanthrene	106-126	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	67-86
3536915-5	1986	On Western (immuno) blot analysis, large increases in this hepatic menadione reductase protein (NMOR1) of 3-methylcholanthrene-treated C57BL/6N but not DBA/2N mice confirmed that induction of this enzyme by 3-methyl-cholanthrene is regulated by the Ah receptor.	Methylcholanthrene	106-126	aryl hydrocarbon receptor	Rattus norvegicus	249-260
3536915-5	1986	On Western (immuno) blot analysis, large increases in this hepatic menadione reductase protein (NMOR1) of 3-methylcholanthrene-treated C57BL/6N but not DBA/2N mice confirmed that induction of this enzyme by 3-methyl-cholanthrene is regulated by the Ah receptor.	Methylcholanthrene	207-228	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	67-86
3099853-6	1986	High performance liquid chromatography of PB-3 and MC-2 on anion-exchangers yielded two additional peaks from the PB-induced major cytochrome P-450 PB-3 and three peaks from the MC-induced major cytochrome P-450 MC-2.	Methylcholanthrene	51-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-152
3026444-1	1986	The chromatin structure of cytochrome P-450c and P-450d genes, which in the liver are highly inducible by 3-methylcholanthrene, was studied in normal and carcinogen-treated rats by using a cDNA probe specific for P-450c and a genomic probe that recognizes both genes.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	27-44
3026444-1	1986	The chromatin structure of cytochrome P-450c and P-450d genes, which in the liver are highly inducible by 3-methylcholanthrene, was studied in normal and carcinogen-treated rats by using a cDNA probe specific for P-450c and a genomic probe that recognizes both genes.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	49-55
3026444-1	1986	The chromatin structure of cytochrome P-450c and P-450d genes, which in the liver are highly inducible by 3-methylcholanthrene, was studied in normal and carcinogen-treated rats by using a cDNA probe specific for P-450c and a genomic probe that recognizes both genes.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-44
3026444-5	1986	Gene induction, by treatment with 3-methylcholanthrene, changes the location of the DNase I site present in the 5" region without affecting the sites present in the 3" region.	Methylcholanthrene	34-54	deoxyribonuclease 1	Rattus norvegicus	84-91
3099853-6	1986	High performance liquid chromatography of PB-3 and MC-2 on anion-exchangers yielded two additional peaks from the PB-induced major cytochrome P-450 PB-3 and three peaks from the MC-induced major cytochrome P-450 MC-2.	Methylcholanthrene	51-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
3096336-9	1986	PB, 3-MC and PCN increased F-UDP-GT activity to 208%, 282% and 342% of vehicle-treated animals, respectively, while F pretreatment did not affect the conjugation of F. In comparison, 1-naphthol glucuronidation was preferentially induced by 3-MC (4.4-fold of control) while estrone glucuronidation was induced by PB and PCN (4.9- and 2.5-fold of control, respectively).	Methylcholanthrene	4-8	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	29-35
3778500-6	1986	In contrast to induction by phenobarbital, induction of cytochrome P-450 by 3-methylcholanthrene enhanced the microsomal oxidation of PAR and its derivatives.	Methylcholanthrene	76-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-72
3801548-0	1986	[Identification and characteristics of mRNA for cytochrome P-450 in the rat liver induced by phenobarbital and 3-methylcholanthrene].	Methylcholanthrene	111-131	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
3778507-0	1986	Structural comparison of monoclonal antibody immunopurified pulmonary and hepatic cytochrome P-450 from 3-methylcholanthrene-treated rats.	Methylcholanthrene	104-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
3778507-1	1986	A pulmonary cytochrome P-450 was purified from lung microsomes of 3-methylcholanthrene (MC)-treated rats by immunoaffinity chromatography using a monoclonal antibody to MC-induced rat liver cytochrome P-450.	Methylcholanthrene	66-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
3801548-3	1986	In contrast, after completion of MC-mRNA translation, the antibodies to major MC-induced cytochrome MC-2 precipitated from the incubation mixture 4-5 polypeptides, of which the largest one with an apparent molecular weight of 58,000 corresponded to cytochrome P-450 MC-2.	Methylcholanthrene	78-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	249-265
3778507-1	1986	A pulmonary cytochrome P-450 was purified from lung microsomes of 3-methylcholanthrene (MC)-treated rats by immunoaffinity chromatography using a monoclonal antibody to MC-induced rat liver cytochrome P-450.	Methylcholanthrene	88-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
3778507-1	1986	A pulmonary cytochrome P-450 was purified from lung microsomes of 3-methylcholanthrene (MC)-treated rats by immunoaffinity chromatography using a monoclonal antibody to MC-induced rat liver cytochrome P-450.	Methylcholanthrene	169-171	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
3778507-1	1986	A pulmonary cytochrome P-450 was purified from lung microsomes of 3-methylcholanthrene (MC)-treated rats by immunoaffinity chromatography using a monoclonal antibody to MC-induced rat liver cytochrome P-450.	Methylcholanthrene	169-171	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	190-206
3778507-2	1986	The isolated pulmonary cytochrome P-450 was MC-inducible and had an apparent molecular weight of 57 kD on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE).	Methylcholanthrene	44-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
2875791-1	1986	Augmentation of specific chemoimmunotherapy by daily, intrasplenic injection of interleukin-2 (IL-2) was assessed in a methylcholanthrene (MCA)-induced fibrosarcoma model in C3H/HeJ mice.	Methylcholanthrene	119-137	interleukin 2	Mus musculus	80-93
3778507-3	1986	The molecular weight, as well as the NH2-terminal sequence of the first nine amino acids of the pulmonary cytochrome P-450, was identical to that of an epitopically related MC-induced rat liver cytochrome P-450.	Methylcholanthrene	173-175	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
2875791-1	1986	Augmentation of specific chemoimmunotherapy by daily, intrasplenic injection of interleukin-2 (IL-2) was assessed in a methylcholanthrene (MCA)-induced fibrosarcoma model in C3H/HeJ mice.	Methylcholanthrene	119-137	interleukin 2	Mus musculus	95-99
3778507-3	1986	The molecular weight, as well as the NH2-terminal sequence of the first nine amino acids of the pulmonary cytochrome P-450, was identical to that of an epitopically related MC-induced rat liver cytochrome P-450.	Methylcholanthrene	173-175	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	194-210
2875791-1	1986	Augmentation of specific chemoimmunotherapy by daily, intrasplenic injection of interleukin-2 (IL-2) was assessed in a methylcholanthrene (MCA)-induced fibrosarcoma model in C3H/HeJ mice.	Methylcholanthrene	139-142	interleukin 2	Mus musculus	80-93
2875791-1	1986	Augmentation of specific chemoimmunotherapy by daily, intrasplenic injection of interleukin-2 (IL-2) was assessed in a methylcholanthrene (MCA)-induced fibrosarcoma model in C3H/HeJ mice.	Methylcholanthrene	139-142	interleukin 2	Mus musculus	95-99
3778507-5	1986	Treatment of rats with MC, therefore, induces a pulmonary cytochrome P-450 which is structurally identical to the MC-induced hepatic enzyme by several criteria.	Methylcholanthrene	23-25	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
3756914-2	1986	The distribution of total 3-methylcholanthrene (3-MC)-associated radioactivity in maternal, placental, and fetal tissues of beta-naphthoflavone-pretreated pregnant B6 and D2 mice was determined up to 12 h after p.o.	Methylcholanthrene	48-52	defensin beta 2	Mus musculus	164-173
3756916-6	1986	Complete tumor regression was observed in the methylcholanthrene induced tumor bearing mice in 90% of the mice treated with TNF (100 micrograms/kg), 67% treated with TNF (50 micrograms/kg), and 34% treated with TNF (25 micrograms/kg).	Methylcholanthrene	46-64	tumor necrosis factor	Mus musculus	124-127
3756916-6	1986	Complete tumor regression was observed in the methylcholanthrene induced tumor bearing mice in 90% of the mice treated with TNF (100 micrograms/kg), 67% treated with TNF (50 micrograms/kg), and 34% treated with TNF (25 micrograms/kg).	Methylcholanthrene	46-64	tumor necrosis factor	Mus musculus	166-169
3756916-6	1986	Complete tumor regression was observed in the methylcholanthrene induced tumor bearing mice in 90% of the mice treated with TNF (100 micrograms/kg), 67% treated with TNF (50 micrograms/kg), and 34% treated with TNF (25 micrograms/kg).	Methylcholanthrene	46-64	tumor necrosis factor	Mus musculus	166-169
3464941-1	1986	The synthesis of cytochrome P-450c is induced remarkably in cultured cells as well as animal tissues in response to added chemicals such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzodioxin.	Methylcholanthrene	140-160	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	17-34
3769142-0	1986	High frequency of c-K-ras activation in 3-methylcholanthrene-induced mouse thymomas.	Methylcholanthrene	40-60	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	18-25
3098723-0	1986	Expression of H-2 antigens and inducibility of antitumor immune responses in various tumor cell clones established from methylcholanthrene-induced fibrosarcomas.	Methylcholanthrene	120-138	histocompatibility-2, MHC	Mus musculus	14-17
3768039-6	1986	The aminoazo dye-induced enzymes differ in their substrate specificities from those induced with 3-methylcholanthrene or phenobarbital, and the induced enzyme was identified to be cytochrome P-448H, as determined by an enzyme-linked immunosorbent assay and immunoblotting with use of anti-cytochrome P-448 monoclonal antibodies.	Methylcholanthrene	97-117	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	180-196
3780371-4	1986	The intron locations in these genes are identical to those in the genes for rat cytochrome P-450b/e, members of the other phenobarbital-inducible subfamily, but completely different from those in the 3-methylcholanthrene-inducible cytochrome P-450 genes.	Methylcholanthrene	200-220	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-97
3551427-9	1986	Patients on both acute and chronic therapy with insulin show T-cell sensitization to MC insulin and its components.	Methylcholanthrene	85-87	insulin	Homo sapiens	48-55
3551427-9	1986	Patients on both acute and chronic therapy with insulin show T-cell sensitization to MC insulin and its components.	Methylcholanthrene	85-87	insulin	Homo sapiens	88-95
3094515-0	1986	Purification and characterization of a form of cytochrome P-450 with high specificity for aflatoxin B1 from 3-methylcholanthrene-treated hamster liver.	Methylcholanthrene	108-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
3094515-1	1986	A form of cytochrome P-450 highly active in inducing mutagenicity of aflatoxin B1 was purified to a specific content of 15.1 nmol/mg of protein from 3-methylcholanthrene-treated hamster liver.	Methylcholanthrene	149-169	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	10-26
3094515-2	1986	This species of cytochrome P-450, having its absorption maximum at 448.5 nm in carbon monoxide-complex of reduced form and low spin ferric ion, is of molecular weight of 56,000 and distinctly different in physicochemical and catalytic properties from major forms of cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rat liver.	Methylcholanthrene	315-335	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
3094931-0	1986	Polychlorinated biphenyls, classified as either phenobarbital- or 3-methylcholanthrene-type inducers of cytochrome P-450, are both hepatic tumor promoters in diethylnitrosamine-initiated rats.	Methylcholanthrene	66-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
2425856-6	1986	Antibodies against PB-cytochrome P-450 inhibited by 50-70% the benzphetamine-N-demethylase and aldrin-epoxidase activities, whereas the antibodies to methylcholanthrene-induced cytochrome P-450 were fairly ineffective.	Methylcholanthrene	150-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	22-38
3800318-6	1986	It is concluded that the metabolic activation of 2-naphthylamine proceeds via N-hydroxylation which is preferentially catalysed by the 3-methylcholanthrene inducible forms of cytochrome P-450, whereas ring-hydroxylation appears to be a deactivation pathway.	Methylcholanthrene	135-155	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	175-191
3528287-4	1986	In a single cell agarose assay, MC of Mac-1-deficient patients formed fewer effector-target cell conjugates in the presence of specific anti-HSV antibody.	Methylcholanthrene	32-34	integrin subunit alpha M	Homo sapiens	38-43
3331675-1	1986	In accordance with previous studies the bioactivation of 2-amino-3-methylimidazo(4,5-f)quinoline (IQ) to mutagens in the Ames test was preferentially catalysed by the 3-methyl-cholanthrene-induced cytochromes P-448, in contrast to the phenobarbital-induced forms of the cytochrome.	Methylcholanthrene	167-188	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	209-214
3768313-3	1986	The major hepatic microsomal cytochrome P-450 forms inducible by PB and 3-MC, respectively designated P-450s PB-4 and BNF-B, were shown to be the principal polypeptides labeled by [125I]TID in the correspondingly induced microsomes.	Methylcholanthrene	72-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
3099765-7	1986	Induction of cytochrome P-450 by 3-methylcholanthrene and beta-naphthoflavone increased cytochrome P-450 content and aryl-hydrocarbon hydroxylase activity by 2-fold in the cortex and medulla, and this correlated with a 2-fold increase in arachidonic acid metabolites via the cytochrome P-450 pathway.	Methylcholanthrene	33-53	cytochrome P-450	Oryctolagus cuniculus	13-29
3099765-7	1986	Induction of cytochrome P-450 by 3-methylcholanthrene and beta-naphthoflavone increased cytochrome P-450 content and aryl-hydrocarbon hydroxylase activity by 2-fold in the cortex and medulla, and this correlated with a 2-fold increase in arachidonic acid metabolites via the cytochrome P-450 pathway.	Methylcholanthrene	33-53	cytochrome P-450	Oryctolagus cuniculus	88-104
3099765-7	1986	Induction of cytochrome P-450 by 3-methylcholanthrene and beta-naphthoflavone increased cytochrome P-450 content and aryl-hydrocarbon hydroxylase activity by 2-fold in the cortex and medulla, and this correlated with a 2-fold increase in arachidonic acid metabolites via the cytochrome P-450 pathway.	Methylcholanthrene	33-53	cytochrome P-450	Oryctolagus cuniculus	88-104
3099767-4	1986	An endogenous substrate has not yet been identified for the p-nitrophenol (3-methylcholanthrene-inducible) UDP-glucuronosyltransferase.	Methylcholanthrene	75-95	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	107-134
3488741-0	1986	Induction of cytochrome P-450 and related drug-metabolizing activities in the livers of different rodent species by 2-acetylaminofluorene or by 3-methylcholanthrene.	Methylcholanthrene	144-164	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3488741-8	1986	Thus, it is quite clear that in quantitative terms the hepatic microsomal cytochrome P-450-catalyzed activities and their inducibility by 2-acetylaminofluorene or 3-methylcholanthrene in the male Sprague-Dawley rat are not representative for other rodent species or even for the female of the same species.	Methylcholanthrene	163-183	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
3758926-4	1986	The patients treated with MC insulin developed significant levels of insulin antibodies, however, at lower levels and appearing later in comparison to those with beef NPH.	Methylcholanthrene	26-28	insulin	Homo sapiens	29-36
3758926-4	1986	The patients treated with MC insulin developed significant levels of insulin antibodies, however, at lower levels and appearing later in comparison to those with beef NPH.	Methylcholanthrene	26-28	insulin	Homo sapiens	69-76
3758926-8	1986	While in the MC-treated patients there was some positive correlation between the insulin dose and the level of Abl no significant correlation was found between the diabetes control and insulin antibody titers in both groups of patients.	Methylcholanthrene	13-15	insulin	Homo sapiens	81-88
3096979-0	1986	Pulmonary microsomal cytochrome P-450 from 3-methylcholanthrene-treated hamsters: purification, characterization, and metabolism of benzo(a)pyrene.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	32-37
3096979-1	1986	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 165-fold from lung microsomes of 3-methylcholanthrene (MC)-treated hamsters.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-42
3096979-1	1986	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 165-fold from lung microsomes of 3-methylcholanthrene (MC)-treated hamsters.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	54-61
3096979-1	1986	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 165-fold from lung microsomes of 3-methylcholanthrene (MC)-treated hamsters.	Methylcholanthrene	59-61	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-42
2425856-6	1986	Antibodies against PB-cytochrome P-450 inhibited by 50-70% the benzphetamine-N-demethylase and aldrin-epoxidase activities, whereas the antibodies to methylcholanthrene-induced cytochrome P-450 were fairly ineffective.	Methylcholanthrene	150-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	177-193
3011254-1	1986	In laboratory animals and in mouse hepatoma cells in culture the Ah receptor previously has been shown to mediate induction of aryl hydrocarbon hydroxylase (cytochrome P1-450) by 3-methylcholanthrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds.	Methylcholanthrene	179-199	aryl-hydrocarbon receptor	Mus musculus	65-76
3011254-1	1986	In laboratory animals and in mouse hepatoma cells in culture the Ah receptor previously has been shown to mediate induction of aryl hydrocarbon hydroxylase (cytochrome P1-450) by 3-methylcholanthrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds.	Methylcholanthrene	179-199	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	127-155
3013548-5	1986	The other family has cDNA inserts for the major 3-methylcholanthrene-inducible species, P-450c and P-450d.	Methylcholanthrene	48-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	88-105
3718496-6	1986	Xenobiotics such as phenobarbital, 3-methylcholanthrene, and trans-stilbene oxide induce rat liver GSH S-transferase activities, especially the Ya- and Yb-subunit containing isozymes.	Methylcholanthrene	35-55	glutathione synthetase	Rattus norvegicus	99-104
3707616-3	1986	In the pretreatment with 3MC, the administration of CHCl3 brought about a marked decrease in the content to 24% of control after 12 hr, while CCl4 reduced the content only to one-half of control.	Methylcholanthrene	25-28	C-C motif chemokine ligand 4	Rattus norvegicus	142-146
3707616-7	1986	These findings indicate that cytochrome P450 species induced with 3MC as well as PB are highly susceptible to CHCl3 intoxication, whereas the administration of CCl4 depletes the PB-induced species without affecting the 3MC-induced species.	Methylcholanthrene	219-222	C-C motif chemokine ligand 4	Rattus norvegicus	160-164
3753450-0	1986	Purification and characterization of a previously unreported form of cytochrome P-448 from the liver of 3-methylcholanthrene-pretreated rats.	Methylcholanthrene	104-124	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	69-85
3753450-1	1986	At least four hepatic isoenzymes of cytochrome P-450 were purified and characterized from rats treated with 3-methylcholanthrene.	Methylcholanthrene	108-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	36-52
3753450-4	1986	Cytochrome P-450 MC-B has a minimum Mr of 53,000, a CO-reduced spectral maximum at 448 nm, a Soret maximum of 417 nm in the absolute oxidized spectrum and a pattern of substrate preferences that differs from those of the other methylcholanthrene-induced forms.	Methylcholanthrene	227-245	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
2872200-10	1986	However, they differed in their basal ALDH activities and in ALDH inducibility by 3-methylcholanthrene, benzo(a)pyrene, and phenobarbital.	Methylcholanthrene	82-102	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	61-65
2422427-1	1986	In vivo treatment of randombred Swiss Webster mice with polyriboinosinic-polyribocytidylic acid (poly l X poly C) inhibited the induction of cytochrome P-450"s by both 3-methylcholanthrene [(MCA) CAS: 56-49-5] and phenobarbitol [(PB) CAS: 50-06-6].	Methylcholanthrene	168-188	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	141-157
3729978-1	1986	Twelve homologous and regioisomeric pyridylalkanamides were examined spectrally for their binding affinity to cytochrome P-450 in phenobarbital- and 3-methylcholanthrene-induced rat liver microsomes.	Methylcholanthrene	149-169	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	110-126
3957930-4	1986	Microsomes from 3-methylcholanthrene-treated rats and cytochrome P-450c in the reconstituted system form exclusively the diol expoxide-1 diastereomer, in which the benzylic hydroxyl group and oxirane oxygen are cis to each other, from the (+)-(3S,4S)-dihydrodiol.	Methylcholanthrene	16-36	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	54-71
3083888-0	1986	[Cytochrome P-450 isoforms in the liver of rats treated with phenobarbital, 3-methylcholanthrene and Aroclor 1254 studied by monoclonal antibodies].	Methylcholanthrene	76-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	1-17
3004700-1	1986	We recently reported trophic response of transplantable mouse colon cancer cells (MC-26) to pentagastrin, in vivo, and demonstrated gastrin receptors on MC-26 cells, in vitro.	Methylcholanthrene	82-84	gastrin	Mus musculus	97-104
3004700-2	1986	In the present study, growth of MC-26 cells in mice, in response to pentagastrin, was studied in relation to binding kinetics and capacity of gastrin receptor.	Methylcholanthrene	32-34	gastrin	Mus musculus	73-80
3085962-8	1986	The data presented give direct proof that HCB exemplifies an individual chemical compound which is able to initiate the synthesis of both PB-form and MC-form of the cytochrome P-450.	Methylcholanthrene	150-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
3515163-4	1986	MC pretreatment decreased maximum levels of 2AA mutagenicity and increased maximum levels of BAP mutagenicity mediated by S9 from both species.	Methylcholanthrene	0-2	prohibitin 2	Rattus norvegicus	93-96
3515163-6	1986	A similar alteration in the pattern of dependence of BAP mutagenicity on the concentration of S9 protein was also observed with S9 from MC-pretreated toadfish.	Methylcholanthrene	136-138	prohibitin 2	Rattus norvegicus	53-56
3515163-8	1986	The changes in the pattern of dependence of 2AA and BAP mutagenicities on the concentration of S9 protein effected by MC pretreatment of toadfish were confirmed in a separate group of experiments.	Methylcholanthrene	118-120	prohibitin 2	Rattus norvegicus	52-55
3515163-9	1986	A third group of experiments was designed to examine the effects of alpha-naphthoflavone (ANF) on the mutagenicities of 2AA and BAP mediated by UI and MC S9 from toadfish.	Methylcholanthrene	151-153	prohibitin 2	Rattus norvegicus	128-131
3515163-10	1986	Although ANF did not affect the 2AA mutagenicity mediated by UI S9, a significant decrease in 2AA mutagenicity and a significant increase in BAP mutagenicity mediated by MC S9 and a significant decrease in BAP mutagenicity mediated by UI S9 were observed.	Methylcholanthrene	170-172	prohibitin 2	Rattus norvegicus	141-144
3517618-1	1986	The rat 3-methylcholanthrene-inducible family of liver cytochromes P-450 contains two proteins (P-450c and P-450d) that are immunochemically related, possess 68% total sequence homology, and are induced by a number of toxic or carcinogenic compounds.	Methylcholanthrene	8-28	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	96-113
3517618-6	1986	We conclude that, in man, there is a cytochrome P-450 family composed of two isozymes (HLc and HLd) that are immunochemically and structurally related to the 3-methylcholanthrene-inducible family observed in several other species.	Methylcholanthrene	158-178	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	37-53
3715917-2	1986	Corticosterone inhibited aryl hydrocarbon hydroxylase (AHH) activity nonlinearly in hepatic microsomes from uninduced, phenobarbital-induced, or 3-methylcholanthrene-induced rats.	Methylcholanthrene	145-165	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	25-53
3715917-2	1986	Corticosterone inhibited aryl hydrocarbon hydroxylase (AHH) activity nonlinearly in hepatic microsomes from uninduced, phenobarbital-induced, or 3-methylcholanthrene-induced rats.	Methylcholanthrene	145-165	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	55-58
3754327-3	1986	On the basis of experiments involving cell-free translation and hybridization to the cloned probe, it was shown that prototype inducers of cytochrome P-450 such as phenobarbitone and 3-methylcholanthrene as well as inhibitors such as CoCl2 and 3-amino-1,2,4-triazole enhanced the glutathione transferase (Ya+Yc) messenger RNA contents in rat liver.	Methylcholanthrene	183-203	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
3754327-3	1986	On the basis of experiments involving cell-free translation and hybridization to the cloned probe, it was shown that prototype inducers of cytochrome P-450 such as phenobarbitone and 3-methylcholanthrene as well as inhibitors such as CoCl2 and 3-amino-1,2,4-triazole enhanced the glutathione transferase (Ya+Yc) messenger RNA contents in rat liver.	Methylcholanthrene	183-203	glutathione S-transferase alpha 4	Rattus norvegicus	280-303
3964682-3	1986	The oxidation-reduction potentials for the rabbit liver microsomal cytochrome P-450 induced by 3-methylcholanthrene and the mitochondrial cytochrome for steroid 11 beta-hydroxylation were found as -360 and -286 mV, respectively.	Methylcholanthrene	95-115	cytochrome P-450	Oryctolagus cuniculus	67-83
3717918-7	1986	Phenobarbital is a more strong and selective inductor of this form of cytochrome P-450 than 3-methylcholanthrene.	Methylcholanthrene	92-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3731348-0	1986	Different depressing effects of lentinan on the increases of cytochrome P-450-dependent monooxygenase activities induced in mice by phenobarbital and by 3-methylcholanthrene.	Methylcholanthrene	153-173	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
2856069-5	1986	This report shows for the first time that AHH induction by 3-methylcholanthrene can occur in the Ahd phenotype mouse.	Methylcholanthrene	59-79	aryl-hydrocarbon receptor	Mus musculus	42-45
3086298-0	1986	Effects of phenobarbital, 3-methylcholanthrene and polychlorinated biphenyls on sex-specific forms of cytochrome P-450 in liver microsomes of rats.	Methylcholanthrene	26-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	102-118
3086298-1	1986	The effects of treatment with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyls (PCB) on the amounts of sex-specific forms of cytochrome P-450, namely P-450-male and P-450-female, in male and female rats were studied.	Methylcholanthrene	45-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
3086298-2	1986	Although treatment with phenobarbital, 3-methylcholanthrene or PCB markedly increased the total amount of hepatic cytochrome P-450, P-450-male and P-450-female were rather decreased or not significantly changed.	Methylcholanthrene	39-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
3952654-11	1986	The effects of gastrin treatment on the growth of MC-26 colon cancer persist after treatment is discontinued; mice with tumors that were treated with gastrin for either 7 or 14 days and in which the treatment was stopped were all dead by 35 or 28 days, respectively, after the end of treatment.	Methylcholanthrene	50-52	gastrin	Mus musculus	15-22
3007551-1	1986	Cytochrome P-450 from rat liver microsomes treated with phenobarbital (PB) was separated into six fractions, as was cytochrome P-450 treated with 3-methylcholanthrene (MC), by high-performance liquid chromatography (HPLC) with an anion-exchange column.	Methylcholanthrene	168-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3007551-1	1986	Cytochrome P-450 from rat liver microsomes treated with phenobarbital (PB) was separated into six fractions, as was cytochrome P-450 treated with 3-methylcholanthrene (MC), by high-performance liquid chromatography (HPLC) with an anion-exchange column.	Methylcholanthrene	168-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	116-132
3007551-2	1986	PB and MC induced three forms and one form of cytochrome P-450, respectively.	Methylcholanthrene	7-9	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
3002384-0	1986	Cytochrome P-450 induction by 3-methylcholanthrene and its antagonism by 2,2-dimethyl-5-t-butyl-1,3-benzodioxole.	Methylcholanthrene	30-50	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
3002384-1	1986	Previous studies in this laboratory have shown 2,2-dimethyl-5-t-butyl-1,3-benzodioxole (DBBD) to antagonize 3-methylcholanthrene induction of cytochrome P-450 in Dub:ICR mice yet have no effect on phenobarbital induction.	Methylcholanthrene	108-128	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
3002384-3	1986	The hypothesis that DBBD, although not a cytochrome P-450 inducer, competes with 3-methylcholanthrene for binding to the Ah receptor was tested.	Methylcholanthrene	81-101	aryl-hydrocarbon receptor	Mus musculus	121-132
3002384-6	1986	However, in in vivo experiments, DBBD treatment of Dub:ICR mice caused Ah receptor depression at 6 and 24 hr with complete recovery in between, while 3-methylcholanthrene treatment caused a 2-fold Ah receptor reduction at 2 hr followed by complete recovery after 12 hr.	Methylcholanthrene	150-170	aryl-hydrocarbon receptor	Mus musculus	197-208
3002384-7	1986	When 3-methylcholanthrene and DBBD were coadministered, the depression of the Ah receptor was additive.	Methylcholanthrene	5-25	aryl-hydrocarbon receptor	Mus musculus	78-89
3002384-8	1986	DBBD-pretreated mice had a 2.25-fold reduction in Ah receptor level, effectively blocking the ability of 3-methylcholanthrene to increase the cytochrome P-450 content and either benzo[a]pyrene hydroxylase or ethoxyresorufin O-deethylase activities.	Methylcholanthrene	105-125	aryl-hydrocarbon receptor	Mus musculus	50-61
3002384-8	1986	DBBD-pretreated mice had a 2.25-fold reduction in Ah receptor level, effectively blocking the ability of 3-methylcholanthrene to increase the cytochrome P-450 content and either benzo[a]pyrene hydroxylase or ethoxyresorufin O-deethylase activities.	Methylcholanthrene	105-125	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
3002384-9	1986	Sodium dodecyl sulfate-polyacrylamide gel electrophoresis confirmed that 3-methylcholanthrene induction of cytochrome P-450 was inhibited by DBBD pretreatment.	Methylcholanthrene	73-93	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	107-123
3002384-10	1986	Hence, although DBBD does not displace 3-methylcholanthrene from the Ah receptor in vitro, it does antagonize 3-methylcholanthrene induction of cytochrome P-450 and also reduces the amount of available receptor in vivo.	Methylcholanthrene	110-130	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
2422427-1	1986	In vivo treatment of randombred Swiss Webster mice with polyriboinosinic-polyribocytidylic acid (poly l X poly C) inhibited the induction of cytochrome P-450"s by both 3-methylcholanthrene [(MCA) CAS: 56-49-5] and phenobarbitol [(PB) CAS: 50-06-6].	Methylcholanthrene	191-194	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	141-157
3788368-5	1986	The 35 000-Mr polypeptide which is normally absent found in the hnRNP particles of the young rats prior to the 11th day of life appears on the 10th day after 24 h 3-MC exposition.	Methylcholanthrene	163-167	heterogeneous nuclear ribonucleoprotein A2/B1	Rattus norvegicus	64-69
3788368-8	1986	Thus, the apparent accelerating effect of 3-MC on the liver development is also valid at the level of hnRNP particles.	Methylcholanthrene	42-46	heterogeneous nuclear ribonucleoprotein A2/B1	Rattus norvegicus	102-107
3532714-0	1986	H-2 modulation of aryl hydrocarbon hydroxylase induction and the mutagenicity of benzo(a)pyrene after 3-methylcholanthrene treatment.	Methylcholanthrene	102-122	homeotic protein knotted-1	Zea mays	0-3
3103934-10	1987	The kinetic characteristics of BP metabolism by UT-microsomes are highly sensitive to the presence of very small but variable amounts (2-25 pmol/mg) of the very active cytochrome P-450c, which is the predominant form in MC-microsomes.	Methylcholanthrene	220-222	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	168-185
3533258-1	1986	Spleen cells of BALB/c mice hyperimmunized with a transplantable methylcholanthrene-induced sarcoma Meth A (Meth A-Im-SPL) inhibited the growth of Meth A tumor in vivo in a tumor neutralizing test.	Methylcholanthrene	65-83	plasma serotonin level	Mus musculus	118-121
3942812-1	1986	Simple and informative method for the elucidation of de novo synthesized forms of microsomal cytochrome P-448 induced by 3-methylcholanthrene and 2,3,7,8-tetrachlordibenzo-p-dioxine has been developed.	Methylcholanthrene	121-141	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	93-109
3942812-3	1986	At least two forms of cytochrome P-448 (with molecular weight of 56000 and 53000) were shown to be de novo synthesized under the influence of 3-methylcholanthrene and 2,3,7,8-tetrachlodbibenzo-p-dioxine.	Methylcholanthrene	142-162	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	22-38
3530494-2	1986	The steroid-secreting cells, i.e., Leydig cells of the testis, and theca interna cells, interstitial gland cells, and corpus luteum cells of the ovary of 3-methylcholanthrene-treated mice show a strong positive reaction to the antiserum against, hepatic microsomal cytochrome P-450, of liver which is the terminal oxidase of the drug-metabolizing enzyme complex.	Methylcholanthrene	154-174	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	265-281
3488924-0	1986	Local treatment with human recombinant interleukin 2 inhibits growth of MC-induced sarcomas in syngeneic mice.	Methylcholanthrene	72-74	interleukin 2	Homo sapiens	39-52
3488924-1	1986	In previous communications we have demonstrated that crude rat interleukin 2 and partially purified mouse interleukin 2 were capable of inhibiting growth of transplantable, MC-induced mouse sarcomas in syngeneic recipients.	Methylcholanthrene	173-175	interleukin 2	Rattus norvegicus	63-76
3488924-1	1986	In previous communications we have demonstrated that crude rat interleukin 2 and partially purified mouse interleukin 2 were capable of inhibiting growth of transplantable, MC-induced mouse sarcomas in syngeneic recipients.	Methylcholanthrene	173-175	interleukin 2	Mus musculus	106-119
3492396-3	1986	The immunotherapeutic effect of human recombinant interleukin 2 was examined with a panel of MC-induced murine sarcomas carrying individual tumour-specific transplantation antigens.	Methylcholanthrene	93-95	interleukin 2	Homo sapiens	50-63
3492396-6	1986	Since the IL-2-sensitive and IL-2-resistant sarcomas were induced with MC in mice of identical genotype and share most of their characteristics, they represent a useful model for investigation of structural target cell determinants and functional target cell properties responsible for the sensitivity of tumours to the immunotherapeutic effects of IL-2.	Methylcholanthrene	71-73	interleukin 2	Mus musculus	10-14
3492396-6	1986	Since the IL-2-sensitive and IL-2-resistant sarcomas were induced with MC in mice of identical genotype and share most of their characteristics, they represent a useful model for investigation of structural target cell determinants and functional target cell properties responsible for the sensitivity of tumours to the immunotherapeutic effects of IL-2.	Methylcholanthrene	71-73	interleukin 2	Mus musculus	29-33
3492396-6	1986	Since the IL-2-sensitive and IL-2-resistant sarcomas were induced with MC in mice of identical genotype and share most of their characteristics, they represent a useful model for investigation of structural target cell determinants and functional target cell properties responsible for the sensitivity of tumours to the immunotherapeutic effects of IL-2.	Methylcholanthrene	71-73	interleukin 2	Mus musculus	29-33
3758464-1	1986	The activities of cytochrome P-450-dependent monooxygenases has been investigated in the liver microsomes of newborn rats (3-16 days after birth) induced with PB or 3-MC.	Methylcholanthrene	165-169	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	18-34
3758464-2	1986	It has been shown that the induction by PB and 3-MC results in the increase of both the total amount of cytochrome P-450 as determined by the CO-reduced spectrum and the amount of induced forms P-450b/e and P-450c respectively.	Methylcholanthrene	47-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
3758464-2	1986	It has been shown that the induction by PB and 3-MC results in the increase of both the total amount of cytochrome P-450 as determined by the CO-reduced spectrum and the amount of induced forms P-450b/e and P-450c respectively.	Methylcholanthrene	47-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	194-200
3758464-2	1986	It has been shown that the induction by PB and 3-MC results in the increase of both the total amount of cytochrome P-450 as determined by the CO-reduced spectrum and the amount of induced forms P-450b/e and P-450c respectively.	Methylcholanthrene	47-51	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	207-213
3758464-3	1986	In the course of induction of the specific forms of cytochrome P-450 BP-hydroxylase and 7-ER-O-deethylase activities increased at 3-MC-induction, while BPh-N-demethylase and BP-hydroxylase increased at PB-induction.	Methylcholanthrene	130-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
3758464-7	1986	This fact shows the higher catalytic activity of this cytochrome P-450 in the neonates compared to similar characteristics of P-450c in the 3-MC-induced microsomes.	Methylcholanthrene	140-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
3758464-7	1986	This fact shows the higher catalytic activity of this cytochrome P-450 in the neonates compared to similar characteristics of P-450c in the 3-MC-induced microsomes.	Methylcholanthrene	140-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	126-132
3942007-3	1986	Preincubation of 3-methylcholanthrene (3-MC)-pretreated rat liver microsomes with chrysotile depresses the overall metabolism of [G-3H]benzo[a]pyrene (BaP).	Methylcholanthrene	17-37	prohibitin 2	Rattus norvegicus	151-154
3942007-3	1986	Preincubation of 3-methylcholanthrene (3-MC)-pretreated rat liver microsomes with chrysotile depresses the overall metabolism of [G-3H]benzo[a]pyrene (BaP).	Methylcholanthrene	39-43	prohibitin 2	Rattus norvegicus	151-154
4084302-2	1985	The 3-MeO-AAB-induced cytochrome P-450 (3-MeO-AAB-P-450) was examined for the molecular character by immuno-Western blotting using monoclonal antibody to 3-methylcholanthrene-induced cytochrome P-448 (P-448H; m.w.	Methylcholanthrene	154-174	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	183-199
3935115-6	1985	The P-450 hemoproteins involved primarily in both the NADH- and NADPH-supported deethylation of NP are the P1-450 type, i.e. they are markedly induced by MC and inhibited by alpha-napthoflavone.	Methylcholanthrene	154-156	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	107-113
4083893-0	1985	Induction of specific cytochrome P-450 isozymes by methylenedioxyphenyl compounds and antagonism by 3-methylcholanthrene.	Methylcholanthrene	100-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
4083893-9	1985	They are intensified by coadministration of 3-MC with BD and may represent either modified isozyme-metabolite adducts or degradation products of P-450d.	Methylcholanthrene	44-48	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	145-151
4083893-14	1985	Coadministration of 3-MC with BD blocked induction of P-450b by 80% and produced a similar repression of its translatable mRNA.	Methylcholanthrene	20-24	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	54-60
4083893-15	1985	This finding indicates that 3-MC type inducers not only induce certain cytochrome P-450 isozymes, but also repress synthesis of other isozymes.	Methylcholanthrene	28-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
2416310-1	1985	The epitope-specific cytochrome P-450 content of animal livers was analysed by radioimmunoassay using a panel of seven monoclonal antibodies (MAbs) made to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	158-178	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
2416310-1	1985	The epitope-specific cytochrome P-450 content of animal livers was analysed by radioimmunoassay using a panel of seven monoclonal antibodies (MAbs) made to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	158-178	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	197-213
2413863-11	1985	Induction of cytochrome P-450 by phenobarbital (PB) and 3-methylcholanthrene (MC) under fed and fasted conditions was also investigated in male and female rats.	Methylcholanthrene	56-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2413863-11	1985	Induction of cytochrome P-450 by phenobarbital (PB) and 3-methylcholanthrene (MC) under fed and fasted conditions was also investigated in male and female rats.	Methylcholanthrene	78-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3935092-1	1985	Incubation of 14C-labeled 3,4,3",4"-tetrachlorobiphenyl (TCB) with a reconstituted monooxygenase system containing cytochrome P-450 isolated from 3-methylcholanthrene (MC)-treated rats caused an increase in incorporation of radioactivity to added rat erythrocytes and resulted in covalent binding of reactive metabolites to hemoglobin.	Methylcholanthrene	146-166	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
3935092-1	1985	Incubation of 14C-labeled 3,4,3",4"-tetrachlorobiphenyl (TCB) with a reconstituted monooxygenase system containing cytochrome P-450 isolated from 3-methylcholanthrene (MC)-treated rats caused an increase in incorporation of radioactivity to added rat erythrocytes and resulted in covalent binding of reactive metabolites to hemoglobin.	Methylcholanthrene	168-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
2992769-1	1985	Fusion products of spleen cells of W/FuDp rats immunized with a methylcholanthrene-induced BALB/c sarcoma, CA-2, and mouse myeloma cells were screened in an attempt to identify a monoclonal antibody defining the individually distinct tumor-specific transplantation antigen of CA-2.	Methylcholanthrene	64-82	carbonic anhydrase 2	Rattus norvegicus	91-111
2996532-1	1985	Sonic disrupted mitoplasts from 3-methylcholanthrene (MCA) treated rats can catalyze the formation of benzo(a)pyrene (BaP) adducts with calf thymus DNA in the presence of an NADPH generating system.	Methylcholanthrene	32-52	prohibitin 2	Rattus norvegicus	118-121
2996532-1	1985	Sonic disrupted mitoplasts from 3-methylcholanthrene (MCA) treated rats can catalyze the formation of benzo(a)pyrene (BaP) adducts with calf thymus DNA in the presence of an NADPH generating system.	Methylcholanthrene	54-57	prohibitin 2	Rattus norvegicus	118-121
2994583-3	1985	A transplantable mouse colon adenocarcinoma cell line (MC-26) contains gastrin receptors; growth of MC-26 colon cancer in vivo is stimulated by pentagastrin (PG).	Methylcholanthrene	55-57	gastrin	Mus musculus	71-78
2994583-4	1985	The purpose of this study was to determine whether a gastrin-receptor antagonist, proglumide (PGL), would inhibit growth of MC-26 colon cancer and prolong survival in tumor-bearing mice.	Methylcholanthrene	124-127	gastrin	Mus musculus	53-60
2411220-0	1985	Transcriptional regulation of rat liver glutathione S-transferase genes by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	93-113	hematopoietic prostaglandin D synthase	Rattus norvegicus	40-65
2996791-3	1985	In in vivo experiments, treatment of C57BL/6 mice with 3-methylcholanthrene caused a 4-fold reduction in Ah receptor binding 2 h after i.p.	Methylcholanthrene	55-75	aryl-hydrocarbon receptor	Mus musculus	105-116
2408745-3	1985	The antigens expressed by the 3-methylcholanthrene-induced fibrosarcomas MCA-D, MCA-F, and MCA-2A fulfill the requirements of a TSTA; namely, immunization of syngeneic hosts with irradiated cells or soluble extracts engenders a tumor-specific immune response such that animals resist challenge with the same, but not another, tumor.	Methylcholanthrene	30-50	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	128-132
2863118-7	1985	Debrisoquine 4-hydroxylase activity was inducible by both 3-methylcholanthrene and phenobarbital in DA and Fischer rats.	Methylcholanthrene	58-78	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	0-26
4012798-0	1985	Foetal and neonatal development of cytochrome P-450 and cytochrome P-448 catalysed mixed function oxidases in the rat: induction by 3-methylcholanthrene.	Methylcholanthrene	132-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-72
4012798-1	1985	Benzphetamine N-demethylase (cytochrome P-450) and ethoxyresorufin O-deethylase activities (cytochrome P-448) were determined in the growing neonate and foetus of control and 3-methylcholanthrene-pretreated rats.	Methylcholanthrene	175-195	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-79
3873598-1	1985	Cytochrome P-450-dependent aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin O-deethylase activities of a cloned line of human lymphoblastoid AHH-1 cells are inhibited by a monoclonal antibody (MAb 1-7-1) prepared to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	225-245	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
3873598-1	1985	Cytochrome P-450-dependent aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin O-deethylase activities of a cloned line of human lymphoblastoid AHH-1 cells are inhibited by a monoclonal antibody (MAb 1-7-1) prepared to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	225-245	aryl hydrocarbon receptor repressor	Homo sapiens	57-60
3873598-1	1985	Cytochrome P-450-dependent aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin O-deethylase activities of a cloned line of human lymphoblastoid AHH-1 cells are inhibited by a monoclonal antibody (MAb 1-7-1) prepared to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	225-245	aryl hydrocarbon receptor repressor	Homo sapiens	148-151
3873598-1	1985	Cytochrome P-450-dependent aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin O-deethylase activities of a cloned line of human lymphoblastoid AHH-1 cells are inhibited by a monoclonal antibody (MAb 1-7-1) prepared to a 3-methylcholanthrene-induced rat liver cytochrome P-450.	Methylcholanthrene	225-245	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	264-280
4004253-4	1985	The results of these studies demonstrate that 3-methylcholanthrene does not significantly influence the transcription of the rat serum albumin gene, but does increase the transcription of the cytochrome P-450c gene.	Methylcholanthrene	46-66	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	192-209
4004253-10	1985	The mRNA coding for cytochrome P-450c was induced maximally in hepatic nuclei at 3 h following 3-methylcholanthrene administration.	Methylcholanthrene	95-115	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	20-37
4004253-11	1985	Maximal accumulation of cytochrome P-450c mRNA in hepatic cytosol has been previously shown to occur at approximately 15 h following 3-methylcholanthrene administration (Bresnick, E., Brosseau, M., Levin, W., Reik, L., Ryan, D. E., and Thomas, P. E. (1981) Proc.	Methylcholanthrene	133-153	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	24-41
4004255-0	1985	Kinetic isotope effects on cytochrome P-450-catalyzed oxidation reactions: full expression of the intrinsic isotope effect during the O-deethylation of 7-ethoxycoumarin by liver microsomes from 3-methylcholanthrene-induced hamsters.	Methylcholanthrene	194-214	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-43
4004255-3	1985	122-152, University Park Press, Baltimore] for the microsomal cytochrome P-448 system from 3-methylcholanthrene-induced hamster livers.	Methylcholanthrene	91-111	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	62-78
4004255-6	1985	The decrease in the rate of product formation, occurring as a consequence of deuterium substitution, resulted in a reduction in the quantity of substrate metabolized but was not accompanied by the change in regiospecificity observed in previous studies with a hepatic cytochrome P-448 isozyme purified from 3-methylcholanthrene-induced rats.	Methylcholanthrene	307-327	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	268-284
3921402-7	1985	However, characteristic of P-450 forms, the synthesis of these proteins was suppressed by 3-methylcholanthrene treatment.	Methylcholanthrene	90-110	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-32
3922372-0	1985	Different effects of cyanide on the activities of 7-ethoxycoumarin O-deethylation catalyzed by two forms of cytochrome P-450 purified from 3-methylcholanthrene-treated rats.	Methylcholanthrene	139-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-124
3922372-1	1985	The effect of cyanide on 7-ethoxycoumarin O-deethylation by two cytochrome P-450 isozymes obtained from 3-methylcholanthrene treated rat liver microsomes was investigated.	Methylcholanthrene	104-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
3985997-12	1985	These results suggest the following: NDMA demethylation is catalyzed by PB-induced cytochrome P-450 species (P450-PB) and MC-induced cytochrome P-450 species (P448-MC).	Methylcholanthrene	122-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	133-149
3986002-0	1985	Altered induction response of hepatic cytochrome P-450 to phenobarbital, 3-methylcholanthrene, and beta-naphthoflavone in organotin-treated animals.	Methylcholanthrene	73-93	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-54
3986002-1	1985	The effects of tricyclohexyltin hydroxide on the induction of cytochrome P-450 in liver by phenobarbital, 3-methylcholanthrene and beta-naphthoflavone were studied.	Methylcholanthrene	106-126	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-78
4024668-1	1985	The formation of ligand complexes between hepatic microsomal cytochrome P-450 and safrole, isosafrole and other methylenedioxyphenyl compounds was studied in vivo and in vitro in rats pretreated with either phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	224-244	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
3856417-1	1985	The effects of methylcholanthrene (MC) treatment of male rats on the regioselectivity of hydroxylation of prostaglandins E1 and E2 (PGE1 and PGE2) by liver microsomes, supplemented with NADPH or H2O2, was examined.	Methylcholanthrene	15-33	carboxylesterase 1C	Rattus norvegicus	121-145
3856417-1	1985	The effects of methylcholanthrene (MC) treatment of male rats on the regioselectivity of hydroxylation of prostaglandins E1 and E2 (PGE1 and PGE2) by liver microsomes, supplemented with NADPH or H2O2, was examined.	Methylcholanthrene	35-37	carboxylesterase 1C	Rattus norvegicus	121-145
3856417-12	1985	The above findings indicate that the high regioselectivity of hydroxylation of PGE1 and PGE2, resulting in the formation of 18-hydroxy-PGE1 and 18-hydroxy-PGE2, respectively, is catalyzed by P-450 isozyme(s) which are induced by MC, possibly by P-450c.	Methylcholanthrene	229-231	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	245-251
3995102-0	1985	[Isolation and characterization of multiple forms of cytochrome P-450 from liver microsomes of 3-methylcholanthrene-induced Wistar rats].	Methylcholanthrene	95-115	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
3868365-1	1985	A single intraperitoneal administration of 3-methylcholanthrene (3MC) or beta-naphthoflavone (BNF) increased aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (EROD) activities.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-142
3868365-1	1985	A single intraperitoneal administration of 3-methylcholanthrene (3MC) or beta-naphthoflavone (BNF) increased aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (EROD) activities.	Methylcholanthrene	65-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-142
3967341-13	1985	The results of this study suggest that the formation of phenolic and N-hydroxy metabolites of 2-FAA in both hepatic and mammary microsomes of lactating rats is catalyzed by similar form(s) of cytochrome P-450 induced by pretreatment with 3-MC or beta-NF.	Methylcholanthrene	238-242	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	192-208
3891197-3	1985	For example, rat liver has much greater microsomal benzo[a]pyrene (BP) hydroxylase (AHH) activity than lung, both in control rats and in rats pretreated with the enzyme inducer, 3-methylcholanthrene (3MC).	Methylcholanthrene	178-198	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	84-87
3891197-3	1985	For example, rat liver has much greater microsomal benzo[a]pyrene (BP) hydroxylase (AHH) activity than lung, both in control rats and in rats pretreated with the enzyme inducer, 3-methylcholanthrene (3MC).	Methylcholanthrene	200-203	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	84-87
2861016-1	1985	In vivo treatment of chicks, quail and rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylcholanthrene (MC) caused a dose-dependent increase in hepatic microsomal aryl hydrocarbon hydroxylase activity.	Methylcholanthrene	95-115	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	176-204
2861016-1	1985	In vivo treatment of chicks, quail and rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylcholanthrene (MC) caused a dose-dependent increase in hepatic microsomal aryl hydrocarbon hydroxylase activity.	Methylcholanthrene	117-119	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	176-204
3965304-0	1985	Catalytic activity of the membrane-bound methylcholanthrene-inducible cytochrome P-450.	Methylcholanthrene	41-59	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-86
3965304-1	1985	The benzopyrene hydroxylase activity of the methylcholanthrene-inducible form of cytochrome P-450 (P-448) has been studied in native and reconstituted liver microsomal membranes.	Methylcholanthrene	44-62	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	81-97
4043714-1	1985	Chromatofocusing between pH 7.4 and 5.0 was introduced as a final step for the resolution of multiple forms of cytochrome P-450 from control, phenobarbital and 3-methylcholanthrene-pretreated rat liver microsomal fractions.	Methylcholanthrene	160-180	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
4044306-2	1985	Immunoblot analyses performed prior to immunohistochemistry revealed the presence of a protein - possible equivalent to cytochrome P-450 found in the liver microsomes of MC-treated male rats - in the adrenal homogenate of MC-treated female mice.	Methylcholanthrene	170-172	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-136
4044306-2	1985	Immunoblot analyses performed prior to immunohistochemistry revealed the presence of a protein - possible equivalent to cytochrome P-450 found in the liver microsomes of MC-treated male rats - in the adrenal homogenate of MC-treated female mice.	Methylcholanthrene	222-224	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-136
3996731-2	1985	An excellent direct correlation (r = 0.95) has been observed between ethoxyresorufin O-deethylase and the metabolic activation of benzo[a]pyrene to mutagens when the fraction of cytochromes P-450 present as cytochrome P-448 was altered by the administration of phenobarbitone and 3-methylcholanthrene alone or in combination with 9-hydroxyellipticine.	Methylcholanthrene	280-300	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	207-223
3917507-5	1985	Inhibition by piperine of arylhydrocarbon hydroxylase (AHH) from 3-methylcholanthrene-treated rats was comparable to that observed with 7,8-benzoflavone.	Methylcholanthrene	65-85	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	26-53
3917507-5	1985	Inhibition by piperine of arylhydrocarbon hydroxylase (AHH) from 3-methylcholanthrene-treated rats was comparable to that observed with 7,8-benzoflavone.	Methylcholanthrene	65-85	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	55-58
3917507-6	1985	Piperine caused noncompetitive inhibition of hepatic microsomal AHH from the untreated and 3-methylcholanthrene-treated rats with a Ki of 30 microM which was close to the apparent Km of AHH observed in the controls.	Methylcholanthrene	91-111	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-67
3917507-6	1985	Piperine caused noncompetitive inhibition of hepatic microsomal AHH from the untreated and 3-methylcholanthrene-treated rats with a Ki of 30 microM which was close to the apparent Km of AHH observed in the controls.	Methylcholanthrene	91-111	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	186-189
3965924-4	1985	In cultures prepared from untreated rats or from rats treated with phenobarbital or with 3-methylcholanthrene, individual forms of cytochrome P-450 declined at markedly differing rates.	Methylcholanthrene	89-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
3965925-7	1985	Other ligands of the Ah receptor, namely 3-methylcholanthrene and beta-naphthoflavone, were inactive at the highest concentrations tested (10(-6) M).	Methylcholanthrene	41-61	aryl-hydrocarbon receptor	Mus musculus	21-32
3877941-6	1985	This is in contrast to the effect of the commonly used cytochrome P-450 inhibitor 7,8-benzoflavone, which inhibits the hepatic AHH of MC-treated rats and has no effects on the AHH of control or PB-treated rats.	Methylcholanthrene	134-136	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	127-130
4059325-3	1985	some flavones (maackiain acetate, flavanone, mollisacacidin, embinin, sciadopitysin) activated, while most of the tested compounds inhibited the MC-induced type of AHH.	Methylcholanthrene	145-147	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	164-167
3991787-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and noramidopyrine-methanesulfonate sodium (metamizol, Analgin) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Methylcholanthrene	34-54	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
3991787-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and noramidopyrine-methanesulfonate sodium (metamizol, Analgin) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Methylcholanthrene	34-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-81
3855567-7	1985	Of 3 thymomas in 6-month-old 3-methylcholanthrene-treated AKR mice, all expressed c-myb and 2 expressed c-myc.	Methylcholanthrene	29-49	myeloblastosis oncogene	Mus musculus	82-87
3920836-5	1985	PB, PCB and MC treatments enhanced the activity of enzymes involved in conjugation reactions, UDP-glucuronyltransferase and glutathione S-transferase, whereas the dietary manipulation and ethanol consumption produced no significant effect on these enzymes.	Methylcholanthrene	12-14	hematopoietic prostaglandin D synthase	Rattus norvegicus	124-149
6334605-3	1984	The nature of the cytochromes P-450 mediating AE, ECDE and AHH activities was analysed using monoclonal antibodies (MAb) made to the major 3-methylcholanthrene-induced cytochrome P-450 (MAb-MC) or phenobarbital-induced cytochrome P-450 (MAb-PB) from rat liver.	Methylcholanthrene	141-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	168-184
6334605-12	1984	The results show that the hepatoma cells examined express to various degrees phenobarbital-inducible cytochrome P-450 and/or 3-methylcholanthrene-inducible cytochrome P-450.	Methylcholanthrene	125-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	156-172
6439215-7	1984	In contrast, cytochrome P-450 content and benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase activities were less in mice treated with 3-methylcholanthrene + DBBD than in animals treated with 3-methylcholanthrene alone.	Methylcholanthrene	144-164	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	13-29
6439215-8	1984	SDS-PAGE confirmed that induction of cytochrome P-450 by 3-methylcholanthrene was reduced by DBBD, suggesting that the latter compound may be an antagonist to the Ah cytosolic receptor.	Methylcholanthrene	57-77	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	37-53
6439217-2	1984	Cytochrome P-450 (termed MC P-4481 and MC P-4482) purified from liver microsomes of 3-methyl-cholanthrene-treated rats was active in both 2- and 4-hydroxylation of biphenyl but cytochrome P-450 (termed PB P-450) purified from liver microsomes of phenobarbital-treated rats was active in 4-hydroxylation of biphenyl only.	Methylcholanthrene	84-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6439217-2	1984	Cytochrome P-450 (termed MC P-4481 and MC P-4482) purified from liver microsomes of 3-methyl-cholanthrene-treated rats was active in both 2- and 4-hydroxylation of biphenyl but cytochrome P-450 (termed PB P-450) purified from liver microsomes of phenobarbital-treated rats was active in 4-hydroxylation of biphenyl only.	Methylcholanthrene	84-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	177-193
6094223-0	1984	Increased transcription of the c-myc oncogene in two methylcholanthrene-induced quail fibroblastic cell lines.	Methylcholanthrene	53-71	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	31-36
6392865-1	1984	We present and evaluate a dual assay, the CYPIA (Cytochrome P-450 induction assay) for the detection and the simultaneous identification of chemicals belonging either to the 3-methylcholanthrene or phenobarbital classes of cytochrome P-450 monooxygenase inducers.	Methylcholanthrene	174-194	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	223-253
6531938-1	1984	Liver homogenates from rats injected with 3-methylcholanthrene were employed for metabolism of benzo[a]pyrene (BP) and in assays of aryl hydrocarbon hydroxylase (AHH) activity in vitro.	Methylcholanthrene	42-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-160
6531938-1	1984	Liver homogenates from rats injected with 3-methylcholanthrene were employed for metabolism of benzo[a]pyrene (BP) and in assays of aryl hydrocarbon hydroxylase (AHH) activity in vitro.	Methylcholanthrene	42-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	162-165
6438082-8	1984	This difference probably reflects the much higher affinity of cytochrome P-450c for BP (Kd = 6 nM), as compared to 7,8-dihydrodiol (Kd = 175 nM) that was established spectrophotometrically both for the purified cytochrome and for MC microsomes.	Methylcholanthrene	230-232	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	62-79
6208847-4	1984	Two protein-staining bands immunorelated to cytochromes P-450c and P-450d were observed in all animals treated with 3-methylcholanthrene (rabbit, hamster, guinea pig, and C57BL/6J mouse) except the DBA/2J mouse, where no polypeptide immunorelated to cytochrome P-450c was detected.	Methylcholanthrene	116-136	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	56-73
6208847-4	1984	Two protein-staining bands immunorelated to cytochromes P-450c and P-450d were observed in all animals treated with 3-methylcholanthrene (rabbit, hamster, guinea pig, and C57BL/6J mouse) except the DBA/2J mouse, where no polypeptide immunorelated to cytochrome P-450c was detected.	Methylcholanthrene	116-136	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	250-267
6240243-5	1984	The inhibition of demethylase by alpha-naphthoflavone in MC-treated microsomes also suggested that cytochrome P-450 species induced by MC are active in demethylating NDMA.	Methylcholanthrene	57-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
6240243-5	1984	The inhibition of demethylase by alpha-naphthoflavone in MC-treated microsomes also suggested that cytochrome P-450 species induced by MC are active in demethylating NDMA.	Methylcholanthrene	135-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
6435901-2	1984	The major 3-methylcholanthrene (MC) inducible cytochrome P-450 (form c) exhibits the greatest activity toward both benzo[a]pyrene (BP) (58 min-1) and 7,12-dimethylbenz[a]anthracene (DMBA) (29 min-1) and forms substantially high spin, high affinity complexes (Kd = 10 nM) with both hydrocarbons.	Methylcholanthrene	10-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
6435901-2	1984	The major 3-methylcholanthrene (MC) inducible cytochrome P-450 (form c) exhibits the greatest activity toward both benzo[a]pyrene (BP) (58 min-1) and 7,12-dimethylbenz[a]anthracene (DMBA) (29 min-1) and forms substantially high spin, high affinity complexes (Kd = 10 nM) with both hydrocarbons.	Methylcholanthrene	32-34	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
6435901-3	1984	Cytochrome P-450d, a minor MC-inducible form, has far lower activity for metabolism of both polycyclic aromatic hydrocarbons (PAH), yet also forms high affinity complexes (Kd approximately 100 nM) with both PAH, retaining the full high spin state of the free cytochrome.	Methylcholanthrene	27-29	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	0-17
6488182-8	1984	Benzo(a)pyrene, 3-methylcholanthrene, and phenobarbital induce hepatic ALDH activity after treatment in vivo.	Methylcholanthrene	16-36	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	71-75
6488182-10	1984	Treatment of cell cultures for 72 hr with 3-methylcholanthrene (1.0 mM) increases the NADP-dependent ALDH activity in H4-II-EC3 and McA-RH7777 cell lines up to 34- and 11-fold, respectively.	Methylcholanthrene	42-62	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	101-105
6488182-12	1984	Treatment with 3-methylcholanthrene or benzo(a)pyrene increases ALDH activity 2-fold in HTC and JM2 but does not increase NADP-dependent ALDH activity in JM1.	Methylcholanthrene	15-35	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	64-68
6436235-3	1984	Both phenobarbital (PB) and 3-methylcholanthrene (3-MC) induce the level of mitochondrial cytochrome P-450 by 2.0- to 2.5-fold above the level of control mitoplasts.	Methylcholanthrene	28-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6436235-3	1984	Both phenobarbital (PB) and 3-methylcholanthrene (3-MC) induce the level of mitochondrial cytochrome P-450 by 2.0- to 2.5-fold above the level of control mitoplasts.	Methylcholanthrene	50-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6436235-8	1984	The activity, however, was restored to preparations from both PB-induced and 3-MC-induced mitochondrial enzymes (AFB1 activation, ethylmorphine, and benzphetamine deamination and BaP metabolism) by addition of purified rat liver cytochrome P-450 reductase, and beef adrenodoxin and adrenodoxin reductase.	Methylcholanthrene	77-81	cytochrome p450 oxidoreductase	Rattus norvegicus	229-255
6436235-8	1984	The activity, however, was restored to preparations from both PB-induced and 3-MC-induced mitochondrial enzymes (AFB1 activation, ethylmorphine, and benzphetamine deamination and BaP metabolism) by addition of purified rat liver cytochrome P-450 reductase, and beef adrenodoxin and adrenodoxin reductase.	Methylcholanthrene	77-81	ferredoxin reductase	Rattus norvegicus	282-303
6436235-11	1984	Anti-P-450b and anti-P-450c provided Ouchterlony precipitin bands against PB- and 3-MC induced mitoplasts, respectively.	Methylcholanthrene	82-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
6436235-11	1984	Anti-P-450b and anti-P-450c provided Ouchterlony precipitin bands against PB- and 3-MC induced mitoplasts, respectively.	Methylcholanthrene	82-86	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	21-27
6480608-2	1984	RIAs based on MAb 1-7-1 and MAb 1-31-2, both to the major 3-methylcholanthrene (MC)-induced rat liver microsomal cytochrome P-450, detected antigenically related forms of cytochrome P-450 in liver microsomes from MC-induced rats, C57BL/6 and DBA/2 mice, hamsters, and guinea pigs, and in lung and kidney microsomes of MC-induced rats.	Methylcholanthrene	58-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-187
6480608-2	1984	RIAs based on MAb 1-7-1 and MAb 1-31-2, both to the major 3-methylcholanthrene (MC)-induced rat liver microsomal cytochrome P-450, detected antigenically related forms of cytochrome P-450 in liver microsomes from MC-induced rats, C57BL/6 and DBA/2 mice, hamsters, and guinea pigs, and in lung and kidney microsomes of MC-induced rats.	Methylcholanthrene	80-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-187
6480608-2	1984	RIAs based on MAb 1-7-1 and MAb 1-31-2, both to the major 3-methylcholanthrene (MC)-induced rat liver microsomal cytochrome P-450, detected antigenically related forms of cytochrome P-450 in liver microsomes from MC-induced rats, C57BL/6 and DBA/2 mice, hamsters, and guinea pigs, and in lung and kidney microsomes of MC-induced rats.	Methylcholanthrene	213-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-187
6480608-2	1984	RIAs based on MAb 1-7-1 and MAb 1-31-2, both to the major 3-methylcholanthrene (MC)-induced rat liver microsomal cytochrome P-450, detected antigenically related forms of cytochrome P-450 in liver microsomes from MC-induced rats, C57BL/6 and DBA/2 mice, hamsters, and guinea pigs, and in lung and kidney microsomes of MC-induced rats.	Methylcholanthrene	213-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-187
6510637-8	1984	These results indicate that in MC-microsomes, the N-hydroxylation of MAB is catalyzed by both FMO and MC-P-448, but in untreated and PB-microsomes the reaction is catalyzed exclusively by FMO.	Methylcholanthrene	31-33	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	105-110
6435285-5	1984	The 3,3",4,4"-TCPB, a 3-MC-type inducer of cytochrome P-450, resembled 3-methylcholanthrene (3-MC) in its inability to induce susceptibility to bromobenzene.	Methylcholanthrene	22-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
6506750-7	1984	Administration of 3-methylcholanthrene and phenobarbital to pigeons resulted in the induction of demethylase and benzo[a]pyrene hydroxylase activities and in cytochrome P-450 levels.	Methylcholanthrene	18-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	158-174
6433897-6	1984	In contrast, 4-nitrophenol UDP-glucuronosyltransferase activity was not affected by steroid hormones, but was highly induced by 3-methylcholanthrene.	Methylcholanthrene	128-148	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	27-54
6744296-0	1984	Metabolism of 2-acetylaminofluorene by two 3-methylcholanthrene-inducible forms of rat liver cytochrome P-450.	Methylcholanthrene	43-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
6744296-1	1984	The present study examines the contribution of two major 3-methylcholanthrene (3-MC)-inducible forms of rat liver cytochrome P-450 (P-448MC and P-448HCB) to the metabolism of 2-acetylaminofluorene (AAF).	Methylcholanthrene	57-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
6744296-1	1984	The present study examines the contribution of two major 3-methylcholanthrene (3-MC)-inducible forms of rat liver cytochrome P-450 (P-448MC and P-448HCB) to the metabolism of 2-acetylaminofluorene (AAF).	Methylcholanthrene	79-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
6744296-14	1984	These data suggest that, in rat liver, two 3-MC-inducible izozymes of cytochrome P-450 metabolize AAF; however, N-hydroxylation is catalyzed primarily by one of these isozymes, cytochrome P-448HCB.	Methylcholanthrene	43-47	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
6548461-0	1984	Isolation and characterization of full-length mouse cDNA and genomic clones of 3-methylcholanthrene-inducible cytochrome P1-450 and P3-450.	Methylcholanthrene	79-99	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	121-127
6548743-0	1984	Characterization of complementary DNA clones coding for two forms of 3-methylcholanthrene-inducible rat liver cytochrome P-450.	Methylcholanthrene	69-89	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	110-126
6548743-2	1984	Twenty clones were verified to carry a complementary DNA (cDNA) insert coding for MC-inducible cytochrome P-450 by positive hybridization translation assay and immunochemical assay with anti-cytochrome P-450 antibody.	Methylcholanthrene	82-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
6548743-2	1984	Twenty clones were verified to carry a complementary DNA (cDNA) insert coding for MC-inducible cytochrome P-450 by positive hybridization translation assay and immunochemical assay with anti-cytochrome P-450 antibody.	Methylcholanthrene	82-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	191-207
6438379-1	1984	Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)).	Methylcholanthrene	212-232	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
6438379-1	1984	Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)).	Methylcholanthrene	212-232	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-16
6494651-5	1984	Not only the microsomal monooxygenase but also amidase was strongly induced by pretreatment with phenobarbital, 3-methylcholanthrene and rifampicin, respectively.	Methylcholanthrene	112-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-37
6442038-0	1984	[Immunological study of the identity of cytochrome P-448 in the mouse and rat liver after induction with 3-methylcholanthrene].	Methylcholanthrene	105-125	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	40-56
6442038-1	1984	As shown by means of Ouchterlony double immunodiffusion technique after induction with 3-methyl cholanthrene the antibodies towards cytochrome P-448 from rat liver tissue developed a clear-cut precipitation line with homologous antigen and interacted also with cytochrome P-448 from mice liver tissue although the precipitation was less distinct.	Methylcholanthrene	87-108	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	132-148
6442038-1	1984	As shown by means of Ouchterlony double immunodiffusion technique after induction with 3-methyl cholanthrene the antibodies towards cytochrome P-448 from rat liver tissue developed a clear-cut precipitation line with homologous antigen and interacted also with cytochrome P-448 from mice liver tissue although the precipitation was less distinct.	Methylcholanthrene	87-108	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	261-277
6547950-1	1984	By sequence analysis of the cloned cDNA or genomic DNA, we have recently deduced the complete primary structures of two forms of 3-methylcholanthrene-inducible cytochromes P-450 (P-450c and P-450d).	Methylcholanthrene	129-149	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	172-177
6547950-1	1984	By sequence analysis of the cloned cDNA or genomic DNA, we have recently deduced the complete primary structures of two forms of 3-methylcholanthrene-inducible cytochromes P-450 (P-450c and P-450d).	Methylcholanthrene	129-149	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	179-185
6547950-1	1984	By sequence analysis of the cloned cDNA or genomic DNA, we have recently deduced the complete primary structures of two forms of 3-methylcholanthrene-inducible cytochromes P-450 (P-450c and P-450d).	Methylcholanthrene	129-149	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	190-196
6547950-4	1984	In RNA blot analysis with unfractionated mRNA isolated from 3-methylcholanthrene-treated rat livers, Probe A (specific to P-450c sequence) hybridized with mRNA around 23 S, while Probe B (specific to P-450d sequence) hybridized with mRNA around 18 S. When common sequence between P-450c and P-450d was used as the probes (Probe C or D), two bands were clearly observed around 23 and 18 S mRNAs.	Methylcholanthrene	60-80	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	122-128
6547950-6	1984	3-Methylcholanthrene increased both P-450c and P-450d mRNA levels by 50 and 10 times above the control at 17 h after the administration, respectively.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	36-42
6547950-6	1984	3-Methylcholanthrene increased both P-450c and P-450d mRNA levels by 50 and 10 times above the control at 17 h after the administration, respectively.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	47-53
6433911-1	1984	Antibody to mouse UDP glucuronosyltransferase, previously shown to cross-react with rat transferase [1], immunoadsorbed 3 electrophoretically distinct transferase forms from the microsomes of untreated and phenobarbital-treated rats and 4 forms from 3-methylcholanthrene treated animals.	Methylcholanthrene	250-270	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	18-45
6490752-1	1984	The major forms of cytochrome P-450 in the hepatic microsomes of rats pretreated with phenobarbital (PB) or 3-methylcholanthrene (3MC) were isolated by sequential chromatography on n-octylamino-Sepharose 4B and DEAE-cellulose columns.	Methylcholanthrene	108-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6490752-1	1984	The major forms of cytochrome P-450 in the hepatic microsomes of rats pretreated with phenobarbital (PB) or 3-methylcholanthrene (3MC) were isolated by sequential chromatography on n-octylamino-Sepharose 4B and DEAE-cellulose columns.	Methylcholanthrene	130-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6490752-3	1984	High-performance liquid chromatography (HPLC) of these preparations on an anion-exchange column yielded three peaks from the PB-induced major cytochrome P-450 and a single peak from the 3MC-induced major cytochrome P-450.	Methylcholanthrene	186-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	204-220
6465891-2	1984	The kinetics of cytochrome P-450 mRNA induction by 3-methylcholanthrene and by phenobarbital were examined, and differences in the types of cytochrome P-450 mRNAs induced by 3-methylcholanthrene (MC), beta-naphthoflavone (BNF), and phenobarbital (PB) in male and female rats were determined.	Methylcholanthrene	51-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
6465891-2	1984	The kinetics of cytochrome P-450 mRNA induction by 3-methylcholanthrene and by phenobarbital were examined, and differences in the types of cytochrome P-450 mRNAs induced by 3-methylcholanthrene (MC), beta-naphthoflavone (BNF), and phenobarbital (PB) in male and female rats were determined.	Methylcholanthrene	174-194	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
6465891-2	1984	The kinetics of cytochrome P-450 mRNA induction by 3-methylcholanthrene and by phenobarbital were examined, and differences in the types of cytochrome P-450 mRNAs induced by 3-methylcholanthrene (MC), beta-naphthoflavone (BNF), and phenobarbital (PB) in male and female rats were determined.	Methylcholanthrene	196-198	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
6465891-15	1984	3-Methylcholanthrene caused parallel increases in AHH activity and translatable cytochrome P-450 mRNA, but when translatable mRNA began to decrease after about 24 h, AHH activity remained high, suggesting that this P-450 mRNA was less stable than the enzyme for which it coded.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-53
6465891-15	1984	3-Methylcholanthrene caused parallel increases in AHH activity and translatable cytochrome P-450 mRNA, but when translatable mRNA began to decrease after about 24 h, AHH activity remained high, suggesting that this P-450 mRNA was less stable than the enzyme for which it coded.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
6611212-1	1984	Intratumor host cells of methylcholanthrene-induced fibrosarcoma(s) were shown to enhance the in vivo outgrowth of syngeneic homologous tumors (MC1A, Mc2A, Mc2B) but not two heterologous T-lymphomas (EL4 and TLX9) in the Winn adoptive transfer assay.	Methylcholanthrene	25-43	epilepsy 4	Mus musculus	200-203
6332881-1	1984	The direct cell-mediated antitumor cytotoxicity induced by coupling a murine methylcholanthrene-induced sarcoma with N-acetylmuramyl-L-alanyl-D-isoglutamine (adjuvant peptide) was eliminated by treatment of effector cells with anti-Thy 1.2 or anti-Lyt 2.2 monoclonal antibody and complement.	Methylcholanthrene	77-95	thymus cell antigen 1, theta	Mus musculus	232-239
6332881-1	1984	The direct cell-mediated antitumor cytotoxicity induced by coupling a murine methylcholanthrene-induced sarcoma with N-acetylmuramyl-L-alanyl-D-isoglutamine (adjuvant peptide) was eliminated by treatment of effector cells with anti-Thy 1.2 or anti-Lyt 2.2 monoclonal antibody and complement.	Methylcholanthrene	77-95	CD8 antigen, alpha chain	Mus musculus	248-253
6378929-4	1984	RNA extracted from Fu5-C8 cells directed the in vitro synthesis of immune-precipitable cytochrome P-450(MC) only after treatment of the cells with 3-methylcholanthrene.	Methylcholanthrene	147-167	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	87-107
6378929-5	1984	Kinetic analysis of the response of these cells to 3-methylcholanthrene induction revealed detectable levels of immune-precipitable cytochrome P-450(MC) 2 h after drug treatment with maximal induction occurring between 12 and 16 h of exposure.	Methylcholanthrene	51-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
6378929-7	1984	Exposure of confluent monolayers to either phenobarbital or 3-methylcholanthrene resulted in an induction of cytochrome P-450(PB) or cytochrome P-450(MC), respectively.	Methylcholanthrene	60-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-129
6378929-7	1984	Exposure of confluent monolayers to either phenobarbital or 3-methylcholanthrene resulted in an induction of cytochrome P-450(PB) or cytochrome P-450(MC), respectively.	Methylcholanthrene	60-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	133-153
6089174-0	1984	Distinct organization of methylcholanthrene- and phenobarbital-inducible cytochrome P-450 genes in the rat.	Methylcholanthrene	25-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
6089174-1	1984	The complete nucleotide sequence of the methylcholanthrene-inducible cytochrome P-450c gene was determined by sequence analysis of cloned genomic DNA and the sequence, consisting of 524 amino acids, of the protein was deduced therefrom.	Methylcholanthrene	40-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	69-86
6433344-4	1984	When animals were administered 3-methylcholanthrene, a typical inducer of these mRNAs in normal animals, a further increase in the glutathione transferase Yb mRNA(s) and DT-diaphorase mRNA was observed in the nodules; however, the Ya/Yc mRNA levels remained unaffected.	Methylcholanthrene	31-51	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	170-183
6433344-5	1984	Our data indicate that during chemically induced neoplastic transformation, the mRNA levels for the Yb subunit of glutathione transferase and DT-diaphorase are increased in the nodules but still retain the capacity to be regulated by 3-methylcholanthrene.	Methylcholanthrene	234-254	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	142-155
6204978-4	1984	The MAb 1-7-1-sensitive cytochrome P-450 is a major contributor to aryl hydrocarbon hydroxylase in rat liver, lung, and kidney of 3-methylcholanthrene-treated rats, C57BL/6 mice, guinea pigs, and hamsters; this type is also present in lesser amounts in the extrahepatic tissues of the control and PB-treated animals, and in the lungs of the relatively "noninducible" DBA/2 mice treated with 3-methylcholanthrene.	Methylcholanthrene	130-150	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6204978-4	1984	The MAb 1-7-1-sensitive cytochrome P-450 is a major contributor to aryl hydrocarbon hydroxylase in rat liver, lung, and kidney of 3-methylcholanthrene-treated rats, C57BL/6 mice, guinea pigs, and hamsters; this type is also present in lesser amounts in the extrahepatic tissues of the control and PB-treated animals, and in the lungs of the relatively "noninducible" DBA/2 mice treated with 3-methylcholanthrene.	Methylcholanthrene	391-411	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6430894-1	1984	Absolute configurations of the arene 1,2-oxides formed from napththalene and anthracene by cytochrome P-450c, the predominant isozyme of cytochrome P-450 found in the livers of rats treated with 3-methylcholanthrene, were determined via two different approaches.	Methylcholanthrene	195-215	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	91-108
6430894-1	1984	Absolute configurations of the arene 1,2-oxides formed from napththalene and anthracene by cytochrome P-450c, the predominant isozyme of cytochrome P-450 found in the livers of rats treated with 3-methylcholanthrene, were determined via two different approaches.	Methylcholanthrene	195-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-107
6430240-0	1984	Rat liver DT-diaphorase: regulation of functional mRNA levels by 3-methylcholanthrene, trans-stilbene oxide, and phenobarbital.	Methylcholanthrene	65-85	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	10-23
6430240-4	1984	These quantitation results demonstrate that 3-methylcholanthrene leads to an eight-fold elevation in functional DT-diaphorase mRNA at 8 h after a single administration of 3-methylcholanthrene; whereas, trans-stilbene oxide and phenobarbital produced only a modest elevation, two- to three-fold, in the functional DT-diaphorase mRNA level.	Methylcholanthrene	44-64	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	112-125
6430240-4	1984	These quantitation results demonstrate that 3-methylcholanthrene leads to an eight-fold elevation in functional DT-diaphorase mRNA at 8 h after a single administration of 3-methylcholanthrene; whereas, trans-stilbene oxide and phenobarbital produced only a modest elevation, two- to three-fold, in the functional DT-diaphorase mRNA level.	Methylcholanthrene	44-64	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	313-326
6430240-4	1984	These quantitation results demonstrate that 3-methylcholanthrene leads to an eight-fold elevation in functional DT-diaphorase mRNA at 8 h after a single administration of 3-methylcholanthrene; whereas, trans-stilbene oxide and phenobarbital produced only a modest elevation, two- to three-fold, in the functional DT-diaphorase mRNA level.	Methylcholanthrene	171-191	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	112-125
6430240-4	1984	These quantitation results demonstrate that 3-methylcholanthrene leads to an eight-fold elevation in functional DT-diaphorase mRNA at 8 h after a single administration of 3-methylcholanthrene; whereas, trans-stilbene oxide and phenobarbital produced only a modest elevation, two- to three-fold, in the functional DT-diaphorase mRNA level.	Methylcholanthrene	171-191	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	313-326
6430240-5	1984	These data indicate that the increase in the level of DT-diaphorase after 3-methylcholanthrene administration noted previously [B. Hojeberg, K. Blomberg, S. Stenberg, and C. Lind (1981) Arch.	Methylcholanthrene	74-94	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	54-67
6089700-5	1984	On the basis of enzyme activities, ligand-binding spectra and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the PBN mixtures were determined to be 3-methylcholanthrene-type inducers of cytochrome P-450 (P-448), resembling qualitatively the most toxic polyhalogenated biphenyls, dibenzofurans, and dioxins in this respect.	Methylcholanthrene	160-180	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	198-214
6089700-5	1984	On the basis of enzyme activities, ligand-binding spectra and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the PBN mixtures were determined to be 3-methylcholanthrene-type inducers of cytochrome P-450 (P-448), resembling qualitatively the most toxic polyhalogenated biphenyls, dibenzofurans, and dioxins in this respect.	Methylcholanthrene	160-180	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	216-221
6610486-3	1984	Elimination of Lyt 1+ cells abolished the outgrowth inhibitory effect exerted by T-cell-enriched populations derived from syngeneic or semisyngeneic mice immunized with the H-2-carrying MC-induced M-A tumor.	Methylcholanthrene	186-188	CD5 antigen	Mus musculus	15-20
6490599-0	1984	Characterization of three forms of cytochrome P-450 isolated from liver microsomes of rats treated with 3-methylcholanthrene.	Methylcholanthrene	104-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
6490599-1	1984	Three forms of cytochrome P-450, designated as P-450MC-I, P-450MC-II, and P-450MC-III, were isolated from liver microsomes of rats treated with 3-methylcholanthrene (MC) by using a high performance liquid chromatography (HPLC) technique.	Methylcholanthrene	144-164	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-31
6490599-1	1984	Three forms of cytochrome P-450, designated as P-450MC-I, P-450MC-II, and P-450MC-III, were isolated from liver microsomes of rats treated with 3-methylcholanthrene (MC) by using a high performance liquid chromatography (HPLC) technique.	Methylcholanthrene	52-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-31
6609977-8	1984	The T cell replacing factor was found in supernatants of unstimulated cord as well as in adult MC cultures, but was less than 50% as potent.	Methylcholanthrene	95-97	interleukin 5	Homo sapiens	4-27
6589594-0	1984	Structures of cysteine-containing peptides in isosafrole-inducible rat hepatic microsomal cytochrome P-450d: sequence homology with 3-methylcholanthrene-induced cytochrome P-450c.	Methylcholanthrene	132-152	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	90-107
6589594-0	1984	Structures of cysteine-containing peptides in isosafrole-inducible rat hepatic microsomal cytochrome P-450d: sequence homology with 3-methylcholanthrene-induced cytochrome P-450c.	Methylcholanthrene	132-152	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	161-178
6589594-3	1984	Five of the peptides have significant sequence homology (20/22, 10/16, 8/13, 13/18, and 5/9 identical residues) to cysteine-containing peptides in cytochrome P-450c, the major isozyme induced by 3-methylcholanthrene.	Methylcholanthrene	195-215	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	147-164
6438922-7	1984	These results indicate that more than two forms of cytochrome P-450, which are inducible by treatment with PCB or 3-methylcholanthrene, mediate the metabolic activation of heteroaromatic amines in rats and mice.	Methylcholanthrene	114-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
6327765-8	1984	Thus, both generation of MAF by newborn blood MC and response to newborn MAF by newborn M phi were impaired.	Methylcholanthrene	46-48	MAF bZIP transcription factor	Homo sapiens	25-28
6327765-10	1984	Depletion of OKT4 antibody-binding cells abrogated the generation of MAF both by adult and cord blood MC.	Methylcholanthrene	102-104	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	69-72
6477879-0	1984	Structural analysis of the cysteine-containing peptides from the major 3-methylcholanthrene-induced isozyme of cytochrome P-450 (P-450c) in rat liver microsomes.	Methylcholanthrene	71-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
6477879-0	1984	Structural analysis of the cysteine-containing peptides from the major 3-methylcholanthrene-induced isozyme of cytochrome P-450 (P-450c) in rat liver microsomes.	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	129-135
6477879-1	1984	Cytochrome P-450c, the major 3-methylcholanthrene-inducible isozyme of cytochrome P-450 in rat liver microsomes, was subjected to proteolytic digestion after S-carboxymethylation of the protein, and the peptides were resolved by high-pressure liquid chromatography.	Methylcholanthrene	29-49	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-17
6477879-1	1984	Cytochrome P-450c, the major 3-methylcholanthrene-inducible isozyme of cytochrome P-450 in rat liver microsomes, was subjected to proteolytic digestion after S-carboxymethylation of the protein, and the peptides were resolved by high-pressure liquid chromatography.	Methylcholanthrene	29-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
6477879-7	1984	Sequence analysis of a cysteine-containing peptide (T-30) from another 3-methylcholanthrene-inducible rat liver cytochrome P-450 (cytochrome P-450d) revealed 91% homology with peptide T-46 from cytochrome P-450c, but this peptide shows no significant homology with any of the cysteine-containing peptides from other cytochromes P-450.	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	123-128
6477879-7	1984	Sequence analysis of a cysteine-containing peptide (T-30) from another 3-methylcholanthrene-inducible rat liver cytochrome P-450 (cytochrome P-450d) revealed 91% homology with peptide T-46 from cytochrome P-450c, but this peptide shows no significant homology with any of the cysteine-containing peptides from other cytochromes P-450.	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	130-147
6477879-7	1984	Sequence analysis of a cysteine-containing peptide (T-30) from another 3-methylcholanthrene-inducible rat liver cytochrome P-450 (cytochrome P-450d) revealed 91% homology with peptide T-46 from cytochrome P-450c, but this peptide shows no significant homology with any of the cysteine-containing peptides from other cytochromes P-450.	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	194-211
6477879-7	1984	Sequence analysis of a cysteine-containing peptide (T-30) from another 3-methylcholanthrene-inducible rat liver cytochrome P-450 (cytochrome P-450d) revealed 91% homology with peptide T-46 from cytochrome P-450c, but this peptide shows no significant homology with any of the cysteine-containing peptides from other cytochromes P-450.	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	141-146
6325423-1	1984	Complete nucleotide sequence of a glutathione S-transferase mRNA and the regulation of the Ya, Yb, and Yc mRNAs by 3-methylcholanthrene and phenobarbital.	Methylcholanthrene	115-135	hematopoietic prostaglandin D synthase	Rattus norvegicus	34-59
6712731-3	1984	polyribocytidylic acid (poly IC), are known to depress hepatic cytochrome P-450-dependent monooxygenase systems and the induction of these systems by phenobarbital (PB) and 3-methylcholanthrene (MC) in mature male rats.	Methylcholanthrene	173-193	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
6712731-3	1984	polyribocytidylic acid (poly IC), are known to depress hepatic cytochrome P-450-dependent monooxygenase systems and the induction of these systems by phenobarbital (PB) and 3-methylcholanthrene (MC) in mature male rats.	Methylcholanthrene	195-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
2869885-0	1986	Kinetic constant determination of liver microsomal and purified UDP-glucuronosyltransferase after phenobarbital and 3-methylcholanthrene treatments in rats.	Methylcholanthrene	116-136	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	64-91
3098490-6	1986	MC from healthy L4 nonresponders (NR), induced to proliferate with L4 in the presence of responder (R) monocytes, also yielded an elevated mean IL2R-50K value of 31.	Methylcholanthrene	0-2	interleukin 2 receptor subunit alpha	Homo sapiens	144-148
3514588-4	1986	In the microsomal preparation, the DBE-debromination rate per nmol cytochrome P-450 was enhanced by phenobarbital-pretreatment of rabbits compared with the untreated microsomes, whereas it was diminished by 3-methylcholanthrene-pretreatment.	Methylcholanthrene	207-227	cytochrome P-450	Oryctolagus cuniculus	67-83
3079779-1	1986	The activities of aryl hydrocarbon hydroxylase and 7-ethoxycoumarin O-de-ethylase in the rat submandibular gland, both of which are normally very low, were increased about 10- and 25-fold, respectively, by administration of 3-methylcholanthrene.	Methylcholanthrene	224-244	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	18-46
3941398-0	1986	Cytochrome P-450 isoenzyme content and monooxygenase activities in rat liver: effect of ontogenesis and pretreatment by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	138-158	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	14-16	insulin	Homo sapiens	17-24
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	14-16	insulin	Homo sapiens	101-108
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	14-16	insulin	Homo sapiens	101-108
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	98-100	insulin	Homo sapiens	17-24
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	98-100	insulin	Homo sapiens	101-108
3915264-4	1985	Adding native MC insulin to a competitive radioimmunoassay suppressed the IBA titer obtained with MC insulin more than that obtained with Cr insulin.	Methylcholanthrene	98-100	insulin	Homo sapiens	101-108
3915264-5	1985	By adding native proinsulin in a similar assay system, the PBA titer obtained with Cr insulin was suppressed more than that extracted with MC insulin.	Methylcholanthrene	139-141	insulin	Homo sapiens	17-27
3915264-5	1985	By adding native proinsulin in a similar assay system, the PBA titer obtained with Cr insulin was suppressed more than that extracted with MC insulin.	Methylcholanthrene	139-141	insulin	Homo sapiens	20-27
3915264-8	1985	Using MC insulin, instead of Cr insulin, as the ligand in affinity chromatography increased the purity of recovered IBA.	Methylcholanthrene	6-8	insulin	Homo sapiens	9-16
4063404-0	1985	[Induction of cytochrome P-450 forms in liver microsomes of rats in the early neonatal period after administration of phenobarbital and 3-methylcholanthrene].	Methylcholanthrene	136-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
4086481-1	1985	Determination of the heme and protein portions of phenobarbital (PB)-inducible and 3-methylcholanthrene inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), in the liver microsomes of drug-treated animals indicated the presence of 20-30% of apo-cytochrome P-450 in both cases.	Methylcholanthrene	83-103	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	123-139
4095131-2	1985	From the elimination velocity of these model substances conclusions concerning the activity of 3-methylcholanthrene inducible (caffeine elimination) and of phenobarbital inducible (metamizol elimination) isoenzymes of cytochrome P-450 are drawn.	Methylcholanthrene	95-115	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	218-234
4095132-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and metamizol (noramidopyrine methanesulfonate sodium) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Methylcholanthrene	34-54	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
4095132-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and metamizol (noramidopyrine methanesulfonate sodium) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Methylcholanthrene	34-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-81
3839750-4	1985	Translation in vitro of 3-methylcholanthrene-induced mRNA, selected with the human P1-450 genomic clone, detect a protein with Mr 52000, which is immunoprecipitable by the anti-(mouse P1-450) antibody.	Methylcholanthrene	24-44	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	83-89
3839750-4	1985	Translation in vitro of 3-methylcholanthrene-induced mRNA, selected with the human P1-450 genomic clone, detect a protein with Mr 52000, which is immunoprecipitable by the anti-(mouse P1-450) antibody.	Methylcholanthrene	24-44	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	184-190
3839750-5	1985	The isolated human P1-450 genomic clone hybridizes to 3-methylcholanthrene-induced mRNA from monkey liver, benzanthracene and 3-methylcholanthrene-treated human mammary tumor cells (MCF-7), but not to isosafrole-treated human cells.	Methylcholanthrene	54-74	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	19-25
3839750-5	1985	The isolated human P1-450 genomic clone hybridizes to 3-methylcholanthrene-induced mRNA from monkey liver, benzanthracene and 3-methylcholanthrene-treated human mammary tumor cells (MCF-7), but not to isosafrole-treated human cells.	Methylcholanthrene	126-146	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	19-25
4074694-0	1985	Chromatin structure of a 3-methylcholanthrene-induced cytochrome P-450 gene.	Methylcholanthrene	25-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
4074694-1	1985	Plasmids carrying fragments of a cytochrome P-450 gene, inducible by 3-methylcholanthrene, were used to study the chromatin structure of this gene in the liver of normal and carcinogen-treated rats.	Methylcholanthrene	69-89	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
4037801-1	1985	We used primary nonproliferating cultures of adult rat hepatocytes to investigate the regulation of P-450c and P-450d, immunochemically related protein products of separate cytochromes P-450 genes that are coinduced by 3-methylcholanthrene and related compounds.	Methylcholanthrene	219-239	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	100-117
3927907-4	1985	The authors further concluded that the 5R,6S-enantiomer predominates on metabolism of DMBA by cytochrome P450c in liver microsomes from 3-methylcholanthrene-treated rats.	Methylcholanthrene	136-156	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	94-110
4005852-9	1985	Pretreatment of rats with enzyme inducers (phenobarbital and 3-methylcholanthrene) stimulated the activity of DT-diaphorase in liver cytosolic fractions.	Methylcholanthrene	61-81	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	110-123
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	19-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	19-39	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	122-129
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	19-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	161-177
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	41-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	41-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	122-129
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	41-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	161-177
2863157-10	1985	On the other hand, 3-methylcholanthrene (MC, 10 microM) caused an increase of both contents of total cytochrome P-450 and P-450MC, which is the specific form of cytochrome P-450 induced by MC, in primary cultured hepatocytes.	Methylcholanthrene	127-129	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	161-177
3928617-2	1985	They were P-451 I and P-451 II from untreated rats, P-450 II and P-450 III from phenobarbital-treated rats, MC-P-448 L and MC-P-448 H from 3-methylcholanthrene-treated rats, and P-452, P-448 L, and P-448 H from 3,4,5,3",4"-pentachlorobiphenyl-treated rats.	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	126-131
3928617-2	1985	They were P-451 I and P-451 II from untreated rats, P-450 II and P-450 III from phenobarbital-treated rats, MC-P-448 L and MC-P-448 H from 3-methylcholanthrene-treated rats, and P-452, P-448 L, and P-448 H from 3,4,5,3",4"-pentachlorobiphenyl-treated rats.	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	126-131
3928617-2	1985	They were P-451 I and P-451 II from untreated rats, P-450 II and P-450 III from phenobarbital-treated rats, MC-P-448 L and MC-P-448 H from 3-methylcholanthrene-treated rats, and P-452, P-448 L, and P-448 H from 3,4,5,3",4"-pentachlorobiphenyl-treated rats.	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	126-131
3858600-1	1985	Long-term administration of prolactin (PRL) markedly enhanced the induction of epidermal squamous cell carcinomas by a chemical carcinogen, 3-methylcholanthrene [(MCA) CAS: 56-49-5], in Swiss male albino mice.	Methylcholanthrene	140-160	prolactin	Mus musculus	28-37
3858600-1	1985	Long-term administration of prolactin (PRL) markedly enhanced the induction of epidermal squamous cell carcinomas by a chemical carcinogen, 3-methylcholanthrene [(MCA) CAS: 56-49-5], in Swiss male albino mice.	Methylcholanthrene	140-160	prolactin	Mus musculus	39-42
3858600-2	1985	DNA radioactivity and quantitative estimation of autoradiographs with the use of [3H]thymidine revealed a significant increase in DNA content (twofold) and in the percentage of labeled neoplastic nuclei in mice treated with PRL plus MCA (48.50%) as compared to that in mice treated with MCA alone (23.50%).	Methylcholanthrene	287-290	prolactin	Mus musculus	224-227
4004253-0	1985	3-Methylcholanthrene-induced expression of the cytochrome P-450c gene.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	47-64
4004253-1	1985	Transcriptional control of 3-methylcholanthrene-dependent cytochrome P-450c nuclear RNA induction was directly observed in an in vitro rat liver nuclear transcription system.	Methylcholanthrene	27-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	69-75
3888809-8	1985	When specific isozymes of cytochrome P-450 were induced with phenobarbital or 3-methylcholanthrene, the constitutive cytochrome P-450 was localized predominantly in the periportal region.	Methylcholanthrene	78-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	26-42
3888809-8	1985	When specific isozymes of cytochrome P-450 were induced with phenobarbital or 3-methylcholanthrene, the constitutive cytochrome P-450 was localized predominantly in the periportal region.	Methylcholanthrene	78-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
2985574-0	1985	Complete nucleotide sequence of a methylcholanthrene-inducible cytochrome P-450 (P-450d) gene in the rat.	Methylcholanthrene	34-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
2985574-0	1985	Complete nucleotide sequence of a methylcholanthrene-inducible cytochrome P-450 (P-450d) gene in the rat.	Methylcholanthrene	34-52	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	81-87
2985574-1	1985	The rat cytochrome P-450d gene which is inducibly expressed by the administration of 3-methylcholanthrene (MC) has been cloned and analyzed for the complete nucleotide sequence.	Methylcholanthrene	85-105	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	8-25
2985574-1	1985	The rat cytochrome P-450d gene which is inducibly expressed by the administration of 3-methylcholanthrene (MC) has been cloned and analyzed for the complete nucleotide sequence.	Methylcholanthrene	107-109	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	8-25
2985574-3	1985	The insertion sites of the introns in this gene are well-conserved as compared with those of another MC-inducible cytochrome P-450c gene, but are completely different from those of a phenobarbital-inducible cytochrome P-450e gene.	Methylcholanthrene	101-103	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	114-131
2985574-3	1985	The insertion sites of the introns in this gene are well-conserved as compared with those of another MC-inducible cytochrome P-450c gene, but are completely different from those of a phenobarbital-inducible cytochrome P-450e gene.	Methylcholanthrene	101-103	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	207-224
2985574-4	1985	The overall homologies in the coding nucleotide and deduced amino acid sequences were 75% and 68% between the two MC-inducible cytochrome P-450 genes, respectively.	Methylcholanthrene	114-116	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	138-143
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Methylcholanthrene	191-193	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-65
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Methylcholanthrene	191-193	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-76
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Methylcholanthrene	191-193	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-64
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Methylcholanthrene	191-193	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	70-75
2994255-1	1985	The in vitro metabolism of polybrominated biphenyl (PBB) congeners by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes isolated from immature male rats pretreated with 3-methylcholanthrene (MC) or phenobarbital (PB).	Methylcholanthrene	203-223	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
2994255-1	1985	The in vitro metabolism of polybrominated biphenyl (PBB) congeners by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes isolated from immature male rats pretreated with 3-methylcholanthrene (MC) or phenobarbital (PB).	Methylcholanthrene	225-227	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
2994255-9	1985	There was good correlation between the rates of 3,4,3",4"-TBB metabolism, induction of microsomal ethoxyresorufin-O-deethylase activity, and specific content of MC-inducible cytochrome P-450 (P-450 beta NF-B).	Methylcholanthrene	161-163	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
3995102-1	1985	Chromatography on 1.8-diaminooctyl-Sepharose and DEAE-Sephacel resulted in 4 fractions of cytochrome P-450 from liver microsomes of 3-methylcholanthrene-induced Wistar rats.	Methylcholanthrene	132-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
3995102-8	1985	The procedure developed is applicable to the isolation of multiple forms of cytochrome P-450 from liver microsomes of 3-methylcholanthrene-induced rats.	Methylcholanthrene	118-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	76-92
3995102-9	1985	Using rocket immunoelectrophoresis, cytochrome P-450 C possessing a high (as compared to benz(a)pyrene metabolism) activity (18 nmol/min/nmol cytochrome) and a high (60-70%) content in 3-methylcholanthrene-induced rat liver microsomes was shown to give a relatively high yield.	Methylcholanthrene	185-205	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	36-54
3884171-6	1985	Metyrapone, a specific inhibitor of PB-inducible major cytochrome P-450, considerably inhibited mutagenicity, whereas 7,8-benzoflavone, a specific inhibitor of 3-MC-inducible major cytochrome P-448, was totally lacking this effect.	Methylcholanthrene	160-164	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	181-197
2578515-0	1985	Investigations into the nature of Igh-V region-restricted T cell interactions by using antibodies to antigens on methylcholanthrene-induced sarcomas.	Methylcholanthrene	113-131	immunoglobulin heavy locus	Homo sapiens	34-39
3922334-3	1985	Lymphoblastoid cell lines were arbitrarily classified into three groups based on their AHH inducibilities with 3-MC (2.5 microM); low (3-MC/control = I less than 3), middle (3 less than or equal to I less than 6) and high (I greater than or equal to 6).	Methylcholanthrene	111-115	aryl hydrocarbon receptor repressor	Homo sapiens	87-90
2985377-6	1985	It was also observed that in both male and female human cell lines, the degree of AHH inducibilities of these compounds were roughly parallel to that of 3-methylcholanthrene, possibly indicating that genetic susceptibility among human population to the toxic compounds are also present similar to those reported among mouse strains.	Methylcholanthrene	153-173	aryl hydrocarbon receptor repressor	Homo sapiens	82-85
3917648-0	1985	Microsomal monooxygenase system in Morris hepatoma: purification and characterization of cytochromes P-450 from Morris hepatoma 5123D of 3-methylcholanthrene-treated rats.	Methylcholanthrene	137-157	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-24
3842315-3	1985	To summarize the recent findings in our laboratory, proteins p82 and p86 have been isolated and apparently purified from MC-induced sarcomas and from an SV40-induced sarcoma of BALB/c mice.	Methylcholanthrene	121-123	A kinase (PRKA) anchor protein 4	Mus musculus	61-64
3842315-3	1985	To summarize the recent findings in our laboratory, proteins p82 and p86 have been isolated and apparently purified from MC-induced sarcomas and from an SV40-induced sarcoma of BALB/c mice.	Methylcholanthrene	121-123	CD79B antigen like complex	Mus musculus	69-72
6331534-0	1984	[Isolation and characterization of the basic forms of cytochrome P-450 from liver microsomes of C57BL mice after phenobarbital and 3-methylcholanthrene induction].	Methylcholanthrene	131-151	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	54-70
6326866-4	1984	On the other hand, 3-methylcholanthrene, 3,4-benzpyrene and TCDD significantly and equally activates the cytochrome P-448-dependent benzpyrene hydroxylase, since the antibodies against cytochrome P-448 inhibit benzpyrene metabolism in the microsomes by 85-90%.	Methylcholanthrene	19-39	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	105-121
6539207-3	1984	In the sera of animals bearing tumors induced by methylcholanthrene ( MCH2 ) or by spontaneously transformed cells ( EHB ) the level of IgG2 was almost normal but IgG1 was barely detectable, especially in MCH2 tumors.	Methylcholanthrene	49-67	melanin concentrating hormone receptor 2	Homo sapiens	70-74
6464499-0	1984	Induction of cytosolic glutathione transferase and microsomal epoxide hydrolase activities in extrahepatic organs of the rat by phenobarbital, 3-methylcholanthrene and trans-stilbene oxide.	Methylcholanthrene	143-163	epoxide hydrolase 1	Rattus norvegicus	51-79
6464499-1	1984	The effects of treating male Sprague-Dawley rats with phenobarbital, 3-methylcholanthrene or trans-stilbene oxide on cytosolic glutathione transferase and microsomal epoxide hydrolase activities in the liver, intestine, kidney, lung, testis, adrenal, spleen, heart and brain have been investigated.	Methylcholanthrene	69-89	epoxide hydrolase 1	Rattus norvegicus	155-183
6706986-8	1984	Three monoclonal antibodies to the same epitope on cytochrome P-450c, (CD2, CD3, and CD5) cross-reacted strongly with cytochrome P-450d, another isozyme induced by 3-methylcholanthrene treatment of rats.	Methylcholanthrene	164-184	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	51-68
6706986-8	1984	Three monoclonal antibodies to the same epitope on cytochrome P-450c, (CD2, CD3, and CD5) cross-reacted strongly with cytochrome P-450d, another isozyme induced by 3-methylcholanthrene treatment of rats.	Methylcholanthrene	164-184	Cd2 molecule	Rattus norvegicus	71-74
6706986-8	1984	Three monoclonal antibodies to the same epitope on cytochrome P-450c, (CD2, CD3, and CD5) cross-reacted strongly with cytochrome P-450d, another isozyme induced by 3-methylcholanthrene treatment of rats.	Methylcholanthrene	164-184	Cd5 molecule	Rattus norvegicus	85-88
6706986-8	1984	Three monoclonal antibodies to the same epitope on cytochrome P-450c, (CD2, CD3, and CD5) cross-reacted strongly with cytochrome P-450d, another isozyme induced by 3-methylcholanthrene treatment of rats.	Methylcholanthrene	164-184	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	118-135
6326866-0	1984	[Correlation between cytochrome P-448 content and benzopyrene hydroxylase activity during the induction of microsomal monooxygenases using methylcholanthrene-type xenobiotics].	Methylcholanthrene	139-157	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	21-37
6326866-1	1984	Using antibodies against electrophoretically homogeneous cytochrome P-448 from rat liver microsomes induced by 3-methylcholanthrene, the changes in the immunologic identity and contents by cytochrome P-448 induced by 3-methylcholanthrene, 3.4-benzpyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), were studied.	Methylcholanthrene	111-131	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	57-73
6326866-1	1984	Using antibodies against electrophoretically homogeneous cytochrome P-448 from rat liver microsomes induced by 3-methylcholanthrene, the changes in the immunologic identity and contents by cytochrome P-448 induced by 3-methylcholanthrene, 3.4-benzpyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), were studied.	Methylcholanthrene	217-237	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	57-73
6326866-1	1984	Using antibodies against electrophoretically homogeneous cytochrome P-448 from rat liver microsomes induced by 3-methylcholanthrene, the changes in the immunologic identity and contents by cytochrome P-448 induced by 3-methylcholanthrene, 3.4-benzpyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), were studied.	Methylcholanthrene	217-237	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	189-205
6326866-4	1984	On the other hand, 3-methylcholanthrene, 3,4-benzpyrene and TCDD significantly and equally activates the cytochrome P-448-dependent benzpyrene hydroxylase, since the antibodies against cytochrome P-448 inhibit benzpyrene metabolism in the microsomes by 85-90%.	Methylcholanthrene	19-39	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	185-201
6326866-5	1984	The possible reasons for the TCDD-induced increase in the catalytic activity of cytochrome P-448 as compared to the immunologically identical cytochrome P-448 induced by 3-methylcholanthrene and 3,4-benzpyrene, are discussed.	Methylcholanthrene	170-190	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	80-96
6373027-0	1984	A biochemical and electron microscopic study of changes in the content of cytochrome P-450 in rat livers after cessation of treatment with phenobarbital, beta-naphtoflavone or 3-methylcholanthrene.	Methylcholanthrene	176-196	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
6427199-0	1984	Purification and characterization of four forms of cytochrome P-450 from liver microsomes of phenobarbital-treated and 3-methylcholanthrene-treated rats.	Methylcholanthrene	119-139	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
6326348-4	1984	Benzo[a]pyrene (BP)-metabolizing activity, NADPH-cytochrome c reductase activity, and cytochrome P-450 content in 3MC-treated fetuses were significantly increased to 2143.6, 137.6, and 323.8% of the control, respectively.	Methylcholanthrene	114-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
6326348-5	1984	Following 3MC administration, the maximum absorption of the cytochrome P-450-CO difference spectra in liver microsomes of fetuses was observed at 449-450 nm.	Methylcholanthrene	10-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Methylcholanthrene	93-113	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	0-4
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Methylcholanthrene	93-113	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Methylcholanthrene	9-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6427199-9	1984	The quantity of each form of cytochrome P-450 in microsomes was determined by quantitative immunoprecipitation, and selective induction of PB-1 and MC-1 by PB and MC, respectively, was confirmed.	Methylcholanthrene	148-150	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6325878-1	1984	A 53,000-dalton protein (p53) present in large amounts in several types of tumorigenic cells was rapidly degraded in nontumorigenic BALB/c 3T3 fibroblasts (t 1/2, approximately 0.5 h) but not in tumorigenic methylcholanthrene-induced mouse sarcoma cells (t 1/2, greater than 2 h).	Methylcholanthrene	207-225	transformation related protein 53, pseudogene	Mus musculus	25-28
6325878-9	1984	Although the amount of labeled p53 was increased in simian virus 40-transformed and methylcholanthrene-induced mouse sarcoma cells, the amount of p53 labeled during a 3-h pulse in Moloney virus- and Rous sarcoma virus-transformed cells and untransformed 3T3 cells was similar.	Methylcholanthrene	84-102	transformation related protein 53, pseudogene	Mus musculus	31-34
6584898-0	1984	Coding nucleotide sequence of 3-methylcholanthrene-inducible cytochrome P-450d cDNA from rat liver.	Methylcholanthrene	30-50	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	61-78
6584898-1	1984	We determined the coding nucleotide sequence of the mRNA for a 3-methylcholanthrene-inducible cytochrome P-450, P-450d, of rat liver by sequence analysis of cloned cDNAs.	Methylcholanthrene	63-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
6584898-1	1984	We determined the coding nucleotide sequence of the mRNA for a 3-methylcholanthrene-inducible cytochrome P-450, P-450d, of rat liver by sequence analysis of cloned cDNAs.	Methylcholanthrene	63-83	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	112-118
6326866-5	1984	The possible reasons for the TCDD-induced increase in the catalytic activity of cytochrome P-448 as compared to the immunologically identical cytochrome P-448 induced by 3-methylcholanthrene and 3,4-benzpyrene, are discussed.	Methylcholanthrene	170-190	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	142-158
6322806-0	1984	Elevated binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the Ah receptor in hepatic cytosols from phenobarbital-treated rats and mice.	Methylcholanthrene	60-80	aryl hydrocarbon receptor	Rattus norvegicus	88-99
6322806-1	1984	Binding of 3-methylcholanthrene (MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and other "MC-type" inducers to cytosolic Ah receptor sites is the first specific step in induction of aryl hydrocarbon hydroxylase (AHH; cytochrome P1-450) by these compounds.	Methylcholanthrene	11-31	aryl-hydrocarbon receptor	Mus musculus	124-135
6322806-1	1984	Binding of 3-methylcholanthrene (MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and other "MC-type" inducers to cytosolic Ah receptor sites is the first specific step in induction of aryl hydrocarbon hydroxylase (AHH; cytochrome P1-450) by these compounds.	Methylcholanthrene	11-31	aryl-hydrocarbon receptor	Mus musculus	185-213
6322806-1	1984	Binding of 3-methylcholanthrene (MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and other "MC-type" inducers to cytosolic Ah receptor sites is the first specific step in induction of aryl hydrocarbon hydroxylase (AHH; cytochrome P1-450) by these compounds.	Methylcholanthrene	11-31	aryl-hydrocarbon receptor	Mus musculus	215-218
6322806-6	1984	Although PB significantly elevated Ah receptor in hepatic cytosols of responsive rodents, many previous studies have shown that the maximal level of AHH activity in animals given PB and an "MC-type" inducer simultaneously is additive rather than synergistic.	Methylcholanthrene	190-192	aryl-hydrocarbon receptor	Mus musculus	149-152
6693411-1	1984	A rapid solid phase radioimmunoassay (RIA) for cytochromes P-450 has been developed utilizing specific monoclonal antibodies to major forms of rat liver cytochrome P-450 that are induced by 3-methylcholanthrene (MC-P-450) and phenobarbital (PB-P-450).	Methylcholanthrene	190-210	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	153-169
6546728-0	1984	Regulation of glutathione S-transferase mRNAs by phenobarbital and 3-methylcholanthrene: analysis using cDNA probes.	Methylcholanthrene	67-87	glutathione S-transferase kappa 1	Homo sapiens	14-39
6366529-2	1984	Upon incubating emodin with the hepatic S9 derived from PCB-pretreated rats, this anthraquinone exhibited mutagenicity in the presence of NADPH or NADH, and this enzymatic activation, maximal at pH 7.0 and occurring in the microsomes, was induced by the pretreatment of rats with PCB, 3-methyl-cholanthrene or phenobarbital and was inhibited by alpha-naphthoflavone, SKF 525A and carbon monoxide.	Methylcholanthrene	285-306	pyruvate carboxylase	Rattus norvegicus	56-59
6421495-5	1984	Simultaneous administration of Sudan III and 3-methylcholanthene (3-MC) induced cytochrome P-448 up to a level brought about by either Sudan III or 3-MC treatment alone.	Methylcholanthrene	66-70	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	91-96
6421495-5	1984	Simultaneous administration of Sudan III and 3-methylcholanthene (3-MC) induced cytochrome P-448 up to a level brought about by either Sudan III or 3-MC treatment alone.	Methylcholanthrene	148-152	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	91-96
6421495-8	1984	It is concluded that the cytochrome P-448 induced in liver by Sudan III is very similar to that induced by 3-MC.	Methylcholanthrene	107-111	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	25-41
6421502-5	1984	Furthermore, microsomes from MC-treated rats could be replaced by a reconstituted system containing purified cytochrome P-448, NADPH-cytochrome reductase and co-factors.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	109-125
6609319-1	1984	The immunoregulatory effects of TCGF (T-cell growth factor) on the generation and growth of syngeneic murine malignant glioma (20-methylcholanthrene-induced 203-glioma)-specific killer T-cell were investigated in C57BL/6 adult mice in order to clarify the immunopotential usefulness for anti-tumor local adoptive immunotherapy against malignant brain tumor.	Methylcholanthrene	127-148	interleukin 2	Mus musculus	32-36
6609319-1	1984	The immunoregulatory effects of TCGF (T-cell growth factor) on the generation and growth of syngeneic murine malignant glioma (20-methylcholanthrene-induced 203-glioma)-specific killer T-cell were investigated in C57BL/6 adult mice in order to clarify the immunopotential usefulness for anti-tumor local adoptive immunotherapy against malignant brain tumor.	Methylcholanthrene	127-148	interleukin 2	Mus musculus	38-58
6693411-6	1984	Significant increases in the MAb-specific P-450 were observed in MC-treated rats, guinea pigs, and C57BL/6 mice, all highly inducible for aryl hydrocarbon hydroxylase; little increase was observed for the relatively noninducible DBA/2 mouse strain.	Methylcholanthrene	65-67	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	138-166
6565518-2	1984	Cell surface antigens of the 3-methylcholanthrene-induced fibrosarcoma of C3H/HeJ mice, MCA-F, were extracted using 2.5% 1-butanol.	Methylcholanthrene	29-49	chemokine (C-C motif) ligand 2	Mus musculus	88-93
6422942-1	1984	Various substrates of rat liver microsomal UDP-glucuronosyltransferase were classified in vitro as preferred substrates of either 3-methylcholanthrene- or phenobarbital-inducible enzyme forms.	Methylcholanthrene	130-150	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	43-70
6141874-14	1984	3-Methylcholanthrene also caused 1 nm spectral shift in the absorption maxima of CO difference spectrum of the dithionite-reduced liver microsomal cytochrome P-450, forming P-449.	Methylcholanthrene	0-20	cytochrome P450 3A14	Cavia porcellus	147-178
6510338-0	1984	[Effect of the combined use of BCG, PPD, a protein-containing preparation from allogenic tissue and cyclophosphamide in the development of methylcholanthrene-induced tumors].	Methylcholanthrene	139-157	cellular communication network factor 6	Homo sapiens	36-39
6510338-1	1984	The organism resistance to the appearance of 20-methylcholanthrene-induced tumours may be enhanced by application of different immunologic factors (BCG, PPD, low-molecular allogenic protein) in combination with a single administration of cyclophosphane (CPh).	Methylcholanthrene	45-66	cellular communication network factor 6	Homo sapiens	153-156
6209214-1	1984	Suppressor factors in the serum of CBA mice bearing transplanted methylcholanthrene-induced tumours suppressed the leukocyte adherence inhibition reaction between tumour-sensitized peritoneal cells and a sequenced antigen, myelin basic protein (MBP).	Methylcholanthrene	65-83	myelin basic protein	Mus musculus	223-243
6209214-1	1984	Suppressor factors in the serum of CBA mice bearing transplanted methylcholanthrene-induced tumours suppressed the leukocyte adherence inhibition reaction between tumour-sensitized peritoneal cells and a sequenced antigen, myelin basic protein (MBP).	Methylcholanthrene	65-83	myelin basic protein	Mus musculus	245-248
6368742-1	1984	Catalase activity in liver homogenates was studied in normal and low endotoxin (LPS)-responder mice treated with various doses of LPS from S. typhimurium B or bearing tumours induced by 3-methylcholanthrene.	Methylcholanthrene	186-206	catalase	Mus musculus	0-8
6582291-2	1984	Michaelis-Menten kinetics were determined for glutathione S-transferase in pancreatic tissue supernatants from control, phenobarbital (PB), and 3-methylcholanthrene (3MCA)-pretreated Sprague-Dawley male rats.	Methylcholanthrene	166-170	hematopoietic prostaglandin D synthase	Rattus norvegicus	46-71
6228583-1	1984	Spleen cells from BALB/c mice bearing a small, but already clinically evident transplantable methylcholanthrene-induced sarcoma (CE-2) are not able to release interferons, proliferate and perform a cytotoxic response against CE-2 cells, nor able to inhibit their growth in vivo in a Winn-type neutralization assay.	Methylcholanthrene	93-111	catalase activity, kidney	Mus musculus	129-133
6326415-0	1984	Glucose-6-phosphatase activities in the developing rat liver and kidney and after phenobarbital, 3-methylcholanthrene, and actinomycin D pretreatment.	Methylcholanthrene	97-117	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	0-21
6318770-9	1983	In summary, the results described in this report suggest that: (a) induction of AFB1-4-hydroxylase activity by MC (or beta NF) is associated with the depression of AFB1 mutagenesis and with the induction of benzo[a]pyrene mutagenesis; and (b) induction by MC (or beta NF) of AHH activity, AFB1-4-hydroxylase activity and AFB2-4-hydroxylase activity is controlled by either the same or closely linked genetic factors.	Methylcholanthrene	111-113	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	275-278
6315393-5	1983	Cadmium inhalation also inhibited (by 50%) 3-methylcholanthrene (MC) induction of lung AHH when compared with MC-treated controls.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	87-90
6315393-5	1983	Cadmium inhalation also inhibited (by 50%) 3-methylcholanthrene (MC) induction of lung AHH when compared with MC-treated controls.	Methylcholanthrene	65-67	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	87-90
6425489-6	1983	In contrast, a marked enhancement of AHH activity in both organs was caused by pretreatment with the MC-type and mixed type inducers.	Methylcholanthrene	101-103	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-40
6658836-3	1983	The survival times of rats exposed to 65 ppm NO2 were prolonged with increase of 3MC doses, and AHH activity in lungs of rats rose with increase of 3MC doses.	Methylcholanthrene	148-151	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	96-99
6658836-5	1983	Induction of AHH activity of female rats administered 3MC was higher than that of male rats.	Methylcholanthrene	54-57	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-16
6418176-4	1983	Cytochrome P-450-dependent S-oxidation of thiobenzamide was induced in the liver by treatment of mice with phenobarbital and slightly increased by treatment with 3-methylcholanthrene, while in rat liver either of these treatments caused only a small increase in metabolism due to cytochrome P-450.	Methylcholanthrene	162-182	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
6719936-4	1984	Induction of cytochrome P-448, as specifically measured by ethoxyresorufin O-deethylase activity, occurs in rat liver, kidney and lung after administration of the carcinogens, 3-methylcholanthrene, Aroclor 1254, 2-anthramine, safrole, 7,12-dimethylbenz[a]anthracene, MNNG and 2-acetamidofluorene.	Methylcholanthrene	176-196	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	13-29
6416180-1	1983	Three isoenzymes of UDP-glucuronyltransferase (UDPGT) have been separated and purified from liver microsomes of untreated female rats or female rats pretreated with 3-methylcholanthrene.	Methylcholanthrene	165-185	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	20-45
6416180-1	1983	Three isoenzymes of UDP-glucuronyltransferase (UDPGT) have been separated and purified from liver microsomes of untreated female rats or female rats pretreated with 3-methylcholanthrene.	Methylcholanthrene	165-185	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	47-52
6416180-10	1983	This study reports the purification of two separate and distinct rat liver UDPGT isoenzymes capable of conjugating p-nitrophenol, only one of which is inducible by 3-methylcholanthrene treatment.	Methylcholanthrene	164-184	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	75-80
6418176-4	1983	Cytochrome P-450-dependent S-oxidation of thiobenzamide was induced in the liver by treatment of mice with phenobarbital and slightly increased by treatment with 3-methylcholanthrene, while in rat liver either of these treatments caused only a small increase in metabolism due to cytochrome P-450.	Methylcholanthrene	162-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	280-296
6317666-0	1983	Molecular cloning of a complementary DNA to 3-methylcholanthrene-inducible cytochrome P-450 mRNA from rat liver.	Methylcholanthrene	44-64	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	86-91
6651850-1	1983	Several rat liver cytochromes P-450 have been substantially purified in a one-step immunoadsorption procedure using Sepharose-bound monoclonal antibodies (MAbs) to the major forms of rat liver cytochrome P-450 induced by 3-methylcholanthrene and phenobarbital (MC-P-450 and PB-P-450, respectively).	Methylcholanthrene	221-241	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-209
6317666-2	1983	The mRNA was translated in an in vitro rabbit reticulocyte lysate system, and assayed for the synthesis of MC-inducible forms of cytochrome P-450 (cytochrome P-450MC) using anti-cytochrome P-450c antibody which reacted with two types of cytochrome P-450MC, P-450c, and P-450d.	Methylcholanthrene	107-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	140-145
6317666-2	1983	The mRNA was translated in an in vitro rabbit reticulocyte lysate system, and assayed for the synthesis of MC-inducible forms of cytochrome P-450 (cytochrome P-450MC) using anti-cytochrome P-450c antibody which reacted with two types of cytochrome P-450MC, P-450c, and P-450d.	Methylcholanthrene	107-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	158-165
6317666-2	1983	The mRNA was translated in an in vitro rabbit reticulocyte lysate system, and assayed for the synthesis of MC-inducible forms of cytochrome P-450 (cytochrome P-450MC) using anti-cytochrome P-450c antibody which reacted with two types of cytochrome P-450MC, P-450c, and P-450d.	Methylcholanthrene	107-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	248-255
6314605-5	1983	345-HBB is a strict 3-methylcholanthrene (MC) type of hepatic microsomal drug metabolizing enzyme inducer and caused a dose-related increase of cytochrome P-450.	Methylcholanthrene	20-40	hemoglobin subunit beta	Rattus norvegicus	4-7
6314605-5	1983	345-HBB is a strict 3-methylcholanthrene (MC) type of hepatic microsomal drug metabolizing enzyme inducer and caused a dose-related increase of cytochrome P-450.	Methylcholanthrene	42-44	hemoglobin subunit beta	Rattus norvegicus	4-7
6314905-0	1983	Differential metabolism of acetanilide versus ethoxycoumarin and benzo[a]pyrene by two 3-methylcholanthrene-inducible forms of rat liver cytochrome P-450.	Methylcholanthrene	87-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	137-153
6631725-6	1983	CL*int,HB and CL*int,AP were both increased by PB pretreatment, but 3-MC-pretreatment increased CL*int,AP, whereas CL*int,HB was decreased.	Methylcholanthrene	68-72	clathrin interactor 1	Rattus norvegicus	96-105
6631725-6	1983	CL*int,HB and CL*int,AP were both increased by PB pretreatment, but 3-MC-pretreatment increased CL*int,AP, whereas CL*int,HB was decreased.	Methylcholanthrene	68-72	clathrin interactor 1	Rattus norvegicus	115-124
6192910-4	1983	All the cell types except late-passage rat epidermal cells metabolized benzo(a)pyrene at comparable rates, and expressed aryl hydrocarbon hydroxylase maximally inducible by similar concentrations of 3-methylcholanthrene.	Methylcholanthrene	199-219	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	121-149
6314905-1	1983	The present study compares the catalytic activities of two 3-methylcholanthrene (3-MC) inducible forms of cytochrome P-450.	Methylcholanthrene	59-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
6314905-1	1983	The present study compares the catalytic activities of two 3-methylcholanthrene (3-MC) inducible forms of cytochrome P-450.	Methylcholanthrene	81-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
6350300-1	1983	Cathepsin B (EC 3.4.22.1) and an analogous thiol proteinase were isolated from mouse liver and from a transplantable tumor induced by methylcholanthrene, respectively, by a sequence of steps involving salt fractionation and ion exchange and gel permeation chromatography.	Methylcholanthrene	134-152	cathepsin B	Mus musculus	0-11
6640434-2	1983	3-Methylcholanthrene (3-MC) and pregnenolone-16 alpha-carbonitrile (PCN), known to induce different forms of cytochrome P-450, when administered together increased benzo[a]pyrene oxidation to the same level as observed following 3-MC treatment alone.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
6415870-1	1983	The specificity of two major types of cytochrome P-450 of rat liver microsomes induced by phenobarbital (PB) and 3-methylcholanthrene (MC) toward activation of three 14C-labeled tetrachlorobiphenyl (TCB) isomers to protein-bound metabolites was examined by intact microsomal and reconstituted monooxygenase systems.	Methylcholanthrene	113-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
6415870-1	1983	The specificity of two major types of cytochrome P-450 of rat liver microsomes induced by phenobarbital (PB) and 3-methylcholanthrene (MC) toward activation of three 14C-labeled tetrachlorobiphenyl (TCB) isomers to protein-bound metabolites was examined by intact microsomal and reconstituted monooxygenase systems.	Methylcholanthrene	135-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
6415870-3	1983	However, the binding of 3,4,3",4"-[14C]TCB was catalyzed most actively by the system containing a MC-inducible (P-448 type) cytochrome P-450 from rat liver microsomes.	Methylcholanthrene	98-100	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	124-140
6625610-8	1983	Competition studies showed that these proteins were not steroid receptors, and that only polycyclic aromatic hydrocarbons which could induce cytochrome P-450c were able to displace 3-methylcholanthrene from the binding site.	Methylcholanthrene	181-201	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	141-158
6411467-3	1983	The cytochrome P-450 content and response to induction by 3-methylcholanthrene and phenobarbitone; the distribution of lactate dehydrogenase, glucose-6-phosphatase, pyruvate kinase and tyrosine aminotransferase activities in the sub-populations is also reported.	Methylcholanthrene	58-78	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-20
6679338-0	1983	Separation of two forms of cytochrome P-450 with aryl hydrocarbon hydroxylase activity from intestinal mucosa microsomes of rabbits treated with 3-methylcholanthrene.	Methylcholanthrene	145-165	cytochrome P-450	Oryctolagus cuniculus	27-43
6679338-1	1983	Two forms of cytochrome P-450, designated P-448a and P-448b, were purified from intestinal mucosa microsomes of rabbits treated with 3-methylcholanthrene.	Methylcholanthrene	133-153	cytochrome P-450	Oryctolagus cuniculus	13-29
6635324-1	1983	The effect of 3-methylcholanthrene (3-MC), an inducer of the mixed function oxidases system (MFOS), was investigated in male Wistar rats in relation to plasmatic cholesterol and hepatic glucose-6-phosphate dehydrogenase (G-6-PD).	Methylcholanthrene	14-34	glucose-6-phosphate dehydrogenase	Rattus norvegicus	186-219
6635324-1	1983	The effect of 3-methylcholanthrene (3-MC), an inducer of the mixed function oxidases system (MFOS), was investigated in male Wistar rats in relation to plasmatic cholesterol and hepatic glucose-6-phosphate dehydrogenase (G-6-PD).	Methylcholanthrene	14-34	glucose-6-phosphate dehydrogenase	Rattus norvegicus	221-227
6635324-1	1983	The effect of 3-methylcholanthrene (3-MC), an inducer of the mixed function oxidases system (MFOS), was investigated in male Wistar rats in relation to plasmatic cholesterol and hepatic glucose-6-phosphate dehydrogenase (G-6-PD).	Methylcholanthrene	36-40	glucose-6-phosphate dehydrogenase	Rattus norvegicus	186-219
6635324-1	1983	The effect of 3-methylcholanthrene (3-MC), an inducer of the mixed function oxidases system (MFOS), was investigated in male Wistar rats in relation to plasmatic cholesterol and hepatic glucose-6-phosphate dehydrogenase (G-6-PD).	Methylcholanthrene	36-40	glucose-6-phosphate dehydrogenase	Rattus norvegicus	221-227
6635324-4	1983	3-MC treatment resulted also in an increase of hepatic G-6-PD.	Methylcholanthrene	0-4	glucose-6-phosphate dehydrogenase	Rattus norvegicus	55-61
6883573-0	1983	Differential effects of phenobarbitone and 3-methylcholanthrene induction on the hepatic microsomal metabolism and cytochrome P-450-binding of phenoxazone and a homologous series of its n-alkyl ethers (alkoxyresorufins).	Methylcholanthrene	43-63	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	115-131
6411328-0	1983	Antibody inhibition of oxidative activation and inactivation of the carcinogen 2-acetylaminofluorene by purified hepatic cytochrome P-450 from 3-methylcholanthrene pretreated rats.	Methylcholanthrene	143-163	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	121-137
6411328-5	1983	These results suggest that P-450 D is the predominant cytochrome P-450 isozyme responsible for AAF N- and ring-oxidations in liver microsomes from MC-pretreated rats.	Methylcholanthrene	147-149	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	27-34
6411328-5	1983	These results suggest that P-450 D is the predominant cytochrome P-450 isozyme responsible for AAF N- and ring-oxidations in liver microsomes from MC-pretreated rats.	Methylcholanthrene	147-149	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
6872097-3	1983	It is metabolized by microsomes from control rats and by rats treated with phenobarbital or 3-methylcholanthrene at 3.9, 4.2 and 7.8 nmol/nmol cytochrome P-450/min, respectively.	Methylcholanthrene	92-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-163
6137342-3	1983	In microsomes from 3MC-induced rats, only naphthimidazole inhibited metabolism at a concentration of 5 X 10(-4) M, but all four imidazole derivatives increased the proportion of BaP 9,10-dihydrodiol formed.	Methylcholanthrene	19-22	prohibitin 2	Rattus norvegicus	178-181
6137342-8	1983	This study also shows that epoxide hydrolase activity limits the rate of formation of BaP 9,10-dihydrodiol by hepatic microsomes from 3MC-induced rats, but not by hepatic microsomes from control or PB-induced rats.	Methylcholanthrene	134-137	prohibitin 2	Rattus norvegicus	86-89
6617839-3	1983	A similar action under analogous conditions is produced by 3-methylcholanthrene which is widely used as an inductor of cytochrome P-450.	Methylcholanthrene	59-79	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	119-135
6617839-4	1983	The induction of liver cytochrome P-450 by cyclophosphamide or 3-methylcholanthrene is accompanied by pronounced inhibition of immunoreactivity.	Methylcholanthrene	63-83	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	23-39
6617839-6	1983	Apparently, the reciprocal action of cyclophosphamide and 3-methylcholanthrene on cytochrome P-450 and immunity is a consequence of intense formation with the involvement of cytochrome P-450 of highly reactive metabolites interfering with the function of immunocompetent cells.	Methylcholanthrene	58-78	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-98
6617839-6	1983	Apparently, the reciprocal action of cyclophosphamide and 3-methylcholanthrene on cytochrome P-450 and immunity is a consequence of intense formation with the involvement of cytochrome P-450 of highly reactive metabolites interfering with the function of immunocompetent cells.	Methylcholanthrene	58-78	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	174-190
6639678-6	1983	Equilibrium partition studies of the higher-affinity class of microsomal binding site for cimetidine showed that the twofold increase in the cytochrome P-450 content of microsomes effected by 3-methylcholanthrene pretreatment was more than offset by a diminished proportion of the total cimetidine-binding capacity present as the higher-affinity, pharmacologically significant, receptor (18%, cf.	Methylcholanthrene	192-212	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
6640434-2	1983	3-Methylcholanthrene (3-MC) and pregnenolone-16 alpha-carbonitrile (PCN), known to induce different forms of cytochrome P-450, when administered together increased benzo[a]pyrene oxidation to the same level as observed following 3-MC treatment alone.	Methylcholanthrene	22-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
6640434-2	1983	3-Methylcholanthrene (3-MC) and pregnenolone-16 alpha-carbonitrile (PCN), known to induce different forms of cytochrome P-450, when administered together increased benzo[a]pyrene oxidation to the same level as observed following 3-MC treatment alone.	Methylcholanthrene	229-233	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
6882464-3	1983	These reductions and cytochrome P-450-dependent since they are inhibited by CO and metyrapone, and are increased after pretreatment of rats by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	161-181	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
6870906-0	1983	Immunological and enzymatic comparison of hepatic cytochrome P-450 fractions from phenobarbital-, 3-methylcholanthrene-, beta-naphthoflavone- and 2,3,7,8- tetrachlorodibenzo-p-dioxin-treated rats.	Methylcholanthrene	96-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
6870906-7	1983	By these different criteria, beta-naphthoflavone, 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin seem to induce a common cytochrome P-450 species in rat liver.	Methylcholanthrene	50-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	135-151
6601984-1	1983	Cloned lines of the methylcholanthrene-induced DBA/2 low-metastatic T-lymphoma Eb line and its highly metastatic variant ESb line were compared for the ability to degrade proteoglycans in the subendothelial extracellular matrix (ECM) produced by cultured endothelial cells.	Methylcholanthrene	20-38	DBA2	Homo sapiens	47-52
6885735-0	1983	Purification and characterization of pulmonary cytochrome P-450 from 3-methylcholanthrene-treated rats.	Methylcholanthrene	69-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	58-63
6865920-10	1983	For microsomes from control and phenobarbital-treated rats, this ratio was between 3:1 and 4:1 whereas microsomes from 3-methylcholanthrene-treated rats (greater than 70% cytochrome P-450c) gave a ratio of between 1:1.5 and 1:2.	Methylcholanthrene	119-139	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	171-188
6885735-1	1983	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 313 fold from lung microsomes of 3-methylcholanthrene (MC)-treated rats.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-42
6885735-1	1983	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 313 fold from lung microsomes of 3-methylcholanthrene (MC)-treated rats.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	54-61
6885735-1	1983	A major form of pulmonary cytochrome P-450 (pulmonary P-450MC) was purified approximately 313 fold from lung microsomes of 3-methylcholanthrene (MC)-treated rats.	Methylcholanthrene	59-61	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-42
6885735-3	1983	By SDS-polyacrylamide gel electrophoresis, the molecular weight of pulmonary P-450MC was estimated to be 54,000, which is smaller than that of a major form of hepatic cytochrome P-450 (hepatic P-450MC) purified from MC-treated rats.	Methylcholanthrene	82-84	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	193-200
6863437-2	1983	Five mono-, four di- and thirteen trihydroxylated metabolites were found after incubation of MC in mouse liver microsomal fraction for 15 min, in the presence of NADPH.	Methylcholanthrene	93-95	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	162-167
6411562-0	1983	[Hepatic enzyme induction by 3-methylcholanthrene-type PCB and development of its toxicity].	Methylcholanthrene	29-49	pyruvate carboxylase	Homo sapiens	55-58
6885729-0	1983	Phenobarbital- and 3-methylcholanthrene-induced synthesis of two different molecular species of microsomal cytochrome P-450 in rat liver.	Methylcholanthrene	19-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
6885729-6	1983	Similarly, MC administration selectively induced the synthesis of P-450(MC), which was about 24 times the control at 6 h, whereas those of P-450(PB), cytochrome b5, and fpT were not affected by MC.	Methylcholanthrene	11-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	66-74
6885729-9	1983	PB and MC induced the syntheses of P-450(PB) and P-450(MC) by bound ribosomes but not by free ribosomes, and the contribution of bound ribosomes to the syntheses of these two species of cytochrome P-450 was predominant in the case of drug-treated animals.	Methylcholanthrene	7-9	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	49-57
6885729-9	1983	PB and MC induced the syntheses of P-450(PB) and P-450(MC) by bound ribosomes but not by free ribosomes, and the contribution of bound ribosomes to the syntheses of these two species of cytochrome P-450 was predominant in the case of drug-treated animals.	Methylcholanthrene	7-9	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	186-202
6870848-1	1983	A fluorescence-microscopic method has been developed for measurement of the intracellular kinetics of the cytochrome P-450 reaction, ethoxyresorufin O-de-ethylation, in individual hepatocytes in unfixed non-frozen liver sections obtained from control or 3-methylcholanthrene-pretreated mice.	Methylcholanthrene	254-274	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	106-122
6189495-2	1983	The substrate (Trp-P-2) disappearance by hepatocytes from untreated rats was slow, but enhanced by 3-methylcholanthrene (MC) pretreatment of rats.	Methylcholanthrene	99-119	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	15-22
6189495-2	1983	The substrate (Trp-P-2) disappearance by hepatocytes from untreated rats was slow, but enhanced by 3-methylcholanthrene (MC) pretreatment of rats.	Methylcholanthrene	121-123	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	15-22
6189495-5	1983	The covalent binding to Trp-P-2 to DNA, RNA and protein in hepatocytes from untreated rats was about 5-10 times less than that in hepatocytes from MC-pretreated rats.	Methylcholanthrene	147-149	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	24-31
6189495-6	1983	7,8-Benzoflavone strongly inhibited the substrate disappearance and the binding of Trp-P-2 to DNA in hepatocytes from MC-pretreated rats.	Methylcholanthrene	118-120	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	83-90
6189495-7	1983	These results indicate that Trp-P-2 is metabolically activated by the P-448 type of cytochrome P-450 which is induced by MC.	Methylcholanthrene	121-123	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	28-35
6189495-8	1983	Diethylmaleate enhanced by about 50% the binding of Trp-P-2 to DNA in hepatocytes from MC-pretreated rats.	Methylcholanthrene	87-89	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	52-59
6862149-5	1983	V. anguillarum LPS also inhibited the growth of syngeneic fibrosarcoma induced  by 3-methylcholanthrene in C57BL/6 mice.	Methylcholanthrene	83-103	toll-like receptor 4	Mus musculus	15-18
6301823-0	1983	Defective binding of 3-methylcholanthrene to the Ah receptor within C3H/1OT1/2 clone 8 mouse fibroblasts in culture.	Methylcholanthrene	21-41	aryl-hydrocarbon receptor	Mus musculus	49-60
6404267-0	1983	Isolation of a high spin form of cytochrome P-450 induced in rat liver by 3-methylcholanthrene.	Methylcholanthrene	74-94	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
6838626-9	1983	Microsomal monooxygenase oxidized styrene to R-(+)- and S-(-)-phenyloxiranes (ratio 1.3:1), and the ratio was little changed by the pretreatment of the animal with phenobarbital, 3-methylcholanthrene and polychlorinated biphenyls.	Methylcholanthrene	179-199	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-24
6343038-2	1983	After 6 mo of treatment, IgG-insulin antibodies were found in only 14% of the patients receiving homologous MC insulins, but in 29% of the patients on heterologous MC insulins.	Methylcholanthrene	108-110	insulin	Homo sapiens	29-36
6343038-4	1983	The previously reported strong influence of immunogenetic factors in determining the magnitude of the anti-insulin immune response was supported by the findings obtained in the pork MC insulin-treated diabetic individuals.	Methylcholanthrene	182-184	insulin	Homo sapiens	107-114
6343038-4	1983	The previously reported strong influence of immunogenetic factors in determining the magnitude of the anti-insulin immune response was supported by the findings obtained in the pork MC insulin-treated diabetic individuals.	Methylcholanthrene	182-184	insulin	Homo sapiens	185-192
6220407-9	1983	Furthermore, the findings that (a) multiple methylcholanthrene-induced tumors express serologically related antigens (as well as the unique ones that have been previously demonstrated by transplantation tests) and (b) these serologically related antigens can be found on Igh-V-controlled T cell communication molecules raise the intriguing possibility that, like certain viruses, methylcholanthrene reacts with specific regions of cellular DNA that either directly or indirectly regulate the expression of other specific genes (in this particular case the genes that encode the T cell communication molecules).	Methylcholanthrene	44-62	immunoglobulin heavy locus	Homo sapiens	271-276
6687522-6	1983	Radiolabeled pGTB6 was utilized in RNA gel-blot experiments to determine that the size of glutathione S-transferase B mRNA is 980 nucleotides and the degree of induction of the mRNA in response to 3-methylcholanthrene administration is threefold.	Methylcholanthrene	197-217	hematopoietic prostaglandin D synthase	Rattus norvegicus	90-115
6848192-7	1983	The inducing effect of TPA on ODC activity was potentiated by a simultaneous administration of MC to C57BL/6 mice; combined TPA and TCDD to DBA/2 mice exerted an additive effect on hepatic ODC activity.	Methylcholanthrene	95-97	ornithine decarboxylase, structural 1	Mus musculus	30-33
6848192-9	1983	effectively inhibited the induction of ODC activity elicited by TPA, MC, or TCDD either alone or in various combinations but did not interfere with AHH induction.	Methylcholanthrene	69-71	ornithine decarboxylase, structural 1	Mus musculus	39-42
6848192-10	1983	These data indicate that different regulatory factors are involved in the ODC induction process elicited by TPA and polycyclic aromatic compounds and that MC and TCDD may induce ODC activity by different mechanisms.	Methylcholanthrene	155-157	ornithine decarboxylase, structural 1	Mus musculus	178-181
6404899-5	1983	On the other hand, 3-methylcholanthrene (MC) treatment stimulated the formation of 3-hexanol and the formation of the other two isomeric alcohols was rather decreased.	Methylcholanthrene	19-39	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	41-43
6408471-5	1983	The contents of liver microsomal cytochrome p-450 of mice pretreated with PB or MC were about twice those of non-treated mice.	Methylcholanthrene	80-82	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	33-49
6296075-2	1983	Specific immunochemical techniques were used to quantitate the levels of eight isozymes of cytochrome P-450 (P-450) and epoxide hydrolase in liver microsomes of untreated rats and rats treated with phenobarbital, 3-methylcholanthrene, a mixture of these two compounds, nine individual polybrominated biphenyl (PBB) congeners, and a commercial mixture of PBBs.	Methylcholanthrene	213-233	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-107
6231877-7	1983	Further, we found a structural gene on MC-induced tumors that could absorb out this activity, and the structural gene for this antigen is coded for the same region as the Igh gene loci.	Methylcholanthrene	39-41	immunoglobulin heavy locus	Homo sapiens	171-174
6559101-1	1983	Tumor-specific transplantation antigens (TSTA) were purified from 3 M KCl and butanol extracts of C3H/HeJ 3-methylcholanthrene-induced fibrosarcomas by preparative isotachophoresis (pITP).	Methylcholanthrene	106-126	heat shock protein 90 alpha (cytosolic), class B member 1	Mus musculus	41-45
6601512-0	1983	Growth inhibition of an MC-induced mouse sarcoma by TCGF (IL 2)-containing preparations.	Methylcholanthrene	24-26	interleukin 2	Mus musculus	52-56
6601512-0	1983	Growth inhibition of an MC-induced mouse sarcoma by TCGF (IL 2)-containing preparations.	Methylcholanthrene	24-26	interleukin 2	Mus musculus	58-62
6601512-2	1983	Supernatants from Con A-stimulated rat spleen cell cultures containing T cell growth factor inhibited growth of a transplantable 3-methylcholanthrene-induced sarcoma in syngeneic mice.	Methylcholanthrene	129-149	interleukin 2	Rattus norvegicus	71-91
6291757-2	1983	This induced cytochrome(s) was characterized and compared to the major forms of cytochrome P-450 induced by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	126-146	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
6291757-4	1983	The results indicate that 2-acetylaminofluorene induces a form(s) of cytochrome P-450 especially effective in the metabolism of this substance itself (i.e., the process can be called substrate induction) and different from the major forms of cytochrome P-450 induced by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	288-308	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	69-85
6641283-1	1983	After an intra-muscular application of 3-methylcholanthrene (MCA) in a dose of 0.2 mg/animal to SPF mice, strain C57B1/10, changes in the lymphocyte nucleoli activation (LNA) and changes of the mononuclear phagocytic system (MPS) in blood and tissues were monitored.	Methylcholanthrene	39-59	SEC14-like lipid binding 2	Mus musculus	96-99
6189709-2	1983	The action of benzo(a)pyrene, 3-methylcholanthrene and 7,12-dimethylbenzo(a)anthracene in the activity of the rat thymus D-T diaphorase (EC 1.6.99.2) and the NAD(P)H cytochrome C (EC 1.6.99.3) reductases of particulate fractions were studied in intact and adrenalectomized animals.	Methylcholanthrene	30-50	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	121-135
6885120-0	1983	Role of H-2 antigens in the host response against transplanted methylcholanthrene-induced tumors.	Methylcholanthrene	63-81	relaxin 2	Homo sapiens	8-11
6874165-1	1983	The effects of polycyclic aromatic hydrocarbons (PAH) such as benzanthracene (BA) and methylcholanthrene (MCA) on 3H-thymidine incorporation and aryl hydrocarbon hydroxylase (AHH) induction were assayed in mitogen-activated and non-activated splenic lymphocyte cultures derived from three strains of mice (C57BL, C3H and DBA/2).	Methylcholanthrene	86-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	145-173
6874165-3	1983	In mitogen-activated and non-activated lymphocytes from C57BL and C3H mice (AHH responsive strains) the percentage of blastogenesis induced by BA or MCA was higher than in lymphocytes from the non-responsive strain (DBA/2).	Methylcholanthrene	149-152	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	76-79
6677623-2	1983	In order to investigate this process in vitro, cloned lines of the low-metastatic methylcholanthrene-induced DBA/2 T lymphoma Eb and its highly metastatic variant line ESb were compared for their mode of interaction (attachment, invasion and morphological appearance) with a confluent monolayer of cultured vascular endothelial cells and with the subendothelial extracellular matrix (ECM).	Methylcholanthrene	82-100	DBA2	Homo sapiens	109-114
6630281-2	1983	Inhibition by SKF 525 A or dithiocarb as well as induction by pretreatment with phenobarbital or 20-methylcholanthrene suggest participation of cytochrome P-450 in this reaction.	Methylcholanthrene	97-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
6645934-3	1983	The activity of MAO was determined in liver homogenates of young rats at 30, 60 and 90 days of age, using a spectrophotometric method by Mc Even and Cohen with benzylamine as a substrate.	Methylcholanthrene	137-139	monoamine oxidase A	Rattus norvegicus	16-19
6306423-0	1983	Benz[a]anthracene and 3-methylcholanthrene induction of cytochrome P-450 in C3H/10T1/2 mouse fibroblasts.	Methylcholanthrene	22-42	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	56-72
6188731-3	1983	The latter studies showed that specificity detected by the MC-26.1 antibody coprecipitated with determinants detected by conventional anti-MB3 and MT3, but not with HLA-DR4 antisera.	Methylcholanthrene	59-61	metallothionein 3	Homo sapiens	147-150
6188731-6	1983	Coprecipitation studies indicate that the antigen defined by MC-26.1 coprecipitates with MB and MT specificities suggesting that the antibody defines a new specificity on the MB3 and MT3 molecules.	Methylcholanthrene	61-63	metallothionein 3	Homo sapiens	183-186
6408389-0	1983	Immunochemical evidence for two 3-methylcholanthrene-inducible forms of cytochrome P-448 in rat liver microsomes using a double-antibody radioimmunoassay procedure.	Methylcholanthrene	32-52	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	72-88
6408389-4	1983	Utilizing the RIAs, both forms of cytochrome P-448 were found in significant quantities in liver microsomes of rats treated with 3-MC, 3,4,5-HCB, isosafrole, and Aroclor 1254 but only in minute concentrations in untreated and phenobarbital-treated rats.	Methylcholanthrene	129-133	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	34-50
6306424-0	1983	Purification and characterization of three forms of microsomal cytochrome P-450 in liver from 3-methylcholanthrene-treated guinea pigs.	Methylcholanthrene	94-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
6817801-9	1982	Cytochrome P-450c, the predominant isozyme inducible in rat liver by 3-methylcholanthrene, was purified from Holtzman and Long-Evans rats.	Methylcholanthrene	69-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-17
6897517-0	1982	Identification and quantitation of a 2.0-kilobase messenger ribonucleic acid coding for 3-methylcholanthrene-induced cytochrome P-450 using cloned cytochrome P-450 complementary deoxyribonucleic acid.	Methylcholanthrene	88-108	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
6897517-0	1982	Identification and quantitation of a 2.0-kilobase messenger ribonucleic acid coding for 3-methylcholanthrene-induced cytochrome P-450 using cloned cytochrome P-450 complementary deoxyribonucleic acid.	Methylcholanthrene	88-108	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	147-163
6897517-1	1982	We have used a plasmid containing DNA complementary to one of the two size classes of mRNA coding for 3-methylcholanthrene-induced cytochrome P-450 from rat liver to characterize and quantitate that mRNA.	Methylcholanthrene	102-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
6897517-7	1982	It was conclusively shown to contain cytochrome P-450 cDNA sequences by demonstrating that the mRNA which specifically hybridized to nitrocellulose-bound plasmid p23 could be translated in vitro into peptides that were immunoprecipitable with monoclonal antibodies specific for 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	278-298	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
6897517-7	1982	It was conclusively shown to contain cytochrome P-450 cDNA sequences by demonstrating that the mRNA which specifically hybridized to nitrocellulose-bound plasmid p23 could be translated in vitro into peptides that were immunoprecipitable with monoclonal antibodies specific for 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	278-298	RAS related	Rattus norvegicus	162-165
6897517-9	1982	Plasmid p23 hybridized strictly to a single size of mRNA that was about 2000 nucleotides in length, the smaller of the two size classes of mRNA coding for 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	155-175	RAS related	Rattus norvegicus	8-11
6897517-9	1982	Plasmid p23 hybridized strictly to a single size of mRNA that was about 2000 nucleotides in length, the smaller of the two size classes of mRNA coding for 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	155-175	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	184-200
6897517-10	1982	From this we concluded that, at least within the region of the mRNA contained within the insert of plasmid p23, the two size classes of 3-methylcholanthrene-induced cytochrome P-450 mRNA were very different in sequence.	Methylcholanthrene	136-156	RAS related	Rattus norvegicus	107-110
6897517-10	1982	From this we concluded that, at least within the region of the mRNA contained within the insert of plasmid p23, the two size classes of 3-methylcholanthrene-induced cytochrome P-450 mRNA were very different in sequence.	Methylcholanthrene	136-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
6897517-11	1982	The mRNA complementary to plasmid p23 was increased about 4-fold after in vivo administration of 3-methylcholanthrene under conditions that result in maximal induction of 3-methylcholanthrene-induced cytochrome P-450 enzymatic activity.	Methylcholanthrene	97-117	RAS related	Rattus norvegicus	34-37
6897517-11	1982	The mRNA complementary to plasmid p23 was increased about 4-fold after in vivo administration of 3-methylcholanthrene under conditions that result in maximal induction of 3-methylcholanthrene-induced cytochrome P-450 enzymatic activity.	Methylcholanthrene	97-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	200-216
6897517-11	1982	The mRNA complementary to plasmid p23 was increased about 4-fold after in vivo administration of 3-methylcholanthrene under conditions that result in maximal induction of 3-methylcholanthrene-induced cytochrome P-450 enzymatic activity.	Methylcholanthrene	171-191	RAS related	Rattus norvegicus	34-37
6897517-11	1982	The mRNA complementary to plasmid p23 was increased about 4-fold after in vivo administration of 3-methylcholanthrene under conditions that result in maximal induction of 3-methylcholanthrene-induced cytochrome P-450 enzymatic activity.	Methylcholanthrene	171-191	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	200-216
6897517-12	1982	This increase in cytochrome P-450 mRNA parallels the increase in cytochrome P-450 enzymatic activity observed after 3-methylcholanthrene administration.	Methylcholanthrene	116-136	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
6897517-12	1982	This increase in cytochrome P-450 mRNA parallels the increase in cytochrome P-450 enzymatic activity observed after 3-methylcholanthrene administration.	Methylcholanthrene	116-136	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
7150559-5	1982	Cytochromes P-450c and P-450d were coinduced by 3-methylcholanthrene, isosafrole, and Aroclor-1254, but their relative amounts varied.	Methylcholanthrene	48-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	12-29
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Methylcholanthrene	51-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Methylcholanthrene	51-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Methylcholanthrene	150-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Methylcholanthrene	150-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
6290035-2	1982	The BP bound to the carcinogen-binding protein (CBP) was exchangeable in a time- and temperature-dependent fashion and has a Kd of 1.8 X 10(-9) M. Competitive binding studies indicate that chemical carcinogens [3-methylcholanthrene, benz(a)anthracene, dibenz(a,c)anthracene] and other inducers of aryl hydrocarbon hydroxylase (5,6- and 7,8-benzoflavone) compete to varying degrees with BP for binding.	Methylcholanthrene	211-231	CREB binding protein	Mus musculus	20-46
6290035-2	1982	The BP bound to the carcinogen-binding protein (CBP) was exchangeable in a time- and temperature-dependent fashion and has a Kd of 1.8 X 10(-9) M. Competitive binding studies indicate that chemical carcinogens [3-methylcholanthrene, benz(a)anthracene, dibenz(a,c)anthracene] and other inducers of aryl hydrocarbon hydroxylase (5,6- and 7,8-benzoflavone) compete to varying degrees with BP for binding.	Methylcholanthrene	211-231	CREB binding protein	Mus musculus	48-51
6130905-2	1982	UDP-GT activity after 3-methylcholanthrene (3-MC) and phenobarbital (PB) treatment was studied in additional rats for comparative purposes.	Methylcholanthrene	22-42	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
6130905-2	1982	UDP-GT activity after 3-methylcholanthrene (3-MC) and phenobarbital (PB) treatment was studied in additional rats for comparative purposes.	Methylcholanthrene	44-48	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
6130905-5	1982	UDP-GT activity toward group-1 aglycones was increased by 3-MC in Wistar and heterozygous rats but was not enhanced in Gunn rats by any inducer.	Methylcholanthrene	58-62	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
6130905-12	1982	Thus, 3-MC, PB, and PCN induce UDP-GT activities toward different groups of acceptors of glucuronic acid.	Methylcholanthrene	6-10	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-37
6820042-2	1982	In kidney microsomes, both contents of cytochrome P-450 (448) and activity of N4-hydroxylase were markedly increased by pretreatment with 3,4,5,3",4"-pentachlorobiphenyl (PenCB) (about 4 times), although neither one was increased by 3-methylcholanthrene (3-MC) and phenobarbital (PB) pretreatments.	Methylcholanthrene	233-253	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6820042-2	1982	In kidney microsomes, both contents of cytochrome P-450 (448) and activity of N4-hydroxylase were markedly increased by pretreatment with 3,4,5,3",4"-pentachlorobiphenyl (PenCB) (about 4 times), although neither one was increased by 3-methylcholanthrene (3-MC) and phenobarbital (PB) pretreatments.	Methylcholanthrene	255-259	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6820042-3	1982	In liver microsomes, on the other hand, both N4-hydroxylase activity and cytochrome P-450 (448) contents were increased by either PenCB or 3-MC pretreatment, whereas by PB pretreatment, N4-hydroxylase activity was not changed although cytochrome P-450 contents was increased 2-fold.	Methylcholanthrene	139-143	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
6820042-3	1982	In liver microsomes, on the other hand, both N4-hydroxylase activity and cytochrome P-450 (448) contents were increased by either PenCB or 3-MC pretreatment, whereas by PB pretreatment, N4-hydroxylase activity was not changed although cytochrome P-450 contents was increased 2-fold.	Methylcholanthrene	139-143	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
7168193-10	1982	The levels of some of these cytochrome P-450 isozymes have been quantified immunologically in hepatic microsomal preparations from untreated rats and following induction by phenobarbital, 3-methylcholanthrene or Aroclor 1254.	Methylcholanthrene	188-208	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
6295646-7	1982	One of the MC-type PBBs, namely 3,3",4,4"-tetrabromobiphenyl, which has been tentatively identified in the commercial PBB mixture, fireMaster BP-6, was at least 50 times more potent as an inducer of AHH activity than the commercial PBB mixture.	Methylcholanthrene	11-13	Blood pressure QTL 6	Rattus norvegicus	142-146
6295646-7	1982	One of the MC-type PBBs, namely 3,3",4,4"-tetrabromobiphenyl, which has been tentatively identified in the commercial PBB mixture, fireMaster BP-6, was at least 50 times more potent as an inducer of AHH activity than the commercial PBB mixture.	Methylcholanthrene	11-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	199-202
6960973-2	1982	In methylcholanthrene (MC)-induced activities of AHH no significant differences were observed between the above groups.	Methylcholanthrene	3-21	aryl hydrocarbon receptor repressor	Homo sapiens	49-52
6960973-2	1982	In methylcholanthrene (MC)-induced activities of AHH no significant differences were observed between the above groups.	Methylcholanthrene	23-25	aryl hydrocarbon receptor repressor	Homo sapiens	49-52
6890504-7	1982	In vitro, the gallates proved to be potent inhibitors of ethoxycoumarin deethylation in liver microsomes from untreated and phenobarbital-treated rats; however, when cytochrome P-448 had been induced by pretreatment with 3-methylcholanthrene, ethoxycoumarin deethylase was less sensitive to the inhibitory action of the gallates.	Methylcholanthrene	221-241	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	166-182
7108220-6	1982	On the other hand, lymphocytes from mice immunized with bovine alpha-crystallin can be stimulated to proliferate to bovine crystallin, but not to either unfractionated mouse crystallin (MC) or purified mouse alpha-crystallin.	Methylcholanthrene	186-188	crystallin, alpha A	Mus musculus	63-79
7140758-0	1982	Binding of 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin to a common Ah receptor site in mouse and rat hepatic cytosols.	Methylcholanthrene	11-31	aryl-hydrocarbon receptor	Mus musculus	84-95
7142127-0	1982	Multiple forms of cytochrome P-450 in kidney cortex microsomes of rabbits treated with 3-methylcholanthrene.	Methylcholanthrene	87-107	cytochrome P-450	Oryctolagus cuniculus	18-34
7142127-1	1982	Cytochrome P-450 was purified from kidney cortex microsomes of rabbits treated with 3-methylcholanthrene.	Methylcholanthrene	84-104	cytochrome P-450	Oryctolagus cuniculus	0-16
7126636-6	1982	Purified cytochromes P-448 from 3-methylcholanthrene-treated rat had similar spectral properties and activity towards [14C]benzo[a]pyrene suggesting similarities between these forms.	Methylcholanthrene	32-52	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	21-26
6289890-3	1982	Methylcholanthrene treatment introduced typical changes in enzyme composition, mainly an increase of the cytochrome P-448.	Methylcholanthrene	0-18	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	105-121
7132565-3	1982	The effects of the 4"-halo-2,3,4,5-tetrachlorobiphenyls on the microsomal enzyme activities and on the relative peak intensities and spectral shifts of the reduced cytochrome P-450:CO and ethylisocyanide (EIC) binding difference spectra were similar to those observed after coadministration of phenobarbitone (PB) and 3-methylcholanthrene (MC).	Methylcholanthrene	318-338	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
7132565-3	1982	The effects of the 4"-halo-2,3,4,5-tetrachlorobiphenyls on the microsomal enzyme activities and on the relative peak intensities and spectral shifts of the reduced cytochrome P-450:CO and ethylisocyanide (EIC) binding difference spectra were similar to those observed after coadministration of phenobarbitone (PB) and 3-methylcholanthrene (MC).	Methylcholanthrene	340-342	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
6980492-2	1982	Splenocytes from mice immune to a methylcholanthrene-induced sarcoma were expanded in TCGF, both before and after in vitro mixed lymphocyte-tumor cultures, and expressed high levels of cytotoxicity for fresh syngeneic solid tumor cells.	Methylcholanthrene	34-52	interleukin 2	Mus musculus	86-90
6815905-14	1982	Pretreatment with 3-methylcholanthrene resulted in a small increase in cutaneous UDP-glucuronosyltransferase activities in both species.	Methylcholanthrene	18-38	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	81-108
6889862-0	1982	3-Methylcholanthrene induces phenobarbital-induced cytochrome P-450 hemoprotein in fetal liver and not cytochrome P-448 hemoprotein induced in maternal liver of rats.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
6812945-1	1982	Carcinogenic hydrocarbons benz[alpha] anthracene (BA), 7,12-dimethyl-BA (DMBA) and 3-methylcholanthrene (MC), bound non-covalently to bovine serum albumin (BSA), are photo-oxidized and become covalently bound to the protein as a result of irradiation at 365 nm.	Methylcholanthrene	83-103	albumin	Homo sapiens	141-154
6812945-1	1982	Carcinogenic hydrocarbons benz[alpha] anthracene (BA), 7,12-dimethyl-BA (DMBA) and 3-methylcholanthrene (MC), bound non-covalently to bovine serum albumin (BSA), are photo-oxidized and become covalently bound to the protein as a result of irradiation at 365 nm.	Methylcholanthrene	105-107	albumin	Homo sapiens	141-154
6810901-4	1982	Following treatment with 3-methylcholanthrene at a dose of 50 mg/kg body weight, aryl hydrocarbon hydroxylase activity and cytochrome P-450 content in liver were both increased in all the strains used, and the activity of NADPH-cytochrome c reductase in liver was also increased in all strains except No.	Methylcholanthrene	25-45	cytochrome P450 3A14	Cavia porcellus	123-139
7097715-2	1982	Effects of benzimidazole and related compounds on aryl hydrocarbon hydroxylase activity from phenobarbitone and 3-methylcholanthrene induced rats.	Methylcholanthrene	112-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-78
7097715-8	1982	Two 5,6-dimethylbenzimidazoles showed slight inhibitory activity and naphtho[2,3:4",5"]imidazole was only threefold less active toward 3-MC-induced (I50 = 2.6 X 10(-4) M) than PB-induced (I50 = 8.4 X 10(-5) AHH activity.	Methylcholanthrene	135-139	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	207-210
7097715-9	1982	These results suggest that for nitrogen heterocycles there may be a relationship of increasing polycyclic size and increasing inhibitory activity toward AHH activity in 3-MC induced rat liver microsomes.	Methylcholanthrene	169-173	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	153-156
6980417-1	1982	Cytochrome P-450 (P-450)-dependent aryl hydrocarbon hydroxylase (AHHase) and 7-ethoxycoumarin deethylase (ECDEtase) in human tissues were differentially inhibited by monoclonal antibodies (MAbs) that were prepared to inhibit and completely inhibited the activity of 3-methylcholanthrene-induced rat liver P-450.	Methylcholanthrene	266-286	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
6175632-1	1982	Pulse and pulse-chase experiments demonstrated that a heterogeneous polypeptide with an apparent Mr = 68,000 was the first intracellular anti-alpha-fetoprotein (AFP)-precipitable polypeptide synthesized by rat Mc-A-RH-7777 hepatoma cells.	Methylcholanthrene	210-214	alpha-fetoprotein	Rattus norvegicus	142-159
6175632-1	1982	Pulse and pulse-chase experiments demonstrated that a heterogeneous polypeptide with an apparent Mr = 68,000 was the first intracellular anti-alpha-fetoprotein (AFP)-precipitable polypeptide synthesized by rat Mc-A-RH-7777 hepatoma cells.	Methylcholanthrene	210-214	alpha-fetoprotein	Rattus norvegicus	161-164
7104016-1	1982	The in vitro metabolism of biphenyl, 4-fluoro-, 4-chloro-, 4-bromo- and 4-iodobiphenyl by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes from immature male rats pretreated with phenobarbitone or 3-methylcholanthrene.	Methylcholanthrene	232-252	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6177329-1	1982	Mice bearing a methylcholanthrene-induced tumour were tested for their cell mediated reactivity to the experimental allergic encephalomyelitis (EAE) peptide of human myelin basic protein (MBP) in the leucocyte adherence inhibition (LAI) test.	Methylcholanthrene	15-33	myelin basic protein	Homo sapiens	166-186
6177329-1	1982	Mice bearing a methylcholanthrene-induced tumour were tested for their cell mediated reactivity to the experimental allergic encephalomyelitis (EAE) peptide of human myelin basic protein (MBP) in the leucocyte adherence inhibition (LAI) test.	Methylcholanthrene	15-33	myelin basic protein	Homo sapiens	188-191
7116338-0	1982	Dissociation of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene-induced induction in ornithine decarboxylase and aryl hydrocarbon hydroxylase activities in C57BL/6 mouse dermal fibroblasts in culture.	Methylcholanthrene	57-77	ornithine decarboxylase, structural 1	Mus musculus	99-122
7116338-0	1982	Dissociation of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene-induced induction in ornithine decarboxylase and aryl hydrocarbon hydroxylase activities in C57BL/6 mouse dermal fibroblasts in culture.	Methylcholanthrene	57-77	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	127-155
7116338-1	1982	The effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) and 3-methyl-cholanthrene (MC) on ornithine decarboxylase (ODC) and aryl hydrocarbon hydroxylase (AHH) activities were studied in C57BL/6 mouse dermal fibroblasts in culture.	Methylcholanthrene	85-87	ornithine decarboxylase, structural 1	Mus musculus	92-115
7116338-1	1982	The effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) and 3-methyl-cholanthrene (MC) on ornithine decarboxylase (ODC) and aryl hydrocarbon hydroxylase (AHH) activities were studied in C57BL/6 mouse dermal fibroblasts in culture.	Methylcholanthrene	85-87	ornithine decarboxylase, structural 1	Mus musculus	117-120
7116338-2	1982	TPA selectively induced ODC activity and MC selectively induced AHH activity in these cells.	Methylcholanthrene	41-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	64-67
7135999-12	1982	Endotoxin failed to depress the phenobarbitone- or 3-methylcholanthrene-induced forms of cytochrome P-450 and the dependent mono-oxygenase enzymes.	Methylcholanthrene	51-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
7074142-1	1982	When rats were pretreated with 3-methylcholanthrene of beta-naphthoflavone, hepatic nicotine oxidase activity per cytochrome P-448 molecule decreased, but the specific activity of the enzyme remained unchanged.	Methylcholanthrene	31-51	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	114-130
6807317-2	1982	3-Methylcholanthrene preferentially induced UDP-GT1 activities in C57BL/6 mice.	Methylcholanthrene	0-20	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	48-51
6217856-5	1982	DAB azoreductase activity was induced by 20-methylcholanthrene and phenobarbital, and increased in streptozotocin-induced diabetes or fasting.	Methylcholanthrene	41-62	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	4-16
6800653-10	1982	The metabolite patterns and the effects of nonsteroid inhibitors of liver monooxygenases, e.g., alpha-naphthoflavone, SU 9055, and ellipticine, suggest that the properties of this cytochrome P-450 resemble those of the 3-methyl-cholanthrene-inducible cytochrome P-488 from rat liver.	Methylcholanthrene	219-240	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	180-196
7047272-7	1982	Patients treated with porcine or mixed species purified insulin (monocomponent MC) did not differ significantly from a non-diabetic control group, whereas serum samples taken from patients treated with crystallized insulin preparations showed a significantly higher level of insulin specific IgE (p less than 0.05).	Methylcholanthrene	79-81	insulin	Homo sapiens	56-63
7047272-10	1982	In all cases of allergy elicited by purified insulin (monocomponent MC), it was ascertained that the diabetic patients in question had received less pure insulin during earlier treatment.	Methylcholanthrene	68-70	insulin	Homo sapiens	45-52
6811722-6	1982	3-Methylcholanthrene, on the other hand, caused 4 and 2 fold increase in UDPGT activities towards p-nitrophenol and 1-naphthol, respectively, but did not cause significant increase in UDPGT activity towards chloramphenicol.	Methylcholanthrene	0-20	UDP glucuronosyltransferase family 1 member A5	Rattus norvegicus	73-78
6811722-7	1982	It is concluded that m-TAN is a new potent inducer of UDPGT activity with its potency exceeding that of 3-methylcholanthrene and the pattern of induction, a little different from that of 3-methylcholanthrene.	Methylcholanthrene	104-124	UDP glucuronosyltransferase family 1 member A5	Rattus norvegicus	54-59
7120027-5	1982	Treatment of 3-methylcholanthrene nonresponsive DBA/2 strain of mice with this azo compound resulted in a limited (1.5 fold) induction of cytochrome P-450 compared to 2.5 fold induction in responsive C57BL/6 strain of mice.	Methylcholanthrene	13-33	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	138-154
7120027-8	1982	This species of P-450 is spectrally indistinguishable from cytochrome P-448 induced by 3-methylcholanthrene.	Methylcholanthrene	87-107	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-75
6806944-4	1982	Hydroxylation activity is determined by the source of cytochrome P-450 fraction; cytochrome P-450 fraction from MC-pretreated mice is several fold more active than that from controls.	Methylcholanthrene	112-114	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	54-70
6806944-4	1982	Hydroxylation activity is determined by the source of cytochrome P-450 fraction; cytochrome P-450 fraction from MC-pretreated mice is several fold more active than that from controls.	Methylcholanthrene	112-114	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	81-97
6282280-7	1982	Since the enhancement of protein kinase activities was accompanied by the stimulation of nuclear RNA polymerases we suggest that both kinds of enzymes are involved in an epigenetic mechanism of the inducing action of 3-MC on cytochrome P1-450.	Methylcholanthrene	217-221	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	225-242
6124393-7	1982	Purified cytochrome P-448 from MC-treated animals catalyzed DAB demethylation very readily but hydroxylation very poorly.	Methylcholanthrene	31-33	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	9-25
7056021-5	1982	AHH activity in cultured human lymphocytes from the nonsmoking subjects was determined in control and 3-methylcholanthrene-induced cells to obtained inducibility ratios of 4.2 +/- 0.56 (SEM) in the summer and 1.4 +/- 0.14 (SEM) in winter.	Methylcholanthrene	102-122	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	0-3
7117737-1	1982	Local administration of riboflavin 2",3",4",5"-tetrabutyrate (B2-But4) suppressed the induction of skin tumors in mice by 3-methylcholanthrene.	Methylcholanthrene	122-142	bradykinin receptor, beta 2	Mus musculus	62-69
6176233-0	1982	Differential induction of rat hepatic cytochrome P-448 and glutathione S-transferase B messenger RNAs by 3-methylcholanthrene.	Methylcholanthrene	105-125	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	38-54
7054190-0	1982	Effects of 3-methylcholanthrene, beta-naphthoflavone, and phenobarbital on the 3-methylcholanthrene-inducible isozyme of cytochrome P-450 within centrilobular, midzonal, and periportal hepatocytes.	Methylcholanthrene	11-31	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	121-137
7054190-0	1982	Effects of 3-methylcholanthrene, beta-naphthoflavone, and phenobarbital on the 3-methylcholanthrene-inducible isozyme of cytochrome P-450 within centrilobular, midzonal, and periportal hepatocytes.	Methylcholanthrene	79-99	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	121-137
6277340-9	1982	Pretreatment of lactating rats with the inducers of hepatic cytochrome P-448, 3-methylcholanthrene and beta-naphthoflavone, increased the cytochrome content 3- to 10-fold, in the mammary gland and liver microsomes, respectively.	Methylcholanthrene	78-98	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	60-76
6275961-5	1982	The most potent opioid peptide in inducing the MC and electrocortical (ECoG) epileptic pattern was the delta opiate receptor agonist [D-Ala2,D-Leu5]-enkephalin (DADL).	Methylcholanthrene	47-49	proenkephalin	Rattus norvegicus	149-159
6279326-7	1982	The total metabolism of BP was found to be approximately 20-fold greater with the cytochrome P-450 from the 3-methylcholanthrene (P-450 3-MC) and beta-naphthoflavone (P-450 BNF) treated rats than with the phenobarbital preinduced cytochrome P-450 (P-450 BP).	Methylcholanthrene	108-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
6279326-7	1982	The total metabolism of BP was found to be approximately 20-fold greater with the cytochrome P-450 from the 3-methylcholanthrene (P-450 3-MC) and beta-naphthoflavone (P-450 BNF) treated rats than with the phenobarbital preinduced cytochrome P-450 (P-450 BP).	Methylcholanthrene	136-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
6897771-6	1982	The ontogenetic expression of 3-MC-induced P1-450 mRNA (23S) from mouse or rat liver corresponds well to previous developmental studies from this laboratory involving 3-MC-inducible aryl hydrocarbon (benzo[a]pyrene) hydroxylase (AHH) (EC 1.14.14.1) activity.	Methylcholanthrene	30-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	43-49
6897771-6	1982	The ontogenetic expression of 3-MC-induced P1-450 mRNA (23S) from mouse or rat liver corresponds well to previous developmental studies from this laboratory involving 3-MC-inducible aryl hydrocarbon (benzo[a]pyrene) hydroxylase (AHH) (EC 1.14.14.1) activity.	Methylcholanthrene	30-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	229-232
6897771-7	1982	P1-450 mRNA--induced transplacentally by 3-MC given to the mother--is readily detectable by clone 46 as early as gestational day 15.	Methylcholanthrene	41-45	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
6979509-0	1982	Role of H-2 antigens in the host response to methylcholanthrene-induced tumors.	Methylcholanthrene	45-63	histocompatibility-2, MHC	Mus musculus	8-11
7298644-2	1981	Cytochrome P-450 from cholate-solubilized liver microsomes prepared from 3-methylcholanthrene-treated genetically "responsive" C57BL/6N mice (Ahb/Ahb) was partially purified by aminooctyl-Sepharose 4B column chromatography with an elution buffer that included Emulgen 911, followed by hydroxylapatite column chromatography.	Methylcholanthrene	73-93	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
6797484-1	1981	Immunization of rats by a homogeneous cytochrome P-450-LM4 from liver microsomes of rabbits pretreated with 3-methylcholanthrene resulted in antibodies to this hemoprotein - anti-P-450-LM4.	Methylcholanthrene	108-128	cytochrome P450 1A2	Oryctolagus cuniculus	38-58
6800639-2	1981	Nuclei from the livers of rats treated with polychlorinated biphenyl (PCB) or 3-methylcholanthrene (MC) showed high mutagenic activity with Trp-P-2 in the Ames test, but activities with nuclei of untreated or phenobarbital (PB)-treated rat livers were quite low.	Methylcholanthrene	78-98	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	140-147
6800639-2	1981	Nuclei from the livers of rats treated with polychlorinated biphenyl (PCB) or 3-methylcholanthrene (MC) showed high mutagenic activity with Trp-P-2 in the Ames test, but activities with nuclei of untreated or phenobarbital (PB)-treated rat livers were quite low.	Methylcholanthrene	100-102	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	140-147
6800639-3	1981	The formation of N-hydroxy-Trp-P-2 by nuclei of PCB- or MC-treated rat livers was greater than that by nuclei of untreated or PB-treated rat livers.	Methylcholanthrene	56-58	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	27-34
6950396-0	1981	High-frequency cotransfer of the transformed phenotype and a tumor-specific transplantation antigen by DNA from the 3-methylcholanthrene-induced Meth A sarcoma of BALB/c mice.	Methylcholanthrene	116-136	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	61-99
6272979-2	1981	Two methylcholanthrene-induced fibrosarcomas, previously demonstrated to contain a common tumor rejection antigen(s), released infectious ecotropic murine leukemia virus and expressed the murine leukemia virus proteins, a glycoprotein with a molecular weight of 70,000 (gp70) and an envelope protein with a molecular weight of 15,000.	Methylcholanthrene	4-22	embigin	Mus musculus	270-274
7298716-1	1981	Induction of cytochrome P-450s by 3-methylcholanthrene (MC) and phenobarbital (PB) and distribution of P-450s in the rat liver nuclear envelope were investigated by biochemical analyses and ferritin immunoelectron microscopy using specific antibodies against the major molecular species of MC- and PB-induced cytochrome P-450.	Methylcholanthrene	34-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
7298716-1	1981	Induction of cytochrome P-450s by 3-methylcholanthrene (MC) and phenobarbital (PB) and distribution of P-450s in the rat liver nuclear envelope were investigated by biochemical analyses and ferritin immunoelectron microscopy using specific antibodies against the major molecular species of MC- and PB-induced cytochrome P-450.	Methylcholanthrene	56-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
7298716-3	1981	Chem., 1971, 246: 577-581), that the total amount of cytochrome P-450s determined by biochemical analysis was markedly increased by MC, but not by PB, treatment.	Methylcholanthrene	132-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
7309711-1	1981	Cytochrome P-450 was solubilized from kidney cortex microsomes of rabbits treated with 3-methylcholanthrene and partially purified by chromatography on 6-amino-n-hexyl Sepharose 4B and heparin-Sepharose CL-6B columns.	Methylcholanthrene	87-107	cytochrome P-450	Oryctolagus cuniculus	0-16
7302992-1	1981	Styrene and styrene 7,8-oxide were able to bind both to partially purified cytochrome P-450 isolated from phenobarbital (PB)-treated rat liver and to cytochrome P-448 from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats.	Methylcholanthrene	192-212	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	150-166
6975627-0	1981	Cytochrome P-450 and ethoxycoumarin-deethylation in rat gastric microsomes: induction by 3-methylcholanthrene and inhibition by cimetidine.	Methylcholanthrene	89-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7295776-5	1981	This frequency and those of other structure-sensitive bands implied that the heme iron of oxidized P-450SCC adopts the hexa-coordinate high-spin structure, in contrast with the high-spin type cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rabbit liver microsomes which presumably have a penta-coordinate structure.	Methylcholanthrene	241-261	cholesterol side-chain cleavage enzyme, mitochondrial	Bos taurus	99-107
7020934-2	1981	Among four cytochrome P-450 preparations, PCB-P-448 and MC-P-448 purified from liver microsomes of polychlorinated biphenyl (PCB)- and 3-methylcholanthrene-treated rats, respectively, showed higher activities for induction of mutation by Trp-P-2 than did the other two preparations, PCB-P-450 and PB-P-450 purified from PCB-and phenobarbital (PB)-treated rats, respectively.	Methylcholanthrene	135-155	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	11-27
7020934-2	1981	Among four cytochrome P-450 preparations, PCB-P-448 and MC-P-448 purified from liver microsomes of polychlorinated biphenyl (PCB)- and 3-methylcholanthrene-treated rats, respectively, showed higher activities for induction of mutation by Trp-P-2 than did the other two preparations, PCB-P-450 and PB-P-450 purified from PCB-and phenobarbital (PB)-treated rats, respectively.	Methylcholanthrene	135-155	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	238-245
6792322-3	1981	Induction of cytochrome P-448 in microsomes by 3-methylcholanthrene pretreatment did not affect the kinetics of NADPH-mediated reduction of chromate by microsomes.	Methylcholanthrene	47-67	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	13-29
6945571-0	1981	Administration of 3-methylcholanthrene to rats increases the specific hybridizable mRNA coding for cytochrome P-450c.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	99-116
6945571-1	1981	Poly(A)+-RNA obtained from the livers of 3-methylcholanthrene (3MC)-treated rats was translated into cytochrome P-450c in a cell-free reticulocyte system.	Methylcholanthrene	41-61	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-118
6945571-1	1981	Poly(A)+-RNA obtained from the livers of 3-methylcholanthrene (3MC)-treated rats was translated into cytochrome P-450c in a cell-free reticulocyte system.	Methylcholanthrene	63-66	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-118
7256865-1	1981	Results of gel electrophoresis of transplantable rat (RA-2) and murine (MC-53) rhabdomyosarcomas show that the LDH isoenzyme spectrum of tumors growing subcutaneously differ from that of normal muscle tissue, LDH-1 and LDH-2 isoenzyme being absent in zymograms.	Methylcholanthrene	72-74	lactate dehydrogenase A	Mus musculus	111-114
7256865-4	1981	After a 16-18 day cultivation in rat and mouse eye anterior chamber, LDH spectra of RA-2 and MC-53 clones changed sharply, LDH-1 and LDH-2 appearing.	Methylcholanthrene	93-95	lactate dehydrogenase A	Mus musculus	69-72
7336952-6	1981	Cytochrome P-450LM4 isolated after pretreatment with 3-methylcholanthrene or phenobarbital showed roughly the same characteristics except in the formation of 1-hexanol where cytochrome P-450LM4 isolated after phenobarbital treatment was the most effective.	Methylcholanthrene	53-73	cytochrome P450 1A2	Oryctolagus cuniculus	0-19
7214334-1	1981	We examined the ability of human lysozyme (HLZM) to enhance the immunogenicity of a methylcholanthrene-induced murine fibrosarcoma of C57BL/10 mice.	Methylcholanthrene	84-102	lysozyme	Homo sapiens	33-41
7214346-0	1981	Correlation of induction of aryl hydrocarbon hydroxylase in cultured rat hepatocytes with saturable high-affinity binding of 3-methylcholanthrene to a 4S cytoplasmic protein.	Methylcholanthrene	125-145	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	28-56
7214346-1	1981	The binding of 3-methylcholanthrene (3-MC), a potent inducer of aryl hydrocarbon hydroxylase activity, to cytoplasmic proteins of a cloned rat hepatocyte culture, RL-PR-C, was studied by sucrose gradient centrifugation.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-92
7214346-1	1981	The binding of 3-methylcholanthrene (3-MC), a potent inducer of aryl hydrocarbon hydroxylase activity, to cytoplasmic proteins of a cloned rat hepatocyte culture, RL-PR-C, was studied by sucrose gradient centrifugation.	Methylcholanthrene	37-41	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-92
6113928-7	1981	The 3-methylcholanthrene-dependent increases in 2- and 3-hydroxylation appear due to induction of a single form of cytochrome P-450, as indicated by similar dose-response relationships and similar changes in sensitivity to the inhibitors.	Methylcholanthrene	4-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
6113938-6	1981	In contrast, 3-methylcholanthrene increased nuclear AHH to a greater extent than the microsomal enzyme.	Methylcholanthrene	13-33	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	52-55
6792366-0	1981	Partial purification of pulmonary cytochrome P-448 from 3-methylcholanthrene-treated rats.	Methylcholanthrene	56-76	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	34-50
6792366-1	1981	Pulmonary cytochrome P-448 from 3-methylcholanthrene-pretreated rats was partially purified approximately 20-fold.	Methylcholanthrene	32-52	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	10-26
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	296-315	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	296-315	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	296-315	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	316-318	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	316-318	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
6258818-4	1981	Sodium dodecyl sulfate (SDS)-gel electrophoresis indicated that these increases in cytochrome P-450 and cytochrome P-450-dependent monooxygenase activities were accompanied by a dose-dependent intensification of a protein of relative molecular weight (Mr) 55 000 which comigrated with the major 3-methylcholanthrene(MC)-inducible form of cytochrome P-450 (i.e., cytochrome P-448).	Methylcholanthrene	316-318	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
6258818-6	1981	The results indicate that HBBp is a potent inducer of cytochrome P-448 and as such is the third MC-type inducer identified in fireMaster BP-6.	Methylcholanthrene	96-98	Blood pressure QTL 6	Rattus norvegicus	137-141
7269901-2	1981	These substances, acting as inductors of microsomal oxidases with mixed function (cytochrome P-450 and P-448), are phenobarbital, 3-methylcholanthrene, DDT, diphenin, rifampicin, benzodiazepin derivatives (diazepam and phenazepam).	Methylcholanthrene	130-150	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-108
6450647-4	1981	Steroid-16 alpha-hydroxylase is completely independent from cytochrome P1-450 (or P-448), as it is insensitive, in vitro, to alpha-naphthoflavone; (2) AHH is supported by two cytochrome P-450 forms: a specific form which is inducible by methylcholanthrene and inhibited in vitro by alpha-naphthoflavone, but is insensitive to metyrapone and steroids; and another less specific form which is inhibited by metyrapone and steroids in vitro.	Methylcholanthrene	237-255	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	151-154
6165325-1	1981	I. Purification of cytosolic DT-diaphorase from control and 3-methylcholanthrene-treated rats.	Methylcholanthrene	60-80	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	29-42
6165326-2	1981	Purification of mitochondrial and microsomal DT-diaphorase from 3-methylcholanthrene-treated rats.	Methylcholanthrene	64-84	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	45-58
7470383-6	1981	Topical methylcholanthrene is also responsible for a smaller aryl hydrocarbon hydroxylase (AHH) induction when the chemical is applied the same day that the club hairs are plucked.	Methylcholanthrene	8-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	61-89
7470383-6	1981	Topical methylcholanthrene is also responsible for a smaller aryl hydrocarbon hydroxylase (AHH) induction when the chemical is applied the same day that the club hairs are plucked.	Methylcholanthrene	8-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	91-94
6787032-7	1981	These findings and data on the detergent treatment of nuclei suggest that the nuclear cytochrome P-448 system, induced by 3-methylcholanthrene and localized in the outer membrane, catalyzes the aflatoxin M1 formation, and the cytochrome P-450 system induced by phenobarbital biotransforms aflatoxin B1 into aflatoxin Q1.	Methylcholanthrene	122-142	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	86-102
6787032-7	1981	These findings and data on the detergent treatment of nuclei suggest that the nuclear cytochrome P-448 system, induced by 3-methylcholanthrene and localized in the outer membrane, catalyzes the aflatoxin M1 formation, and the cytochrome P-450 system induced by phenobarbital biotransforms aflatoxin B1 into aflatoxin Q1.	Methylcholanthrene	122-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-242
6262772-0	1981	Isolation and characterization of a cloned DNA sequence associated with the murine Ah locus and a 3-methylcholanthrene-induced form of cytochrome P-450.	Methylcholanthrene	98-118	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	135-151
6262772-7	1981	The cDNA made from total mRNA isolated from 3-methylcholanthrene-treated C57BL/6N mice hybridized to the two fragments of Pst I-digested DNA from clone 46, whereas similarly prepared cDNA from 3-methylcholanthrene-treated DBA/2N and control C57BL/6N and DBA/2N mice did not.	Methylcholanthrene	44-64	sulfotransferase family 1A, phenol-preferring, member 1	Mus musculus	122-125
6797751-2	1981	Similar enhancement in epidermal cell phospholipase A2 was observed after application of phorbol-12,13-didecanoate or 3-methylcholanthrene to mouse skin.	Methylcholanthrene	118-138	phospholipase A2, group IB, pancreas	Mus musculus	38-54
7460072-4	1981	The time course of induction of AHH activity by 3-MC was followed from around 60 h after cells were plated until 190 h when cells were at the end of exponential and at the start of stationary growth phase.	Methylcholanthrene	48-52	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	32-35
7460072-7	1981	Cells from aromatic hydrocarbon responsive mice attained maximal AHH activity with inducer concentrations of 0.05--0.10 micrograms 3-MC/ml.	Methylcholanthrene	131-135	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	65-68
7460072-9	1981	The 5--10-fold difference between cells from responsive and non-responsive mice in concentration of 3-MC needed to induce AHH maximally is taken to indicate that genes controlling aromatic hydrocarbon responsiveness in adult mouse livers in vivo also function in fetal mouse liver cells maintained in culture.	Methylcholanthrene	100-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	122-125
6926812-0	1981	Effects of 3-methylcholanthrene and DDT on cholesterol 7 alpha-hydroxylase in rats.	Methylcholanthrene	11-31	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	43-74
6926812-5	1981	3-Methylcholanthrene and DDT, however, both caused a significant decrease in cholesterol 7 alpha-hydroxylase activity.	Methylcholanthrene	0-20	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	77-108
6926812-6	1981	3-Methylcholanthrene, which produced the greatest decrease in cholesterol 7 alpha-hydroxylase activity, also caused a marked elevation in serum cholesterol levels.	Methylcholanthrene	0-20	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	62-93
6926812-7	1981	It seems plausible that the decrease in cholesterol 7 alpha-hydroxylase produced by 3-methylcholanthrene may have produced the elevation in serum cholesterol levels.	Methylcholanthrene	84-104	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	40-71
6926817-0	1981	Dietary fat and 3-MC induction of hepatic nuclear and microsomal cytochrome P-450.	Methylcholanthrene	16-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
6926817-2	1981	Treatment with 3-methylcholanthrene (3-MC) increased the concentrations of cytochrome P-450 (as measured by CO binding spectra) to nearly equal levels in both dietary groups, but the binding of aniline and octylamine to microsomes of rats fed the fat diet exceeded the increase in cytochrome P-450 concentration.	Methylcholanthrene	15-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	75-91
6926817-2	1981	Treatment with 3-methylcholanthrene (3-MC) increased the concentrations of cytochrome P-450 (as measured by CO binding spectra) to nearly equal levels in both dietary groups, but the binding of aniline and octylamine to microsomes of rats fed the fat diet exceeded the increase in cytochrome P-450 concentration.	Methylcholanthrene	15-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	281-297
6926817-2	1981	Treatment with 3-methylcholanthrene (3-MC) increased the concentrations of cytochrome P-450 (as measured by CO binding spectra) to nearly equal levels in both dietary groups, but the binding of aniline and octylamine to microsomes of rats fed the fat diet exceeded the increase in cytochrome P-450 concentration.	Methylcholanthrene	37-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	75-91
6926817-2	1981	Treatment with 3-methylcholanthrene (3-MC) increased the concentrations of cytochrome P-450 (as measured by CO binding spectra) to nearly equal levels in both dietary groups, but the binding of aniline and octylamine to microsomes of rats fed the fat diet exceeded the increase in cytochrome P-450 concentration.	Methylcholanthrene	37-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	281-297
7026457-2	1981	The presence of "foreign" H-2 allospecificities on MC-induced sarcoma cells were detected.	Methylcholanthrene	51-53	histocompatibility-2, MHC	Mus musculus	26-29
6783636-0	1981	Selective induction of two different molecular species of cytochrome P-450 by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	96-116	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Methylcholanthrene	141-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Methylcholanthrene	141-161	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	43-50
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Methylcholanthrene	48-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6783636-8	1981	The administration of MC to PB-treated rats induced a drastic decrease in the P-450PB-dependent oxidations of benzo(a)pyrene and 7-ethoxycoumarin, while the corresponding activities of P-450MC increased sharply, and these changes were much more rapid than the change of the amount of each form of cytochrome P-450.	Methylcholanthrene	22-24	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	185-192
6783636-8	1981	The administration of MC to PB-treated rats induced a drastic decrease in the P-450PB-dependent oxidations of benzo(a)pyrene and 7-ethoxycoumarin, while the corresponding activities of P-450MC increased sharply, and these changes were much more rapid than the change of the amount of each form of cytochrome P-450.	Methylcholanthrene	22-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	297-313
6166001-0	1981	Mg and Mc: mutations within the amino-terminal region of glycophorin A.	Methylcholanthrene	7-9	glycophorin A (MNS blood group)	Homo sapiens	57-70
6166001-10	1981	The finding that Mc contains structural features of both M and N suggests that these two forms of glycophorin A have evolved from a common ancestral gene by single base substitutions at sites in the genome coding for amino acids in positions 1 and 5 of the sequence.	Methylcholanthrene	17-19	glycophorin A (MNS blood group)	Homo sapiens	98-111
6266081-6	1981	Multiple treatments with PBB, PCB or 3MC increased renal and hepatic AHH activities, but NaPB induced hepatic AHH only.	Methylcholanthrene	37-40	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	69-72
6266081-7	1981	Renal AHH activity was increased more rapidly than hepatic AHH after a single treatment with PBB, PCB or 3MC and returned more rapidly to control.	Methylcholanthrene	105-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	6-9
6266081-8	1981	The renal AHH induced by PBB and PCB, like that induced by 3MC, was more sensitive to inhibition by ANF in vitro than was renal AHH from naive rats.	Methylcholanthrene	59-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	10-13
7210704-9	1980	The results of experiments using various inhibitors suggest that the 13-hydroxylation in liver microsomes from 3-methylcholanthrene-treated rats is catalysed by an enzyme system involving an unusual type of cytochrome P-448.	Methylcholanthrene	111-131	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	207-223
7430117-5	1980	The heme-mediated increase of cytochrome P-450 was most pronounced in phenobarbital-pretreated rats (46%), but was detectable also in 3-methylcholanthrene-pretreated (6%) and in untreated animals (7%).	Methylcholanthrene	134-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
7432518-7	1980	We now describe principal differences in the expression of H-2 parental haplotypes between a local F1 methylcholanthrene-induced tumour and its descendant pulmonary metastases.	Methylcholanthrene	102-120	histocompatibility-2, MHC	Mus musculus	59-62
6159495-1	1980	Tumor-specific transplantation antigens (TSTA), extracted from the 3-methylcholanthrene-induced sarcoma MCA-F and partially purified by flat-bed isoelectric focusing, were used to treat syngeneic inbred C3H/HeJ mice bearing supralethal neoplastic challenges.	Methylcholanthrene	67-87	heat shock protein 90 alpha (cytosolic), class B member 1	Mus musculus	41-45
6935662-5	1980	Proteins collected from the major peaks induced by PB or 3-MC treatment were found to retain spectral characteristics of cytochrome P-450.	Methylcholanthrene	57-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	121-137
7251224-1	1980	The fibrosarcoma ST2, induced by 3-methylcholanthrene in BALB/c (H-2d) mice, also expressed alien histocompatibility antigens of the C3Hf and B10 background not encoded by the MHC.	Methylcholanthrene	33-53	interleukin 1 receptor-like 1	Mus musculus	17-20
7002195-1	1980	The subcutaneous growth of 2 antigenically distinct syngeneic methylcholanthrene-induced murine fibrosarcomas, designated H1 and H7, were significantly augmented by the concomitant administration of E. coli endotoxin (LPS).	Methylcholanthrene	62-80	histocompatibility 1	Mus musculus	122-131
7428105-1	1980	The in vitro inhibitor of mixed-function oxidation, 9-hydroxyellipticine, non-competitively inhibited the binding of the type II substrate, aniline, to cytochrome P-448 of hepatic microsomal preparations from rats pretreated with 3-methylcholanthrene.	Methylcholanthrene	230-250	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	152-168
7428105-4	1980	With rats pretreated with 9-hydroxyellipticine and 3-methylcholanthrene, inhibition of ethoxyresorufin O-deethylase was 90%, and cytochrome P-450/P-448, cytochrome P-450 reductase, biphenyl 2- and 4-hydroxylase were inhibited by 30, 15, 50 and 40% respectively.	Methylcholanthrene	51-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	129-145
7428105-4	1980	With rats pretreated with 9-hydroxyellipticine and 3-methylcholanthrene, inhibition of ethoxyresorufin O-deethylase was 90%, and cytochrome P-450/P-448, cytochrome P-450 reductase, biphenyl 2- and 4-hydroxylase were inhibited by 30, 15, 50 and 40% respectively.	Methylcholanthrene	51-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	153-169
7428109-5	1980	Four of the mouse strains (C57BL/6J, BALB/cCr, CBA/J and C57L/J) were highly inducible with respect to liver AHH when pretreated with MC.	Methylcholanthrene	134-136	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	109-112
7428109-6	1980	The induction of AHH by MC in these strains correlated well with the radioactive metabolites of [3H] BP remaining in the alkali extract derived from the AHH assay mixture and with the increased binding of [3H] BP to microsomal protein and DNA.	Methylcholanthrene	24-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	17-20
7428109-6	1980	The induction of AHH by MC in these strains correlated well with the radioactive metabolites of [3H] BP remaining in the alkali extract derived from the AHH assay mixture and with the increased binding of [3H] BP to microsomal protein and DNA.	Methylcholanthrene	24-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	153-156
6780342-9	1980	When cytochrome P-448 purified from hepatic microsomes of 3-methylcholanthrene-treated rats was used, a very low rate of epoxidation was observed which was less than 3% of the activity mediated by cytochrome P-450 under similar assay conditions.	Methylcholanthrene	58-78	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	5-21
6780342-9	1980	When cytochrome P-448 purified from hepatic microsomes of 3-methylcholanthrene-treated rats was used, a very low rate of epoxidation was observed which was less than 3% of the activity mediated by cytochrome P-450 under similar assay conditions.	Methylcholanthrene	58-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	197-213
7389009-4	1980	The capacity of isosafrole and piperonyl butoxide to induced cytochrome P-450 was evaluated by measurement of biphenyl 2- and 4-hydroxylase, ethoxyresofurin O-deethylase and ethylmorphine N-demethylase and by sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis and compared with results obtained for phenobarbitone, 3-methylcholanthrene and pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	329-349	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
7408882-6	1980	The inability of adequately hypothyroid rats to induce the delta 9-desaturase seems to be specific, in that injection of methylcholanthrene successfully induced microsomal benzpyrene monooxygenase activity and increased cytochrome b5 contents in hypothyroid animals.	Methylcholanthrene	121-139	cytochrome b5 type A	Rattus norvegicus	220-233
6252201-4	1980	Both optical absorption and EPR studies have shown that the oxidized forms of P-450(1), P-450(2) (from PB-treated animals), and P-450(3) (from MC-treated animals) are in the low spin state, having a Soret absorption peak at 417-418 nm.	Methylcholanthrene	143-145	cytochrome P450 2C5	Oryctolagus cuniculus	78-86
7419508-3	1980	A method is described for the separation and purification of different forms of cytochrome P-450 from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-pretreated rabbits.	Methylcholanthrene	146-166	cytochrome P-450	Oryctolagus cuniculus	80-96
7419508-3	1980	A method is described for the separation and purification of different forms of cytochrome P-450 from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-pretreated rabbits.	Methylcholanthrene	168-170	cytochrome P-450	Oryctolagus cuniculus	80-96
6771001-8	1980	The treatment of rats with polychlorinated biphenyl mixture and 3-methylcholanthrene resulted in a marked increase in the ability of microsomes to activate Trp-P-1 and Trp-P-2, and the activation reaction required reduced nicotinamide adenine dinucleotide phosphate as a cofactor and was inhibited by carbon monoxide, 7,8-benzoflavone, n-octylamine, and 2-diethylaminoethyl-2,2-diphenylvalerate.	Methylcholanthrene	64-84	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	168-175
7445519-0	1980	Metabolic activation of trp-P-2, a mutagenic amine from tryptophan-pyrolysate, by liver microsomes from 3-methylcholanthrene-responsive and non-responsive mice.	Methylcholanthrene	104-124	polycystin 2, transient receptor potential cation channel	Mus musculus	24-31
7445519-2	1980	The metabolic activation of a tryptophan pyrolysate, Trp-P-2 (3-amino-1-methyl-5H-pyrido[4,3-]indole), was studied using liver microsomes from mice of 3-methylcholanthrene-responsive, C57BL/6N (B6) strain and non-responsive, DBA/2N (D2) strain.	Methylcholanthrene	151-171	polycystin 2, transient receptor potential cation channel	Mus musculus	53-60
7445519-4	1980	The formation of N-hydroxy-Trp-P-2 (3-hydroxylamino-1-methyl-5H-pyrido-[4,3-b]indole) by hepatic microsomes was markedly increased by the pretreatment with 3-methylcholanthrene in B6 mice, but not in D2 mice.	Methylcholanthrene	156-176	polycystin 2, transient receptor potential cation channel	Mus musculus	27-34
7445519-10	1980	Addition of alpha-naphthoflavone to microsomes from control and 3-methyl-cholanthrene-treated B6 mice effectively decreased the activities to convert Trp-P-2 to a mutagen(s) and to N-hydroxylate Trp-P-2.	Methylcholanthrene	64-85	polycystin 2, transient receptor potential cation channel	Mus musculus	150-157
7445519-10	1980	Addition of alpha-naphthoflavone to microsomes from control and 3-methyl-cholanthrene-treated B6 mice effectively decreased the activities to convert Trp-P-2 to a mutagen(s) and to N-hydroxylate Trp-P-2.	Methylcholanthrene	64-85	polycystin 2, transient receptor potential cation channel	Mus musculus	195-202
7397681-0	1980	Correlation of inducibility of aryl hydrocarbon hydroxylase with susceptibility to 3-methylcholanthrene-induced lung cancers.	Methylcholanthrene	83-103	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	31-59
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-3
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	146-149	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-3
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	146-149	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	146-149	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-3	1980	AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment.	Methylcholanthrene	146-149	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	55-58
7397681-5	1980	The AHH responsive C57BL/6Cum, F1, and C57BL/6Cum X F1 animals were much more susceptible to MCA-induced lung cancers than the AHH non-responsive DBA/2Cum mice.	Methylcholanthrene	93-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	4-7
7375915-1	1980	Antibody to the major purified cytochrome P-450 induced by 3-methylcholanthrene in rat liver strongly inhibits aryl hydrocarbon hydroxylase activity of uninduced and benz[a]anthracene-induced human monocytes and lymphocytes.	Methylcholanthrene	59-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-47
7375915-1	1980	Antibody to the major purified cytochrome P-450 induced by 3-methylcholanthrene in rat liver strongly inhibits aryl hydrocarbon hydroxylase activity of uninduced and benz[a]anthracene-induced human monocytes and lymphocytes.	Methylcholanthrene	59-79	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	111-139
7376887-1	1980	Multiple forms of liver microsomal cytochrome P-450 in rats were identified on SDS-polyacrylamide gels stained for protein and peroxidase activity after induction with phenobarbital, 3-methylcholanthrene, and 16 alpha-cyanopregnenolone.	Methylcholanthrene	183-203	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
7415204-0	1980	Methyl red azo-reductase and its induction by 3-methylcholanthrene in the liver by different species.	Methylcholanthrene	46-66	NAD(P)H dehydrogenase, quinone 1	Mus musculus	11-24
7415204-7	1980	Azo-reductase in the cytosol of mouse liver also differed from that of the rat in its resistance to the inductive effects of 3-methylcholanthrene.	Methylcholanthrene	125-145	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-13
6154358-0	1980	Tumor rejection activity of antigens isolated from the membranes of a methylcholanthrene-induced sarcoma, C-1, bearing alien H-2 antigens.	Methylcholanthrene	70-88	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	106-128
7370972-1	1980	A delay in onset of heat-sensitivity was demonstrated for methylcholanthrene-induced tumors implanted in the footpad of BALB/cJ or CAF1/J female mice.	Methylcholanthrene	58-76	chromatin assembly factor 1, subunit A (p150)	Mus musculus	131-135
7356631-1	1980	The synthesis of cytochrome P-450 (phenobarbital inducible) and cytochrome P-448 (3-methylcholanthrene inducible) have been studied in rat liver in vivo and in the wheat germ cell-free system using anti-cytochrome P-450 and anti-cytochrome P-448 antibodies.	Methylcholanthrene	82-102	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	64-80
7356631-4	1980	In the case of 3-methylcholanthrene, the cell-free product immunoprecipitated with anti-cytochrome P-448 antibody shows a molecular weight around 59,000.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	88-104
7356631-6	1980	Phenobarbital and 3-methylcholanthrene enhance the translatable messenger RNA contents for cytochrome P-450 and cytochrome P-448, respectively.	Methylcholanthrene	18-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-128
6105134-4	1980	The numbers of gamma-GT-positive foci induced by B(as)P, 7,12-DMBA, 3-MC and DB (a,h)A were significantly different from all of the parent compounds, anthracene, naphthalene, pyrene and phenanthrene.	Methylcholanthrene	68-72	inactive glutathione hydrolase 2	Homo sapiens	15-23
7424729-1	1980	Ethanol induces in rat liver microsomes a form of cytochrome P-450 differing in substrate specificity from cytochrome P-450 species present in controls or in rats treated with phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	193-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
7424729-1	1980	Ethanol induces in rat liver microsomes a form of cytochrome P-450 differing in substrate specificity from cytochrome P-450 species present in controls or in rats treated with phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	193-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
6254470-7	1980	It is suggested that both kinds of enzymes are involved in the mechanism of the cytochrome P-448-inducing action of 3-MC via stimulating nuclear RNA polymerases.	Methylcholanthrene	116-120	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	80-96
6772436-4	1980	The epoxide hydratase activity was, on the other hand, 38% lower after intragastric administration of 3-methylcholanthrene than after intraperitoneal administration.	Methylcholanthrene	102-122	epoxide hydrolase 2	Rattus norvegicus	4-21
6988329-1	1980	The effect of prolonged immunization of mice with bovine serum albumin (BSA) on tumors elicited by injection of 3-methylcholanthrene was studied.	Methylcholanthrene	112-132	albumin	Mus musculus	57-70
6153226-1	1980	The ability of alpha-fetoprotein (AFP), derived from mouse amniotic fluid, to alter qualitative and quantitative characteristics of pristane-induced plasmacytomas and the carcinogenic action of 3-methylcholanthrene (MCA) and 7,12-dimethylbenz]a[-anthracene (DMBA) was studied and compared to analogous treatment with murine albumin and transferrin in BALB/c mice.	Methylcholanthrene	194-214	alpha fetoprotein	Mus musculus	15-32
6153226-1	1980	The ability of alpha-fetoprotein (AFP), derived from mouse amniotic fluid, to alter qualitative and quantitative characteristics of pristane-induced plasmacytomas and the carcinogenic action of 3-methylcholanthrene (MCA) and 7,12-dimethylbenz]a[-anthracene (DMBA) was studied and compared to analogous treatment with murine albumin and transferrin in BALB/c mice.	Methylcholanthrene	194-214	alpha fetoprotein	Mus musculus	34-37
6769180-1	1980	In C57BL/6 mice, aryl hydrocarbon hydroxylase (AHH) increased 1 day after treatment with 3-methylcholanthrene, and induction of UDP-glucuronyl transferases for 3-hydroxybenzo(a)pyrene, p-nitrophenol and bilirubin in the liver microsomes was observed 2 to 5 days later.	Methylcholanthrene	89-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	17-45
6769180-1	1980	In C57BL/6 mice, aryl hydrocarbon hydroxylase (AHH) increased 1 day after treatment with 3-methylcholanthrene, and induction of UDP-glucuronyl transferases for 3-hydroxybenzo(a)pyrene, p-nitrophenol and bilirubin in the liver microsomes was observed 2 to 5 days later.	Methylcholanthrene	89-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	47-50
7006198-7	1980	It was found that bovine MC insulin and porcine MC insulin possess the same immunological activity, i.e. no antibody formation to either of the two insulins was demonstrable.	Methylcholanthrene	25-27	insulin	Bos taurus	28-35
7006198-7	1980	It was found that bovine MC insulin and porcine MC insulin possess the same immunological activity, i.e. no antibody formation to either of the two insulins was demonstrable.	Methylcholanthrene	48-50	insulin	Bos taurus	51-58
119159-4	1979	Treatments with 3-methylcholanthrene and PCB also increased the rate of synthesis of cytochrome b5 and its reductase in both the microsome and outer mitochondrial membrane.	Methylcholanthrene	16-36	cytochrome b5	Oryctolagus cuniculus	85-98
317704-4	1979	It was striking that in the nuclei those activities (benzpyrene hydroxylase, 7-ethoxyresorufin deethylase, 7-ethoxycoumarin deethylase) were preferably induced which can be attributed to the methyl-cholanthrene-induced form of the cytochrome P-450 (cytochrome P-448).	Methylcholanthrene	191-210	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	231-247
317704-4	1979	It was striking that in the nuclei those activities (benzpyrene hydroxylase, 7-ethoxyresorufin deethylase, 7-ethoxycoumarin deethylase) were preferably induced which can be attributed to the methyl-cholanthrene-induced form of the cytochrome P-450 (cytochrome P-448).	Methylcholanthrene	191-210	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	249-265
118380-9	1979	MC induces AHH in hamster lung and intestinal mucosa.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	11-14
387773-0	1979	Specificity of phospholipases in methylcholanthrene-transformed mouse fibroblasts activated by bradykinin, thrombin, serum, and ionophore A23187.	Methylcholanthrene	33-51	coagulation factor II	Mus musculus	107-115
387773-1	1979	Methylcholanthrene-transformed mouse fibroblasts synthesize prostaglandins in response to bradykinin, thrombin, serum, and the ionophore A23187.	Methylcholanthrene	0-18	coagulation factor II	Mus musculus	102-110
500620-1	1979	Genetic and immunochemical evidence for two forms of mouse liver cytochrome P-450 induced by 3-methylcholanthrene.	Methylcholanthrene	93-113	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	65-81
118814-1	1979	Aryl hydrocarbon hydroxylase (AHH) activity and epoxyde hydrase (EH) activity have been found in Rat liver nucleoli obtained from untreated (C) and methylcholanthrene (MC) pretreated Rats.	Methylcholanthrene	148-166	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-28
118814-1	1979	Aryl hydrocarbon hydroxylase (AHH) activity and epoxyde hydrase (EH) activity have been found in Rat liver nucleoli obtained from untreated (C) and methylcholanthrene (MC) pretreated Rats.	Methylcholanthrene	148-166	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-33
118814-1	1979	Aryl hydrocarbon hydroxylase (AHH) activity and epoxyde hydrase (EH) activity have been found in Rat liver nucleoli obtained from untreated (C) and methylcholanthrene (MC) pretreated Rats.	Methylcholanthrene	168-170	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-28
118814-1	1979	Aryl hydrocarbon hydroxylase (AHH) activity and epoxyde hydrase (EH) activity have been found in Rat liver nucleoli obtained from untreated (C) and methylcholanthrene (MC) pretreated Rats.	Methylcholanthrene	168-170	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-33
118814-5	1979	AHH was inducible by MC in nuclei but not in nucleoli.	Methylcholanthrene	21-23	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-3
121315-4	1979	The mutagenic activity of the compounds was clearly correlated to 3-methylcholanthrene-induced cytochrome P-450.	Methylcholanthrene	66-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
550122-1	1979	Using the very well investigated and sensitive microsomal monooxynogenase aryl hydrocarbon hydrolase (AHH), we investigated the dose-response relations between an inducer, 3-methylcholanthrene (3-MC), and an inhibitor of transcription, actinomycin D (ACT D), in 10 days old rats.	Methylcholanthrene	172-192	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	102-105
550122-1	1979	Using the very well investigated and sensitive microsomal monooxynogenase aryl hydrocarbon hydrolase (AHH), we investigated the dose-response relations between an inducer, 3-methylcholanthrene (3-MC), and an inhibitor of transcription, actinomycin D (ACT D), in 10 days old rats.	Methylcholanthrene	194-198	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	102-105
550122-3	1979	With increasing doses of ACT D the inhibition of 3-MC-mediated AHH induction increased up to 88%.	Methylcholanthrene	49-53	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	63-66
550122-6	1979	After 3-MC induction a nearly uniform ANF-mediated inhibition by about 50% of the hepactic AHH activity was observed: in older animals the percentage became slightly higher.	Methylcholanthrene	6-10	natriuretic peptide A	Rattus norvegicus	38-41
550122-6	1979	After 3-MC induction a nearly uniform ANF-mediated inhibition by about 50% of the hepactic AHH activity was observed: in older animals the percentage became slightly higher.	Methylcholanthrene	6-10	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	91-94
550122-7	1979	The investigation appears to confirm the change in cytochrome pattern,--especially as for the participation of cytochrome P-448,--according to the age and induction stimulus by 3-MC.	Methylcholanthrene	177-181	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-127
399151-2	1979	The smaller amount of anti-insulin antibody produced by MC insulin bound pork insulin more strongly than beef insulin in both displacement and direct binding studies of 125I-insulin.	Methylcholanthrene	56-58	insulin	Homo sapiens	27-34
399151-2	1979	The smaller amount of anti-insulin antibody produced by MC insulin bound pork insulin more strongly than beef insulin in both displacement and direct binding studies of 125I-insulin.	Methylcholanthrene	56-58	insulin	Homo sapiens	59-66
399151-2	1979	The smaller amount of anti-insulin antibody produced by MC insulin bound pork insulin more strongly than beef insulin in both displacement and direct binding studies of 125I-insulin.	Methylcholanthrene	56-58	insulin	Homo sapiens	59-66
399151-2	1979	The smaller amount of anti-insulin antibody produced by MC insulin bound pork insulin more strongly than beef insulin in both displacement and direct binding studies of 125I-insulin.	Methylcholanthrene	56-58	insulin	Homo sapiens	59-66
510719-0	1979	Effect of protein synthesis inhibitors on the induction of rat liver microsomal cytochrome P-448 by 3-methylcholanthrene [proceedings].	Methylcholanthrene	100-120	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	80-96
40702-11	1979	The 56 000 Mr band had the same mobility in the gel as an MC-induced protein likely to be cytochrome P-448.	Methylcholanthrene	58-60	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	90-106
115598-3	1979	The addition of dimethylbenz[a]anthracene (DMBA), benz[a]anthracene (BA), or 3-methylcholanthrene (3-MC) to the cell culture medium increased AHH activity 5.3-, 4.7- and 2.4-fold, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	142-145
115598-3	1979	The addition of dimethylbenz[a]anthracene (DMBA), benz[a]anthracene (BA), or 3-methylcholanthrene (3-MC) to the cell culture medium increased AHH activity 5.3-, 4.7- and 2.4-fold, respectively.	Methylcholanthrene	99-103	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	142-145
118106-5	1979	Addition of phenobarbital or methylcholanthrene at day 5 in culture caused an increase in cytochromes P-450 and P-448, respectively, only in hepatocytes cultured on collagen membranes and confluent fibroblasts.	Methylcholanthrene	29-47	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	102-117
109438-0	1979	Amino acid compositions and partial amino acid sequences of three highly purified forms of liver microsomal cytochrome P-450 from rats treated with polychlorinated biphenyls, phenobarbital, or 3-methylcholanthrene.	Methylcholanthrene	193-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-124
6097582-3	1983	The potentials of various derivatives of phorbol ester, indole alkaloid, and polyacetate for enhancing transformation in 3-methylcholanthrene-initiated cells were, in general, in parallel with their potentials for inhibiting phorbol-12, 13-dibutyrate-binding and for inducing early responses such as the reduction of epidermal growth factor (EGF)-binding to cell surface receptors, the increase in glucose uptake and release of arachidonic acid, and the stimulation of DNA synthesis in cells arrested at G0.	Methylcholanthrene	121-141	epidermal growth factor	Mus musculus	317-340
6097582-3	1983	The potentials of various derivatives of phorbol ester, indole alkaloid, and polyacetate for enhancing transformation in 3-methylcholanthrene-initiated cells were, in general, in parallel with their potentials for inhibiting phorbol-12, 13-dibutyrate-binding and for inducing early responses such as the reduction of epidermal growth factor (EGF)-binding to cell surface receptors, the increase in glucose uptake and release of arachidonic acid, and the stimulation of DNA synthesis in cells arrested at G0.	Methylcholanthrene	121-141	epidermal growth factor	Mus musculus	342-345
540966-1	1979	A methylcholanthrene induced tumor of BALBc (H-2d) origin had a high rate of spontaneous regression when transplanted into syngeneic animals.	Methylcholanthrene	2-20	histocompatibility 2, D region	Mus musculus	45-49
496999-0	1979	Regulation of rat liver epoxide hydratase activity by phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	72-92	epoxide hydrolase 2	Rattus norvegicus	24-41
6131891-0	1983	The accumulation of distinct mRNAs for the immunochemically related cytochromes P-450c and P-450d in rat liver following 3-methylcholanthrene treatment.	Methylcholanthrene	121-141	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	80-97
108265-2	1979	An azoreductase has been purified to apparent homogeneity from the hepatic 105,000 x g supernatant fraction of 3-methylcholanthrene-treated rats.	Methylcholanthrene	111-131	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	3-15
6131891-1	1983	Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	170-187
6131891-1	1983	Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c.	Methylcholanthrene	23-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	170-186
6131891-1	1983	Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	426-443
6131891-1	1983	Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c.	Methylcholanthrene	199-219	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	170-187
6131891-1	1983	Treatment of rats with 3-methylcholanthrene leads not only to a marked accumulation in the liver of translatable mRNA coding for a 56-kilodalton polypeptide representing cytochrome P-450c, the major 3-methylcholanthrene-induced cytochrome P-450 of rat liver, but also to the accumulation of comparable amounts of mRNA encoding a 52-kilodalton polypeptide which is immunoprecipitated with antibodies prepared against rat liver cytochrome P-450c.	Methylcholanthrene	199-219	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	170-186
582345-1	1979	Crude membranes (CM) were obtained from in vivo subcutaneous nodules of the methylcholanthrene-induced BALB/c fibrosarcoma C-1 by forcing tumor fragments through a mechanical press and subsequent differential centrifugation.	Methylcholanthrene	76-94	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	123-126
474152-4	1979	In methylcholanthrene-induced rat lung, the metabolism of BP was inhibited by alpha-naphthoflavone, an inhibitor of monooxygenase, and less with diethylmaleate, a depletor of glutathione, with salicylamide, an inhibitor of conjugases, and, astonishingly, with D-saccharo-1,4-lactone, an inhibitor of beta-glucuronidase.	Methylcholanthrene	3-21	glucuronidase, beta	Rattus norvegicus	300-318
222183-10	1979	The cytochrome which is induced by commercial PCB and PBB mixtures appears to be identical to a mixture of cytochromes from phenobarbital- and 3-MC-treated rats.	Methylcholanthrene	143-147	pyruvate carboxylase	Rattus norvegicus	46-49
457816-3	1979	Binding assay showed that at the saturation level of the antibodies, microsomes from untreated, phenobarbital- and methylcholanthrene-treated rats bind 0.25, 0.41 and 0.14 mol of the antibody per mol of cytochrome P-450, respectively.	Methylcholanthrene	115-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	203-219
109558-0	1979	Parameters influencing quantitation of 3-methylcholanthrene-induced aryl hydrocarbon hydroxylase activity in cultured human lymphocytes.	Methylcholanthrene	39-59	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	68-96
286324-0	1979	Biochemical characterization of alien H-2 antigens expressed on a methylcholanthrene-induced tumor.	Methylcholanthrene	66-84	relaxin 2	Homo sapiens	38-41
286324-1	1979	A methylcholanthrene-induced tumor of BALB/c (H-2d) origin had been shown to express H-2 antigens normally associated with the H-2k haplotype.	Methylcholanthrene	2-20	relaxin 2	Homo sapiens	46-49
229677-0	1979	Comparison of spectral properties of 3-MC induced cytochrome P-448 from rabbits and rats.	Methylcholanthrene	37-41	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	50-66
105007-0	1979	Separation and characterization of highly purified forms of liver microsomal cytochrome P-450 from rats treated with polychlorinated biphenyls, phenobarbital, and 3-methylcholanthrene.	Methylcholanthrene	163-183	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
229677-4	1979	Contrary to the 3-methylcholanthrene induced cytochrome P-448 from rats, that from rabbits does not bind 3-methylcholanthrene.	Methylcholanthrene	16-36	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	45-61
229677-5	1979	A particular protein structure establishing the high spin state and an absent binding site for type I substrates is assumed to be responsible for these and other peculiarities of cytochrome P-448 from 3-methylcholanthrene-induced rabbits.	Methylcholanthrene	201-221	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	179-195
229678-1	1979	The paper presents results of a comparative study of the haem environment, by proton magnetic relaxation, in P-450 and P-448 monooxygenases from rat and rabbit, induced by phenobarbital and 3-methylcholanthrene, in both species.	Methylcholanthrene	190-210	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	109-124
106274-9	1979	AR and MC are very good inducers of AHH activity in livers of mice classified as aromatic hydrocarbon responsive, but not in those classified as hydrocarbon nonresponsive.	Methylcholanthrene	7-9	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	36-39
719633-2	1978	The increases in epoxide hydratase activities produced by BHA were far greater (11-fold) than were those produced by the administration of well-known enzyme inducers such as 3-methylcholanthrene, phenobarbital, and Aroclor 1254 (2- to 3-fold).	Methylcholanthrene	174-194	epoxide hydrolase 2, cytoplasmic	Mus musculus	17-34
719999-8	1978	Study in vitro of the kinetics of two reactions, namely aminopyrine N-demethylation and 3,4-benzpyrene hydroxylation, catalysed by the hepatic microsomal cytochrom P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450 with different catalytic properties from those of forms induced by either phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	447-467	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	246-262
153061-8	1978	Treatment of control and diabetic female rats with 3-methylcholanthrene resulted in larger increases in hepatic AHH activity in control animals, but similar increases in cytochrome P-448 content occurred in both treatment groups.	Methylcholanthrene	51-71	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	112-115
153061-8	1978	Treatment of control and diabetic female rats with 3-methylcholanthrene resulted in larger increases in hepatic AHH activity in control animals, but similar increases in cytochrome P-448 content occurred in both treatment groups.	Methylcholanthrene	51-71	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	170-186
719999-8	1978	Study in vitro of the kinetics of two reactions, namely aminopyrine N-demethylation and 3,4-benzpyrene hydroxylation, catalysed by the hepatic microsomal cytochrom P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450 with different catalytic properties from those of forms induced by either phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	447-467	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	339-355
699173-3	1978	Nuclear AHH was induced upon administration of 3-methylcholanthrene (3-MC) to rats.	Methylcholanthrene	47-67	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	8-11
708784-4	1978	Comparison of these distributions leads to the conclusion that the benzpyrene monooxygenase system and epoxide hydratase may form a complex of unique stoichiometry in the membrane of microsomes from control rats, but that such a complex is not consistent with the distributions obtained after methylcholanthrene induction.	Methylcholanthrene	293-311	epoxide hydrolase 2	Rattus norvegicus	103-120
699173-3	1978	Nuclear AHH was induced upon administration of 3-methylcholanthrene (3-MC) to rats.	Methylcholanthrene	69-73	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	8-11
699173-6	1978	The greatest fold increase in nuclear AHH after 3-MC administration was observed in the 6--8 g, or 1--2-day-old rat.	Methylcholanthrene	48-52	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-41
699173-7	1978	Fetal rat liver nuclear AHH was also induced after 3-MC administration to the dam.	Methylcholanthrene	51-55	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	24-27
96118-1	1978	Hepatic microsomal azoreductase activity with amaranth (3-hydroxy-4[(4-sulfo-1-naphthalenyl)azo]-2,7-naphthalenedisulfonic acid trisodium salt) as a substrate is proportional to the levels of microsomal cytochrome P-450 from control or phenobarbital-pretreated rats and mice or cytochrome P-448 from 3-methylchol-anthrene-pretreated animals.	Methylcholanthrene	300-321	NAD(P)H dehydrogenase, quinone 1	Mus musculus	19-31
101214-1	1978	After the administration of 3-methylcholanthrene to adult male rats, activities of hepatic UDP-glucuronosyltransferase towards six from a group of 12 substrates were stimulated by 250-350%.	Methylcholanthrene	28-48	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	91-118
694712-5	1978	There was a significantly lower mean maximum binding and titre of insulin and PP antibodies and total circulating insulin (i.e. antibody bound and free) in patients receiving MC insulin.	Methylcholanthrene	175-177	insulin	Homo sapiens	66-73
694712-5	1978	There was a significantly lower mean maximum binding and titre of insulin and PP antibodies and total circulating insulin (i.e. antibody bound and free) in patients receiving MC insulin.	Methylcholanthrene	175-177	pancreatic polypeptide	Homo sapiens	78-80
694712-5	1978	There was a significantly lower mean maximum binding and titre of insulin and PP antibodies and total circulating insulin (i.e. antibody bound and free) in patients receiving MC insulin.	Methylcholanthrene	175-177	insulin	Homo sapiens	114-121
694712-5	1978	There was a significantly lower mean maximum binding and titre of insulin and PP antibodies and total circulating insulin (i.e. antibody bound and free) in patients receiving MC insulin.	Methylcholanthrene	175-177	insulin	Homo sapiens	114-121
96118-2	1978	In the "inducible" C57B/6J strain of mice, 3-methylcholanthrene and phenobarbital pretreatment cause an increase in cytochrome P-448 and P-450 levels, respectively, which is directly proportional to the increase of azoreductase activity.	Methylcholanthrene	43-63	NAD(P)H dehydrogenase, quinone 1	Mus musculus	215-227
581059-4	1978	Induction of AHH by MC was markedly inhibited by SO2, only slightly by mixture of NO2-SO2 but not with NO2 alone.	Methylcholanthrene	20-22	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-16
694712-6	1978	In patients treated with MC insulins for longer than 2 years there was a significant fall in the mean maximum binding of insulin and total serum insulin, but no consistent change in diabetes control and daily insulin dose.	Methylcholanthrene	25-27	insulin	Homo sapiens	28-35
694712-6	1978	In patients treated with MC insulins for longer than 2 years there was a significant fall in the mean maximum binding of insulin and total serum insulin, but no consistent change in diabetes control and daily insulin dose.	Methylcholanthrene	25-27	insulin	Homo sapiens	121-128
694712-6	1978	In patients treated with MC insulins for longer than 2 years there was a significant fall in the mean maximum binding of insulin and total serum insulin, but no consistent change in diabetes control and daily insulin dose.	Methylcholanthrene	25-27	insulin	Homo sapiens	121-128
79560-1	1978	The studies reported here explore the relationship between tumor-specific transplantation antigens (TSTA) and (1) the expression of serologically defined specificities, and (2) the immunogenicity of H-2K- or H-2D-determined alloantigens on methylcholanthrene (MCA)-induced murine fibrosarcomas.	Methylcholanthrene	240-258	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	100-104
79560-1	1978	The studies reported here explore the relationship between tumor-specific transplantation antigens (TSTA) and (1) the expression of serologically defined specificities, and (2) the immunogenicity of H-2K- or H-2D-determined alloantigens on methylcholanthrene (MCA)-induced murine fibrosarcomas.	Methylcholanthrene	260-263	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	100-104
566669-3	1978	Insulin binding-capacities below 2 mU/ml (mean value after 12 months: 0.45 mU/ml) were found following MC and considerably higher concentrations (mean value after 12 months: 5.16 mU/ml) following CS administration.	Methylcholanthrene	103-105	insulin	Homo sapiens	0-7
633396-3	1978	The DMF in a highly immunogenic 3-methylcholanthrene-induced C3H fibrosarcoma (FSa) was 1.65 in normal mice and 1.86 in mice immunosuppressed by 600 rads whole-body irradiation 1 day before tumor transplantation.	Methylcholanthrene	32-52	RIKEN cDNA 4932438A13 gene	Mus musculus	61-83
27210-5	1978	The reductase reduced cytochrome P-450 (from phenobarbital-treated rabbits) and cytochrome P-448 (from 3-methylcholanthrene-treated rabbits).	Methylcholanthrene	103-123	cytochrome P-450	Oryctolagus cuniculus	22-38
208548-0	1978	Cytochrome P450 in the liver mitochondrial outer membrane of 20-methyl cholanthrene or Aroclor treated rabbits.	Methylcholanthrene	61-83	cytochrome P-450	Oryctolagus cuniculus	0-15
633074-9	1978	Evidence that these polypeptides are cytochrome P-450 was obtained from heme staining with tetramethylbenzidine and from induction studies with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	162-182	cytochrome P450 3A14	Cavia porcellus	37-53
75855-1	1978	Methylcholanthrene-induced sarcomas of BALB/c mice express unique tumor specific transplantation antigens (TSTA), and weaker, common TSTA.	Methylcholanthrene	0-18	heat shock protein 90 alpha (cytosolic), class B member 1	Mus musculus	107-111
75855-1	1978	Methylcholanthrene-induced sarcomas of BALB/c mice express unique tumor specific transplantation antigens (TSTA), and weaker, common TSTA.	Methylcholanthrene	0-18	heat shock protein 90 alpha (cytosolic), class B member 1	Mus musculus	133-137
626975-1	1978	During the growth of five of ten primary tumors that were induced by 3-methylcholanthrene in BALB/cMk and BALB/cMk X C57BL/6F1 mice, leukemoid reactions, characterized by increase in number of granulocytes in peripheral blood, and splenomegaly were observed.	Methylcholanthrene	69-89	chemokine (C-X-C motif) ligand 9	Mus musculus	98-101
415100-13	1978	The gradient of P-450 (OR P1-450) was less steep in 3-MC-treated cells with pooled fractions 1 and 2 containing an average of 4.62 times as much cytochrome as fractions 11 and 12.	Methylcholanthrene	52-56	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-21
415100-13	1978	The gradient of P-450 (OR P1-450) was less steep in 3-MC-treated cells with pooled fractions 1 and 2 containing an average of 4.62 times as much cytochrome as fractions 11 and 12.	Methylcholanthrene	52-56	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	26-32
106613-3	1978	3-methylcholanthrene induced the aryl hydrocarbon hydroxylase and azoreductase and led to an increase in the demethylation of 4-dimethylaminoazobenzene but not in the ethylmorphine demethylation.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	33-61
620413-4	1978	Methylcholanthrene-transformed C3H/10T 1/2 1/2 CL8 cells adapted to CDM exhibited a regular epithelioid morphology with no cell overlap and formed confluent monolayers of nonproliferating cells at a saturation density of 5 X 10(4) cells/sq cm.	Methylcholanthrene	0-18	cadmus	Drosophila melanogaster	68-71
640318-2	1978	Properties of AHH enzymes in the lung microsomes from mice treated intraperitoneally with 3-methylcholanthrene (induced enzymes) were compared with those treated with corn oil (constitutive enzymes).	Methylcholanthrene	90-110	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	14-17
106613-3	1978	3-methylcholanthrene induced the aryl hydrocarbon hydroxylase and azoreductase and led to an increase in the demethylation of 4-dimethylaminoazobenzene but not in the ethylmorphine demethylation.	Methylcholanthrene	0-20	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	66-78
697926-0	1978	Effect of dietary phenobarbital, 3,4-benzo(alpha)pyrene and 3-methylcholanthrene on hepatic, intestinal and renal glutathione s-transferase activities in the rat.	Methylcholanthrene	60-80	hematopoietic prostaglandin D synthase	Rattus norvegicus	114-139
728164-0	1978	Time course of the induction of aryl hydrocarbon hydroxylase in rat liver nuclei and microsomes by phenobarbital, 3-methylcholanthrene, 2,3,7,8-tetrachloro-dibenzo-p-dioxin, dieldrin and other inducers.	Methylcholanthrene	114-134	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	32-60
898314-4	1977	Administration of actinomycin D simultaneously with polycyclic hydrocarbons prevents intensification of the CCl4 hepatotoxic effect caused by 3-methylcholanthrene and dibenz (a, h) anthracene.	Methylcholanthrene	142-162	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
658547-1	1978	Lymph node cells obtained from B10 mice were sensitized in vitro on monolayers of syngeneic methylcholanthrene-induced sarcoma cells.	Methylcholanthrene	92-110	granzyme C	Mus musculus	31-34
907723-0	1977	3-Methylcholanthrene inducibility of aryl hydrocarbon hydroxylase in cultured human lymphocytes depends upon the extent of blast transformation.	Methylcholanthrene	2-20	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	37-65
69494-0	1977	Biological and biochemical properties of Nonidet P40-solubilized and partially purified tumor-specific antigens of the transplantation type from plasma membranes of a methylcholanthrene-induced sarcoma.	Methylcholanthrene	167-185	interleukin 9	Mus musculus	49-52
70414-1	1977	The presence of alien histocompatibility antigens on the cell surface of the 3-methylcholanthrene-induced BALB/c (H-2d) fibrosarcoma C-1, was investigated by serological and transplantation studied.	Methylcholanthrene	77-97	histocompatibility 2, D region	Mus musculus	114-118
906776-5	1977	When MC"s were abolished by feeding or PG infusion, simultaneous 13-nle-motilin administration was without effect on spike activity, but slightly attenuated the accelerating effect of gastrin on the gastric pacemaker frequency.	Methylcholanthrene	5-7	motilin	Canis lupus familiaris	72-79
407010-7	1977	Both flavones when added directly to the assay tubes inhibited the in vitro epidermal AHH activity from control and MC pretreated mice by greater than 75%.	Methylcholanthrene	116-118	aryl-hydrocarbon receptor	Mus musculus	86-89
142349-4	1977	Significant mesangial cell proliferation and an increase in mesangial matrix were found on treatment with the a+b component whereas the animals treated with MC insulin exhibited only a transient and slight mesangial activation after 30 days.	Methylcholanthrene	157-159	insulin	Oryctolagus cuniculus	160-167
870187-3	1977	AHH inducibility was determined by comparing lymphocytes from the same person cultured with and without the inducer 3-methylcholanthrene.	Methylcholanthrene	116-136	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	0-3
842593-7	1977	It is concluded that in the neonate insulin increases MC as well as substrate uptake.	Methylcholanthrene	54-56	LOC105613195	Ovis aries	36-43
405315-1	1977	The intensity of anaphylactic shock was lower in C3H mice carrying a methylcholanthrene-induced tumour (McC3) than in their normal counterparts when immunized with ovalbumin and challenged i.v.	Methylcholanthrene	69-87	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	164-173
856576-6	1977	In contrast, the reconstituted benzo[a]pyrene hydroxylase system, with purified cytochrome P-448 from 3-methylcholanthrene-induced rats, exhibited a considerably higher sensitivity towards CO (CO/O2 ratio approximately 1), well within the range for mixed-function oxidase reactions.	Methylcholanthrene	102-122	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	80-96
578932-7	1977	All of these data suggested that clinical effects of MC-insulin and commercial insulin treatment on insulin requiring diabetics were comparable except insulin antibody or proinsulinspecific antibody production.	Methylcholanthrene	53-55	insulin	Homo sapiens	56-63
833884-1	1977	To check the suggestion that 3-methylcholanthrene-induced, sarcoma-associated, tumor-specific transplantation antigens (TSTA) could be modified H-2 antigens, reciprocal isoantigenic variants derived from TA3Ha/MSWBS hybrid cells were examined.	Methylcholanthrene	29-49	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	120-124
898289-0	1977	Alien histocompatibility determinants on the cell surface of sarcomas induced by methylcholanthrene.	Methylcholanthrene	81-99	COP9 signalosome subunit 2	Homo sapiens	0-5
833884-1	1977	To check the suggestion that 3-methylcholanthrene-induced, sarcoma-associated, tumor-specific transplantation antigens (TSTA) could be modified H-2 antigens, reciprocal isoantigenic variants derived from TA3Ha/MSWBS hybrid cells were examined.	Methylcholanthrene	29-49	histocompatibility-2, MHC	Mus musculus	144-147
833884-13	1977	These findings argue against the possibility that methylcholanthrene-induced TSTA is a modified form of H-2 or that its structural determinants(s) is localized on chromosome 17.	Methylcholanthrene	50-68	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	77-81
833115-7	1977	All the data are consistent with an hypothesis that two loci (Ox-1 and Ox-2) regulate oxidoreductase induction by 3-methylcholanthrene, that one of the genes is linked to the Ah locus (with an estimated recombination frequency between 2% and 23%), and that the other gene is not linked to the Ah locus.	Methylcholanthrene	114-134	NAD(P)H dehydrogenase, quinone 1	Mus musculus	62-75
833122-1	1977	Solubilized cytochromes P-450 and P-448 have been prepared from liver microsomes of phenobarbital- and 3-methylcholanthrene-pretreated rats, respectively.	Methylcholanthrene	103-123	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	24-39
13937-7	1977	3-MC and PB specifically act on cytochrome P-450 and do not modify the physico-chemical properties of the microsomal membrane as measured by the non-specific binding of benzpyrene (BP).	Methylcholanthrene	0-4	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
20401-0	1977	Glutaminase & glutamine synthetase in 20-methylcholanthrene treated mice.	Methylcholanthrene	42-63	glutamate-ammonia ligase (glutamine synthetase)	Mus musculus	18-38
13970-5	1977	Maximum MC-induction of type I binding and de-ethylase activity coincided with the appearance of a cytochrome P-450 spectrum whose absorption maximum was shifted to 448 nm.	Methylcholanthrene	8-10	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	43-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
63323-1	1976	Interindividual and intraindividual variations in aryl hydrocarbon hydroxylase (AHH) induction by 3-methylcholanthrene were studied in cultured lymphocytes from normal adult volunteers.	Methylcholanthrene	98-118	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	50-78
63323-1	1976	Interindividual and intraindividual variations in aryl hydrocarbon hydroxylase (AHH) induction by 3-methylcholanthrene were studied in cultured lymphocytes from normal adult volunteers.	Methylcholanthrene	98-118	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	80-83
63323-5	1976	Fetal calf serum may contain inducers of AHH activity that vary with the particular lot of serum, thereby rendering the apparent induction ratio an imprecise indicator of genetic susceptibility to induction by 3-methylcholanthrene.	Methylcholanthrene	210-230	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	41-44
63323-6	1976	The index of heritability for AHH fold inducibility in twins studied with different lots of fetal calf serum (0.80) or with a single lot of fetal calf serum (0.77) suggests nonetheless that genetic rather than environmental factors are mainly responsible for interindividual variations in AHH inducibility by 3-methylcholanthrene in human lymphocytes.	Methylcholanthrene	309-329	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	30-33
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-160
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	43-63	cytochrome b5 type A	Rattus norvegicus	344-357
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	65-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	65-67	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-160
10077-1	1976	The hepatic nuclear fraction isolated from 3-methylcholanthrene (MC)-treated rats contained enhanced levels of cytochrome P-450 and aryl hydrocarbon hydroxylase [benzo(a)pyrene (BP) monooxygenase], whereas the activities of epoxide hydrase and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase and the concentration of cytochrome b5 were not altered.	Methylcholanthrene	65-67	cytochrome b5 type A	Rattus norvegicus	344-357
134910-5	1976	The administration of polycyclic aromatic hydrocarbons (e.g., 3-methylcholanthrene (MC)) to certain inbred strains of mice induces aryl hydrocarbon hydroxylase, while other inbred strains fail to respond; and the trait of aryl hydrocarbon responsiveness is inherited as an autosomal dominant.	Methylcholanthrene	62-82	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	131-159
182361-5	1976	Treatment of the rats with 3-methylcholanthrene induced the nuclear aryl hydrocarbon hydroxylase (AHH) activity and also increased the level of carcinogen binding.	Methylcholanthrene	27-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	68-96
182361-5	1976	Treatment of the rats with 3-methylcholanthrene induced the nuclear aryl hydrocarbon hydroxylase (AHH) activity and also increased the level of carcinogen binding.	Methylcholanthrene	27-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	98-101
182361-8	1976	Lung nuclei from control rats had very low AHH activity and did not exhibit appreciable carcinogen binding, whereas those from 3-methylcholanthrene-pretreated animals had slightly higher AHH activity and caused low levels of binding.	Methylcholanthrene	127-147	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	187-190
134910-5	1976	The administration of polycyclic aromatic hydrocarbons (e.g., 3-methylcholanthrene (MC)) to certain inbred strains of mice induces aryl hydrocarbon hydroxylase, while other inbred strains fail to respond; and the trait of aryl hydrocarbon responsiveness is inherited as an autosomal dominant.	Methylcholanthrene	84-86	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	131-159
948753-0	1976	Cytochrome P-450 induction by phenobarbital and 3-methylcholanthrene in primary cultures of hepatocytes.	Methylcholanthrene	48-68	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
10606-3	1976	The reaction was inhibited by 7,8-benzoflavone indicating that it was mediated by the 3MC-inducible form of cytochrome P-450.	Methylcholanthrene	86-89	cytochrome P-450	Oryctolagus cuniculus	108-124
10448-11	1976	Pretreatment with 3-methylcholanthrene partially inhibited the increase of GTase that had been induced by a single dose of 3"-Me-DAB.	Methylcholanthrene	18-38	gamma-glutamyltransferase 1	Rattus norvegicus	75-80
971515-3	1976	3-MC or benzpyrene stimulated aryl hydrocarbon hydroxylase (AHH) activity in C57BL/6J (B6) mice but not in DBA/2J (D2) mice.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	30-58
971515-3	1976	3-MC or benzpyrene stimulated aryl hydrocarbon hydroxylase (AHH) activity in C57BL/6J (B6) mice but not in DBA/2J (D2) mice.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	60-63
1268849-5	1976	3-Methylcholanthrene, phenobarbital, and 2-acetylaminofluorene had a greater inductive effect and cytochrome P-450 in vitamin A-deficient rats.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
793922-2	1976	The pleural fibrosarcomas were induced by a substernal injection of 3-methylcholanthrene into the thoracic cavity of ddO mice.	Methylcholanthrene	68-88	D-aspartate oxidase	Mus musculus	117-120
1260949-8	1976	However, while both phenobarbital and MC powerfully repress the DMN-demethylase, we have confirmed that they are strong inducers of the synthesis of P-450 and P-448, respectively, as estimated from the difference spectra.	Methylcholanthrene	38-40	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	149-164
815258-2	1976	Purified hepatic cytochrome P-448 from 3-methylcholanthrene-treated rats was used to produce antibody in rabbits.	Methylcholanthrene	39-59	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	17-33
815258-12	1976	The observed patterns of immunoprecipitation and inhibition of catalytic activity indicate that (a) cytochrome P-448 from 3-methylcholanthrene-treated rats is immunochemically different from cytochrome P-450 from phenobarbital-treated rats, and (b) there appear to be at least three hemeprotein forms in the purified cytochrome P-450 preparation from phenobarbital-treated rats.	Methylcholanthrene	122-142	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-116
815258-12	1976	The observed patterns of immunoprecipitation and inhibition of catalytic activity indicate that (a) cytochrome P-448 from 3-methylcholanthrene-treated rats is immunochemically different from cytochrome P-450 from phenobarbital-treated rats, and (b) there appear to be at least three hemeprotein forms in the purified cytochrome P-450 preparation from phenobarbital-treated rats.	Methylcholanthrene	122-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	317-333
3285-1	1976	Administration of 3-methylcholanthrene (3MC) to rats greatly enhanced the aryl hydrocarbon hydroxylase (AHH) activity of liver nuclei.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	74-102
3285-1	1976	Administration of 3-methylcholanthrene (3MC) to rats greatly enhanced the aryl hydrocarbon hydroxylase (AHH) activity of liver nuclei.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	104-107
3285-1	1976	Administration of 3-methylcholanthrene (3MC) to rats greatly enhanced the aryl hydrocarbon hydroxylase (AHH) activity of liver nuclei.	Methylcholanthrene	40-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	74-102
3285-1	1976	Administration of 3-methylcholanthrene (3MC) to rats greatly enhanced the aryl hydrocarbon hydroxylase (AHH) activity of liver nuclei.	Methylcholanthrene	40-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	104-107
1259730-0	1976	Purification of a substrate complex of cytochrome P-450 from liver microsomes of 3-methylcholanthrene-treated rabbits.	Methylcholanthrene	81-101	cytochrome P-450	Oryctolagus cuniculus	39-55
5265-5	1976	In the presence of fixed amounts of lipid and NADPH-cytochrome c reductase, the rate of complex formation with cytochrome P-450 isolated from phenobarbital-treated rats was much greater than that observed with cytochrome P-48 from 3-methylcholanthrene-treated rats or rabbits.	Methylcholanthrene	231-251	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
1274375-11	1976	Treatment of 7 day-old chicks with exogenous inducers, 3-methylcholanthrene or phenobarbital sodium (100 mg/kg, intraperitoneally) brought about maximal stimulation of microsomal activity as 18-24 h. The time-course of this induction was reflected by changes in microsomal cytochrome P-450 content and NADPH-cytochrome P=450 reductase activities.	Methylcholanthrene	55-75	cytochrome p450 oxidoreductase	Gallus gallus	302-334
813227-6	1976	Induction with 3-methylcholanthrene gave the largest increases in nuclear activities: 11 times as much hydroxylase, 6 times as much cytochrome P-450, and 4 times as much binding of both hydrocarbons.	Methylcholanthrene	15-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-155
1027349-4	1976	After transfer from conventional to MC insulin treatment it was observed: -- disappearance of allergy and total remission of lipoatrophy, in parallel with a reduction of IB titer; -- decrease in insulin requirement and stabilisation of labile diabetic control, not always in concomitance with IB reduction; -- deterioration of advanced diabetic retinopathy and, or nephropathy in spite of IB reduction.	Methylcholanthrene	36-38	insulin	Homo sapiens	39-46
1087093-6	1976	Rabbits treated with MC insulin showed no significant antibody formation and no significant changes in the glomerular structure.	Methylcholanthrene	21-23	insulin	Oryctolagus cuniculus	24-31
1027349-4	1976	After transfer from conventional to MC insulin treatment it was observed: -- disappearance of allergy and total remission of lipoatrophy, in parallel with a reduction of IB titer; -- decrease in insulin requirement and stabilisation of labile diabetic control, not always in concomitance with IB reduction; -- deterioration of advanced diabetic retinopathy and, or nephropathy in spite of IB reduction.	Methylcholanthrene	36-38	insulin	Homo sapiens	195-202
1027349-5	1976	It is concluded that MC insulin constitutes a major tool in the treatment of the above mentioned diabetic conditions, except for advanced microangiopathy.	Methylcholanthrene	21-23	insulin	Homo sapiens	24-31
1027349-6	1976	Thus a MC insulin treatment should be started, as a rule, in newly diagnosed diabetics, to possibly prevent such complications.	Methylcholanthrene	7-9	insulin	Homo sapiens	10-17
1192552-0	1975	Inhibition of hepatic aryl hydrocarbon hydroxylase by 3-methylcholanthrene, 7,8-benzoflavone and other inducers added in vitro.	Methylcholanthrene	54-74	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	22-50
174812-3	1976	The cis-1,2-dihydroxy, trans-11,12-dihydroxy, and cis-11,12-dihydroxy derivatives of 3-methylcholanthrene exerted little effect.	Methylcholanthrene	85-105	suppressor of cytokine signaling 1	Homo sapiens	4-9
954982-1	1976	Subcutaneous injection of epidermal growth factor 1. significantly shortened the latency period for the appearance of methylcholanthrene induced skin tumors and 2. increased the average number of papillomas elicited per mouse in both the Swiss Webster and C3HeB/FeJ strains.	Methylcholanthrene	118-136	epidermal growth factor	Mus musculus	26-49
3152-9	1975	3) Altered microsomal cytochrome P-450 concentrations in newborn animals, or produced by pretreatment of rats with phenobarbital, 3-methylcholanthrene (MC), or CoCl2 effected similar, but not proportional changes in the rates of irreversible protein and lipid binding.	Methylcholanthrene	130-150	cytochrome P-450	Oryctolagus cuniculus	22-38
3152-9	1975	3) Altered microsomal cytochrome P-450 concentrations in newborn animals, or produced by pretreatment of rats with phenobarbital, 3-methylcholanthrene (MC), or CoCl2 effected similar, but not proportional changes in the rates of irreversible protein and lipid binding.	Methylcholanthrene	152-154	cytochrome P-450	Oryctolagus cuniculus	22-38
3152-10	1975	Upon addition of CCl4 the difference of light absorption of reduced liver microsomes from MC-pretreated rats containing cytochrome P-448 appeared at 452 nm.	Methylcholanthrene	90-92	C-C motif chemokine ligand 4	Rattus norvegicus	17-21
3152-10	1975	Upon addition of CCl4 the difference of light absorption of reduced liver microsomes from MC-pretreated rats containing cytochrome P-448 appeared at 452 nm.	Methylcholanthrene	90-92	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	120-136
131730-1	1975	The protein-bound polysaccharide preparation, PS-K, was found to possess an antitumor effect against 3-methylcholanthrene-induced fibrosarcoma in mice which was shown to have a tumor-specific transplantation antigen.	Methylcholanthrene	101-121	TAO kinase 2	Mus musculus	46-50
148-10	1975	(4) After feeding DAB for 4 weeks the effect of PB and 3-methylcholanthrene (MC) on the activities of DAB-azoreductase, CB10-252-azoreductase and components of the azoreductases-cytochrome P-450, NADPH-cytochrome c reductase, the CO-CB10-252-azoreductase was not induced by PB or MC, and CO did not inhibit its reduction.	Methylcholanthrene	77-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	178-194
51886-4	1975	These same alloantisera, however, produced anomalous positive reactions when tested on cultured MCA-induced sarcoma cells from B10 background H-2 congenic mice.	Methylcholanthrene	96-99	histocompatibility-2, MHC	Mus musculus	142-145
808269-4	1975	After treatment of rats with 3-methylcholanthrene, the specific content of cytochrome P-450 in lung microsomes is doubled and that of cytochrome b5 increases 1.5 times.	Methylcholanthrene	29-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	75-91
809440-1	1975	Solubilized cytochrome P-450 has been prepared from the livers of 3-methylcholanthrene-pretreated rats.	Methylcholanthrene	66-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
1233923-0	1975	[Influence of prolactin on the appearance and development of experimental mammary tumors induced with 20-methylcholanthrene].	Methylcholanthrene	102-123	prolactin	Homo sapiens	14-23
808269-4	1975	After treatment of rats with 3-methylcholanthrene, the specific content of cytochrome P-450 in lung microsomes is doubled and that of cytochrome b5 increases 1.5 times.	Methylcholanthrene	29-49	cytochrome b5 type A	Rattus norvegicus	134-147
808269-9	1975	It is concluded that the cytochrome P-450 present in rat lung microsomes before and after 3-methylcholanthrene treatment of the animals is distinctly different from the liver hemoprotein.	Methylcholanthrene	90-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	25-41
52639-4	1975	In contrast to these enzymes, urate oxidase activity remained unchanged in H, whereas it was decreased in M and increased in L and Mc during the first 5 days after operation.	Methylcholanthrene	131-133	urate oxidase	Rattus norvegicus	30-43
813632-1	1975	The N- and ring-hydroxylation of 2-acetamidofluorene were studied with a reconstituted cytochrome P-450 enzyme from microsomal fractions of liver from both control and 3-methylcholanthrene-pretreated rats.	Methylcholanthrene	168-188	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	87-103
1180881-2	1975	Furthermore, the induction of AHH was investigated using the fetal liver explant model system with 3MC, trans-1,2-dihydroxy-3MC, and 4"-bromoflavone as the inducers.	Methylcholanthrene	99-102	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	30-33
1171804-4	1975	In this study the antigenicity of MC insulin was determined in two groups of diabetic patients.	Methylcholanthrene	34-36	insulin	Homo sapiens	37-44
1171804-5	1975	In group 1, seven patients treated with insulin for the first time were given MC insulin for seven to fifteen months.	Methylcholanthrene	78-80	insulin	Homo sapiens	40-47
1171804-5	1975	In group 1, seven patients treated with insulin for the first time were given MC insulin for seven to fifteen months.	Methylcholanthrene	78-80	insulin	Homo sapiens	81-88
1171804-13	1975	When the purity of the MC insulin was determined, significant contaminants could be demonstrated in all of ten separate batches of MC insulin.	Methylcholanthrene	23-25	insulin	Homo sapiens	26-33
1171804-13	1975	When the purity of the MC insulin was determined, significant contaminants could be demonstrated in all of ten separate batches of MC insulin.	Methylcholanthrene	23-25	insulin	Homo sapiens	134-141
1171804-13	1975	When the purity of the MC insulin was determined, significant contaminants could be demonstrated in all of ten separate batches of MC insulin.	Methylcholanthrene	131-133	insulin	Homo sapiens	26-33
50348-1	1975	A tumor specific transplantation antigen (TSTA) has been detected in a methylcholanthrene (MCA) induced guinea pig tumor.	Methylcholanthrene	91-94	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	42-46
50348-1	1975	A tumor specific transplantation antigen (TSTA) has been detected in a methylcholanthrene (MCA) induced guinea pig tumor.	Methylcholanthrene	71-89	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	42-46
50291-0	1975	Are methylcholanthrene-induced sarcoma-associated, rejection-inducing (TSTA) antigens, modified forms of H-2 or linked determinants?	Methylcholanthrene	4-22	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	71-75
176078-1	1975	Aryl hydrocarbon hydroxylase activity in Morris hepatoma 5123D is very low, but apparently increases by the administration of 3-methylcholanthrene, as demonstrated in the host liver, small intestine, and lung from the rats bearing this tumor.	Methylcholanthrene	126-146	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-28
50291-11	1975	The present paper examined the possibility, often suggested in the literature, that the MC-sarcoma-associated TSTA could be a modified form of H-2.	Methylcholanthrene	88-90	heat shock protein 90, alpha (cytosolic), class A member 1	Mus musculus	110-114
50291-11	1975	The present paper examined the possibility, often suggested in the literature, that the MC-sarcoma-associated TSTA could be a modified form of H-2.	Methylcholanthrene	88-90	histocompatibility-2, MHC	Mus musculus	143-146
168749-0	1975	Studies on the spin state of 3-methylcholanthrene induced cytochrome P-450 from rat liver.	Methylcholanthrene	29-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
805662-2	1975	C57BL/10nSn (B10) mice and their F1 hybrids were given injections of a methylcholanthrene-induced fibrosarcoma of B10 origin.	Methylcholanthrene	71-89	granzyme C	Mus musculus	114-117
1215860-5	1975	It is advised that the use of mc-insulin should be restricted to precise clinical indications until enough pure pig insulin is available for treatment of all insulin-dependent diabetics.	Methylcholanthrene	30-32	insulin	Sus scrofa	33-40
184628-0	1975	On the selectivity of aryl hydrocarbon hydroxylase induction after 3-methylcholanthrene pretreatment.	Methylcholanthrene	67-87	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	22-50
184628-3	1975	3-MC highly specifically influenced the AHH activity, which was increased dose dependent.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	40-43
184628-7	1975	Therefore the 3-MC mediated AHH induction seems to be a suitable model for the examination of dose dependent inducer-inhibitor interactions in the intact animal.	Methylcholanthrene	14-18	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	28-31
808108-3	1975	Partial purification of liver microsomal cytochrome p-450 results in the separation of two forms of cytochrome p-450 from phenobarbital-treated rats and two forms of cytochrome p-44, from 3-methylcholanthrene-treated rats.	Methylcholanthrene	188-208	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
808108-3	1975	Partial purification of liver microsomal cytochrome p-450 results in the separation of two forms of cytochrome p-450 from phenobarbital-treated rats and two forms of cytochrome p-44, from 3-methylcholanthrene-treated rats.	Methylcholanthrene	188-208	mitogen activated protein kinase 3	Rattus norvegicus	177-181
168749-1	1975	The time course of infuction of rat liver microsomal cytochrome P-450 by the polycyclic hydrocarbon 3-methylcholanthrene was followed by measuring the specific content of cytochrome P-450, benzpyrene hydroxylase activity, and the percent of cytochrome P-450 existing as the high-spin form (g equal to 7.9, 3.7 and 1.7) as determined by low temperature EPR spectroscopy.	Methylcholanthrene	100-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
168749-2	1975	Significant increases in benzpyrene hydroxylase, cytochrome P-450 and high-spin ferric hemoprotein are seen twenty-four hours following 3-methylcholanthrene treatment.	Methylcholanthrene	136-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
168749-4	1975	In addition, partially purified cytochrome P-450 can be isolated from liver microsomes of 3-methylcholanthrene treated rats as low-spin ferric hemoprotein containing essentially no high-spin species (smaller than 1 per cent).	Methylcholanthrene	90-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
810814-5	1975	3-Methylcholanthrene was, however, able to maintain or increase mucosal hydroxylative enzymes and UDP glucuronosyltransferase.	Methylcholanthrene	0-20	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	98-125
1131799-1	1975	Mice bearing a 3-methylcholanthrene-induced fibrosarcoma (MCAM-7) transplant in the right leg underwent surgical excision of the tumor and showed specific resistance to subsequent challenges with that identical tumor line.	Methylcholanthrene	15-35	melanoma cell adhesion molecule	Homo sapiens	58-62
4218121-0	1974	Co-carcinogenic effect of DDT and PCB feeding on methylcholanthrene-induced chemical carcinogenesis.	Methylcholanthrene	49-67	pyruvate carboxylase	Homo sapiens	34-37
4431051-0	1974	Prolactin-stimulating effect on 3H-thymidine incorporation in 3-methylcholanthrene-induced cervical carcinomas in normal and estrogenized mice.	Methylcholanthrene	62-82	prolactin	Mus musculus	0-9
4142788-1	1974	The tumorigenic EPO clonal cell line, derived from a methylcholanthrene-induced murine sarcoma, was exposed to increasing concentrations of actinomycin D and gave rise to a subline, resistant to 0.02 mug of actinomycin D per ml of medium, which was designated EPO/ADj.	Methylcholanthrene	53-71	erythropoietin	Mus musculus	16-19
4403783-0	1972	Differential acute effects of phenobarbital and 3-methylcholanthrene pretreatment on CCl 4 -induced hepatotoxicity in rats.	Methylcholanthrene	48-68	C-C motif chemokine ligand 4	Rattus norvegicus	85-90
4720873-0	1973	Evidence of a genetic relationship between susceptibility to 3-methyl-cholanthrene-induced subcutaneous tumors and inducibility of aryl hydrocarbon hydroxylase.	Methylcholanthrene	61-82	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	131-159
5026638-0	1972	[Cell surface antigen--study of localization of rat transplantation antigen and specific antigen of MC-induced sarcoma on the cell surface by ferritin antibody technic].	Methylcholanthrene	100-102	CD53 molecule	Homo sapiens	1-21
4197089-6	1973	These data suggest that Aroclor 1254-induced cytochrome P-448 may be catalytically different from the 3-methylcholanthrene-induced P-448 or that the hemoprotein(s) induced by Aroclor 1254 may be a mixture of cytochromes P-448 and P-450 exhibiting catalytic properties of both cytochromes.	Methylcholanthrene	102-122	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	131-136
5144545-4	1971	The highest degree of binding occurs in washed mitochondria, microsomes, ribosome-free microsomal membranes and their constituent core proteins.Cell sap which contains non-covalently bound 3"-methylcholanthrene was fractionated into pH 5 enzyme and pH 5 supernatant fractions.	Methylcholanthrene	189-210	amyloid P component, serum	Rattus norvegicus	149-152
5083567-0	1972	Regression of established methylcholanthrene tumors by intratumor injections of Vbrio cholerae neuraminidase.	Methylcholanthrene	26-44	neuraminidase 1	Homo sapiens	95-108
5152321-0	1971	[Effect of an increased and lowered production of erythropoietin in mice on the development in them of skin tumors induced by 20-methylcholanthrene].	Methylcholanthrene	126-147	erythropoietin	Mus musculus	50-64
5096510-5	1971	Other drugs and chemicals which cause proliferation of hepatic smooth endoplasmic reticulum and enhancement of drug metabolism, such as allylisopropylacetamide, dieldrin, DDT, 3-methylcholanthrene, and benzpyrene increased Y and BSP K(1) and, where studied, hepatic BSP content.	Methylcholanthrene	176-196	integrin-binding sialoprotein	Rattus norvegicus	229-232
5096510-5	1971	Other drugs and chemicals which cause proliferation of hepatic smooth endoplasmic reticulum and enhancement of drug metabolism, such as allylisopropylacetamide, dieldrin, DDT, 3-methylcholanthrene, and benzpyrene increased Y and BSP K(1) and, where studied, hepatic BSP content.	Methylcholanthrene	176-196	integrin-binding sialoprotein	Rattus norvegicus	266-269
5576331-2	1971	Five methylcholanthrene-induced sarcomas were compared for their capacity to (a) absorb monospecific H-2 antisera, (b) induce tumor-specific immunity in syngeneic mice, and (c) metastasize early to the lungs.	Methylcholanthrene	5-23	histocompatibility-2, MHC	Mus musculus	101-104
5552260-0	1971	Effect of methylcholanthrene or phenobarbital pretreatment of rabbits and rats on the extinction coefficient for cytochrome P-450.	Methylcholanthrene	10-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-129
4318775-0	1970	Electron paramagnetic resonance study of the high- and low-spin forms of cytochrome P-450 in liver and in liver microsomes from a methylcholanthrene-treated rabbit.	Methylcholanthrene	130-148	cytochrome P-450	Oryctolagus cuniculus	73-89
4318775-1	1970	The high- and low-spin forms of cytochrome P-450 were observed by electron paramagnetic resonance (epr) in a liver slice and in hepatic microsomes from a rabbit injected with methylcholanthrene.	Methylcholanthrene	175-193	cytochrome P-450	Oryctolagus cuniculus	32-48
5688265-0	1968	Effect of partial hepatectomy of the responsiveness of microsomal enzymes and cytochrome P-450 to phenobarbital or 3-methylcholanthrene.	Methylcholanthrene	115-135	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-94
14188468-0	1964	3-METHYLCHOLANTHRENE CONCENTRATION AND CLEARANCE IN SOME ADIPOSE TISSUES IN MICE.	Methylcholanthrene	0-20	WD and tetratricopeptide repeats 1	Mus musculus	57-64
13697631-0	1961	Changes in the synthesis of deoxyribonucleic acid (DNA) and in mitotic count in epidermis of hairless mice after a single application of one per cent 3:methyl-cholanthrene in benzene.	Methylcholanthrene	152-171	lysine demethylase and nuclear receptor corepressor	Mus musculus	93-101
14050615-0	1963	EARLY EFFECTS OF A SINGLE APPLICATION OF 3 METHYLCHOLANTHRENE IN BENZENE SOLUTION ON THE EPIDERMIS OF HAIRLESS MICE STUDIED BY MEANS OF A TETRAZOLIUM REDUCTION METHOD.	Methylcholanthrene	41-61	lysine demethylase and nuclear receptor corepressor	Mus musculus	102-110
14054096-0	1963	EFFECT OF 3-METHYLCHOLANTHRENE ON AMINO ACID INCORPORATION INTO RAT LIVER PROTEIN.	Methylcholanthrene	10-30	Yip1 interacting factor homolog A, membrane trafficking protein	Rattus norvegicus	68-81
33765348-2	2021	3MC is caused by biallelic pathogenic variants in MASP1, COLEC11, or COLEC10.	Methylcholanthrene	0-3	mannan-binding lectin serine protease 1	Meleagris gallopavo	50-55
21065029-0	1946	Uptake of P32 in the phospholipid fraction of mouse epidermis undergoing carcinogenesis by methylcholanthrene.	Methylcholanthrene	91-109	complement component 1, q subcomponent binding protein	Mus musculus	10-13
5497719-1	1970	V. Independent formation of cytochromes P-450 and P1-450 in rats treated with phenobarbital and 3-methylcholanthrene simultaneously.	Methylcholanthrene	96-116	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-56
34046774-3	2021	We sought to develop an integrative model for the prediction of TMPG following MitraClip (MC) therapy.	Methylcholanthrene	90-92	CAP-Gly domain containing linker protein 1	Homo sapiens	79-88
33765348-2	2021	3MC is caused by biallelic pathogenic variants in MASP1, COLEC11, or COLEC10.	Methylcholanthrene	0-3	collectin-11	Meleagris gallopavo	57-64
33765348-2	2021	3MC is caused by biallelic pathogenic variants in MASP1, COLEC11, or COLEC10.	Methylcholanthrene	0-3	collectin-10	Meleagris gallopavo	69-76
33472828-13	2021	In contrast, inhibitory DREADDs led to a large increase in GC c-Fos, consistent with a reduction in MC excitation of GABAergic neurons, and reduced inhibition of GCs.	Methylcholanthrene	100-102	guanylate cyclase 2c	Mus musculus	59-63
33472828-13	2021	In contrast, inhibitory DREADDs led to a large increase in GC c-Fos, consistent with a reduction in MC excitation of GABAergic neurons, and reduced inhibition of GCs.	Methylcholanthrene	100-102	FBJ osteosarcoma oncogene	Mus musculus	64-67
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	tumor necrosis factor	Homo sapiens	106-137
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	transforming growth factor beta 1	Homo sapiens	139-143
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	cellular communication network factor 2	Homo sapiens	146-177
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	cellular communication network factor 2	Homo sapiens	179-183
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	insulin like growth factor 1	Homo sapiens	186-214
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	insulin like growth factor 1	Homo sapiens	216-220
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	tenascin C	Homo sapiens	223-233
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	tenascin C	Homo sapiens	235-238
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	fibronectin 1	Homo sapiens	241-252
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	fibronectin 1	Homo sapiens	254-257
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	scleraxis bHLH transcription factor	Homo sapiens	260-269
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	scleraxis bHLH transcription factor	Homo sapiens	271-274
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	fibromodulin	Homo sapiens	277-289
33475929-2	2021	We investigated if the application of MC at 10 muA/90 s could modulate the expression of remodeling genes transforming growth factor beta (Tgfb), connective tissue growth factor (Ctgf), insulin-like growth factor 1 (Igf1), tenascin C (Tnc), Fibronectin (Fn1), Scleraxis (Scx), Fibromodulin (Fmod) and tenomodulin in NIH/3T3 fibroblasts in a wound healing assay.	Methylcholanthrene	38-40	fibromodulin	Homo sapiens	291-295
33790107-4	2021	We showed that treatments with 3MC, BaP, and DMBA strongly suppressed mammosphere formation of the stem cells in an AHR-dependent manner, while other agonists showed weaker suppression.	Methylcholanthrene	31-34	aryl hydrocarbon receptor	Homo sapiens	116-119
33120142-4	2021	In this study, we found that TET1 expression was significantly down-regulated and the methylation level was significantly up-regulated in 3-methylcholanthrene (3-MCA) induced cell malignant transformation model, rat chemical carcinogenesis model, and human lung cancer tissues.	Methylcholanthrene	138-158	tet methylcytosine dioxygenase 1	Rattus norvegicus	29-33
33120142-4	2021	In this study, we found that TET1 expression was significantly down-regulated and the methylation level was significantly up-regulated in 3-methylcholanthrene (3-MCA) induced cell malignant transformation model, rat chemical carcinogenesis model, and human lung cancer tissues.	Methylcholanthrene	160-165	tet methylcytosine dioxygenase 1	Rattus norvegicus	29-33
33408298-5	2021	CYP3A5 mRNA expression was induced by the polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (3MC) and benzo[a]pyrene in HepG2 cells.	Methylcholanthrene	90-110	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	0-6
33176130-5	2021	Here, we show that the HOMEODOMAIN LEUCINE ZIPPER III (HD-ZIPIII) transcription factor PHABULOSA (PHB) is a master regulator of MC formation, controlling the accumulation of CYCD6;1 in the endodermis in a cell non-autonomous manner.	Methylcholanthrene	128-130	Homeobox-leucine zipper family protein / lipid-binding START domain-containing protein	Arabidopsis thaliana	87-96
33176130-5	2021	Here, we show that the HOMEODOMAIN LEUCINE ZIPPER III (HD-ZIPIII) transcription factor PHABULOSA (PHB) is a master regulator of MC formation, controlling the accumulation of CYCD6;1 in the endodermis in a cell non-autonomous manner.	Methylcholanthrene	128-130	Homeobox-leucine zipper family protein / lipid-binding START domain-containing protein	Arabidopsis thaliana	98-101
33176130-5	2021	Here, we show that the HOMEODOMAIN LEUCINE ZIPPER III (HD-ZIPIII) transcription factor PHABULOSA (PHB) is a master regulator of MC formation, controlling the accumulation of CYCD6;1 in the endodermis in a cell non-autonomous manner.	Methylcholanthrene	128-130	Cyclin D6;1	Arabidopsis thaliana	174-181
33408298-5	2021	CYP3A5 mRNA expression was induced by the polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (3MC) and benzo[a]pyrene in HepG2 cells.	Methylcholanthrene	112-115	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	0-6
33408298-9	2021	We found that CYP3A5 mRNA expression was induced by 3MC treatment in AhR rescue cells.	Methylcholanthrene	52-55	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	14-20
33408298-9	2021	We found that CYP3A5 mRNA expression was induced by 3MC treatment in AhR rescue cells.	Methylcholanthrene	52-55	aryl hydrocarbon receptor	Homo sapiens	69-72
32730838-6	2020	3-Methylcholanthrene (3-MC), benz[a]anthracene (B[a]A), benzo[a]pyrene (B[a]P), and valproic acid (VPA) increased the expression of CYP1B1 and CYP1A1.	Methylcholanthrene	0-20	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	132-138
32516650-4	2020	Combining MC and constant current (CC) operation for CA electrolysis resulted in a substantial reduction of the specific energy consumption from 256 to 52.4 kWh kg-1 TOC, due to improvement of the mineralization current efficiency from 17.9 to 77.1%.	Methylcholanthrene	10-12	rhomboid 5 homolog 2	Homo sapiens	166-169
32730838-6	2020	3-Methylcholanthrene (3-MC), benz[a]anthracene (B[a]A), benzo[a]pyrene (B[a]P), and valproic acid (VPA) increased the expression of CYP1B1 and CYP1A1.	Methylcholanthrene	0-20	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	143-149
32730838-7	2020	The potent aryl hydrocarbon receptor antagonist GNF351 significantly suppressed the 3-MC- and VPA-mediated upregulation of CYP1B1 and CYP1A1.	Methylcholanthrene	84-88	aryl hydrocarbon receptor	Homo sapiens	11-36
32730838-7	2020	The potent aryl hydrocarbon receptor antagonist GNF351 significantly suppressed the 3-MC- and VPA-mediated upregulation of CYP1B1 and CYP1A1.	Methylcholanthrene	84-88	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	123-129
32730838-7	2020	The potent aryl hydrocarbon receptor antagonist GNF351 significantly suppressed the 3-MC- and VPA-mediated upregulation of CYP1B1 and CYP1A1.	Methylcholanthrene	84-88	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	134-140
32730838-8	2020	In addition, VPA potentiated the induction of CYP1B1 and CYP1A1 by 3-MC, B[a]A, and B[a]P, although the augmentation of CYP1A1 was more remarkable than that of CYP1B1.	Methylcholanthrene	67-71	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	46-52
32730838-8	2020	In addition, VPA potentiated the induction of CYP1B1 and CYP1A1 by 3-MC, B[a]A, and B[a]P, although the augmentation of CYP1A1 was more remarkable than that of CYP1B1.	Methylcholanthrene	67-71	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	57-63
32730838-11	2020	Therefore, the effects of trichostatin A, a representative HDAC inhibitor, on CYP1 induction by 3-MC were examined.	Methylcholanthrene	96-100	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	78-82
32730838-12	2020	Trichostatin A enhanced the 3-MC-mediated upregulation of CYP1A1 but not CYP1B1.	Methylcholanthrene	28-32	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	58-64
32336047-3	2020	GCP-2 parent plasmid and MC containing GCP-2 were generated.	Methylcholanthrene	25-27	C-X-C motif chemokine ligand 6	Homo sapiens	39-44
32613892-6	2020	The better the environment context the weaker the association between BMI and MC (beta = -2.93, p < .01 to beta = -2.38, p = .33 to beta = 0.26, p = .94).Conclusions: The association between BMI and MC is moderated by environmental contexts.	Methylcholanthrene	78-80	ATPase H+ transporting V0 subunit a2	Homo sapiens	82-91
32613892-6	2020	The better the environment context the weaker the association between BMI and MC (beta = -2.93, p < .01 to beta = -2.38, p = .33 to beta = 0.26, p = .94).Conclusions: The association between BMI and MC is moderated by environmental contexts.	Methylcholanthrene	78-80	ATPase H+ transporting V0 subunit a2	Homo sapiens	107-116
32726451-8	2020	In WT mice, CYP1A1 and 1A2 expression was induced by MC.	Methylcholanthrene	53-55	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	12-26
32166993-2	2020	Metaphyseal chondromatosis with D-2-hydroxyglutaric aciduria (MC-HGA) is a type of D-2-HGA that has been previously reported in ten patients (OMIM 614875), three of whom had somatic mosaicism for R132 variants in isocitrate dehydrogenase 1 (IDH1).	Methylcholanthrene	62-64	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	213-239
32166993-2	2020	Metaphyseal chondromatosis with D-2-hydroxyglutaric aciduria (MC-HGA) is a type of D-2-HGA that has been previously reported in ten patients (OMIM 614875), three of whom had somatic mosaicism for R132 variants in isocitrate dehydrogenase 1 (IDH1).	Methylcholanthrene	62-64	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	241-245
32166993-3	2020	We describe a 3-year-old boy with MC-HGA who subsequently developed acute myeloid leukemia (AML) and was found to have an IDH1 R132C mutation in a leukemic bone marrow sample.	Methylcholanthrene	34-36	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	122-126
32694763-0	2020	Author Correction: Simvastatin reduces the carcinogenic effect of 3-methylcholanthrene in renal epithelial cells through histone deacetylase 1 inhibition and RhoA reactivation.	Methylcholanthrene	66-86	histone deacetylase 1	Homo sapiens	121-142
32694763-0	2020	Author Correction: Simvastatin reduces the carcinogenic effect of 3-methylcholanthrene in renal epithelial cells through histone deacetylase 1 inhibition and RhoA reactivation.	Methylcholanthrene	66-86	ras homolog family member A	Homo sapiens	158-162
32650472-5	2020	Moreover, MC reduced ROS-mediated phosphorylation of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun NH (2)-terminal kinase (JNK) that were also activated in PM exposed cells.	Methylcholanthrene	10-12	mitogen-activated protein kinase 3	Mus musculus	93-134
32650472-5	2020	Moreover, MC reduced ROS-mediated phosphorylation of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun NH (2)-terminal kinase (JNK) that were also activated in PM exposed cells.	Methylcholanthrene	10-12	mitogen-activated protein kinase 3	Mus musculus	136-142
32650472-5	2020	Moreover, MC reduced ROS-mediated phosphorylation of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun NH (2)-terminal kinase (JNK) that were also activated in PM exposed cells.	Methylcholanthrene	10-12	mitogen-activated protein kinase 8	Mus musculus	178-181
32650472-7	2020	These results provide a clear evidence for MC"s potential in attenuating PM-triggered inflammatory responses in MLE-12 cells via repressing TLR2/4/7 and MAPK signaling.	Methylcholanthrene	43-45	toll-like receptor 2	Mus musculus	140-148
32441374-2	2020	3MC is secondary to mutations in the MASP1, MASP3, COLEC11, and COLEC10 genes.	Methylcholanthrene	0-3	MBL associated serine protease 1	Homo sapiens	37-42
32441374-2	2020	3MC is secondary to mutations in the MASP1, MASP3, COLEC11, and COLEC10 genes.	Methylcholanthrene	0-3	MBL associated serine protease 1	Homo sapiens	44-49
32441374-2	2020	3MC is secondary to mutations in the MASP1, MASP3, COLEC11, and COLEC10 genes.	Methylcholanthrene	0-3	collectin subfamily member 11	Homo sapiens	51-58
32441374-2	2020	3MC is secondary to mutations in the MASP1, MASP3, COLEC11, and COLEC10 genes.	Methylcholanthrene	0-3	collectin subfamily member 10	Homo sapiens	64-71
32545838-1	2020	This research revealed the effect of carboxyl-functionalization on the mesoporous carbon (MC)-fixed glucose oxidase (GOx) for promoting the properties of bioelectrodes.	Methylcholanthrene	90-92	hydroxyacid oxidase 1	Homo sapiens	117-120
32438315-5	2020	The endogenous reduction of mc-COX2 can affect mitochondrial functions, suppress cell proliferation, and induce cell apoptosis.	Methylcholanthrene	28-30	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	31-35
32438315-8	2020	We also screened and tested several chemical compounds and small-molecule inhibitors that can decrease the generation of mc-COX2.	Methylcholanthrene	121-123	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	124-128
32438315-9	2020	It was found that the silencing of mc-COX2 in CLL cells strengthened the anti-tumor effects of drugs used in coordination.	Methylcholanthrene	35-37	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	38-42
32336047-4	2020	Human dermal fibroblasts (HDF) were transfected with MC containing GCP-2.	Methylcholanthrene	53-55	C-X-C motif chemokine ligand 6	Homo sapiens	67-72
32336047-10	2020	Taken together, these data suggest that MC-based GCP-2 overexpression could be a promising alternative strategy for promoting wound healing.	Methylcholanthrene	40-42	chemokine (C-X-C motif) ligand 5	Mus musculus	49-54
32670558-0	2020	An androgen-independent mechanism underlying the androgenic effects of 3-methylcholanthrene, a potent aryl hydrocarbon receptor agonist.	Methylcholanthrene	71-91	aryl hydrocarbon receptor	Homo sapiens	102-127
32224228-8	2020	Together, our data suggest that TRPM5-MC-dependent region-specific upregulation of cell proliferation in the majority of the MOE during chemical exposure contributes to the adaptive maintenance of OSNs and olfactory function.	Methylcholanthrene	38-40	transient receptor potential cation channel, subfamily M, member 5	Mus musculus	32-37
32670558-3	2020	To decipher this mechanism, we evaluated the effects of 3-methylcholanthrene (3MC), a potent AhR agonist, on the transcription of AR-regulated genes in three AR-expressing cell lines.	Methylcholanthrene	56-76	aryl hydrocarbon receptor	Homo sapiens	93-96
32670558-3	2020	To decipher this mechanism, we evaluated the effects of 3-methylcholanthrene (3MC), a potent AhR agonist, on the transcription of AR-regulated genes in three AR-expressing cell lines.	Methylcholanthrene	56-76	androgen receptor	Homo sapiens	130-132
32670558-3	2020	To decipher this mechanism, we evaluated the effects of 3-methylcholanthrene (3MC), a potent AhR agonist, on the transcription of AR-regulated genes in three AR-expressing cell lines.	Methylcholanthrene	56-76	androgen receptor	Homo sapiens	158-160
32670558-4	2020	3MC induced the expression of not only three representative AR-regulated chromosomal genes but also the exogenous AR-responsive luciferase reporter gene.	Methylcholanthrene	0-3	androgen receptor	Homo sapiens	60-62
32670558-4	2020	3MC induced the expression of not only three representative AR-regulated chromosomal genes but also the exogenous AR-responsive luciferase reporter gene.	Methylcholanthrene	0-3	androgen receptor	Homo sapiens	114-116
32670558-8	2020	Co-immunoprecipitation revealed that AhR and AR formed a complex in the nucleus of cells treated with 3MC.	Methylcholanthrene	102-105	aryl hydrocarbon receptor	Homo sapiens	37-40
32670558-8	2020	Co-immunoprecipitation revealed that AhR and AR formed a complex in the nucleus of cells treated with 3MC.	Methylcholanthrene	102-105	androgen receptor	Homo sapiens	45-47
31945720-4	2020	However, MC-NH2 (k2 = 0.042 g/mg/min) reacted faster with MC-LR than MC-H during early-stage adsorption due to enhancing electrostatic interactions.	Methylcholanthrene	9-15	pro-melanin concentrating hormone	Homo sapiens	69-73
31999965-12	2020	Thus, the redox- and pH- stimuli stepwise-responsive novel nanomicelles fabricated from the mPEG-SS-g-P(ae-Asp)-MCA-DA-TAT graft copolymer exhibited multifunctionality and displayed great potential for drug delivery.	Methylcholanthrene	112-115	tyrosine aminotransferase	Mus musculus	119-122
32239915-4	2020	Here we report the development of a tantalum oxide nanoparticle (NP)-based mass tag for MC immunoassays.	Methylcholanthrene	88-90	long intergenic non-protein coding RNA 1194	Homo sapiens	80-83
32139999-6	2020	Results: Significantly more patients with Scheuermann"s disease had at least one MC compared to the controls at the level L1/L2 (Odds Ratio [OR] 21.11, 95% Confidence Interval [95% CI] 2.31-192.96), at the level L3/L4 (OR 13.62, 95% CI 1.41-131.26), and at the level L5/S1 (OR 6.11, 95% CI 1.50-24.83).	Methylcholanthrene	81-83	L1 cell adhesion molecule	Homo sapiens	122-127
30608348-9	2020	The standard MC image (84.0%), green-blue-enhanced image (84.0%), IR (78.7%), and GR (80%) delineated the boundaries of SRF more effectively than CFP (44%).	Methylcholanthrene	13-15	serum response factor	Homo sapiens	120-123
30608348-14	2020	CONCLUSION: As an adjunct to SD-OCT, the MC image can delineate the extent or boundaries of SRF more effectively than CFP.	Methylcholanthrene	41-43	serum response factor	Homo sapiens	92-95
31041718-8	2020	The cumulative overall survival rates in patients with MIM without MVI (potential MC) was significantly better than that in patients with both MIM and MVI (P = 0.022).	Methylcholanthrene	82-84	MTSS I-BAR domain containing 1	Homo sapiens	55-58
31776611-9	2020	However, both 3-MC and TCDD potently induced CYP1A1 gene expression and modestly increased CYP1A1 enzyme activity in human islets after 48 h. The induction of CYP1A1 in human islets by TCDD was prevented by cotreatment with a cytokine mixture.	Methylcholanthrene	14-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	45-51
32166665-4	2020	The results showed that the levels of NQO1, gamma-GCS and Nrf2 were significantly increased in the MC group and the RSG group as compared with those in the NC group (P<0.01).	Methylcholanthrene	99-101	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	38-42
32166665-4	2020	The results showed that the levels of NQO1, gamma-GCS and Nrf2 were significantly increased in the MC group and the RSG group as compared with those in the NC group (P<0.01).	Methylcholanthrene	99-101	NFE2 like bZIP transcription factor 2	Rattus norvegicus	58-62
31776611-9	2020	However, both 3-MC and TCDD potently induced CYP1A1 gene expression and modestly increased CYP1A1 enzyme activity in human islets after 48 h. The induction of CYP1A1 in human islets by TCDD was prevented by cotreatment with a cytokine mixture.	Methylcholanthrene	14-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	91-97
31776611-9	2020	However, both 3-MC and TCDD potently induced CYP1A1 gene expression and modestly increased CYP1A1 enzyme activity in human islets after 48 h. The induction of CYP1A1 in human islets by TCDD was prevented by cotreatment with a cytokine mixture.	Methylcholanthrene	14-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	91-97
31888209-2	2019	Here, we report on the biological activity of a dual-KDM inhibitor (MC3324), obtained by coupling the chemical properties of tranylcypromine, a known LSD1 inhibitor, with the 2OG competitive moiety developed for JmjC inhibition.	Methylcholanthrene	68-74	lysine (K)-specific demethylase 1A	Mus musculus	150-154
31722089-7	2020	By contrast, when BH4 or BH5 was co-cultured with previously established bovine liver sinusoidal cell lines and treated with 3-MC, the gene expression levels of CYP1A1, CYP1A2, and CYP1B1 increased by 38~290%, compared with those in BH4 or BH5 cells cultured alone.	Methylcholanthrene	125-129	cytochrome P450 1A1	Bos taurus	161-167
31722089-7	2020	By contrast, when BH4 or BH5 was co-cultured with previously established bovine liver sinusoidal cell lines and treated with 3-MC, the gene expression levels of CYP1A1, CYP1A2, and CYP1B1 increased by 38~290%, compared with those in BH4 or BH5 cells cultured alone.	Methylcholanthrene	125-129	cytochrome P450 1B1	Bos taurus	181-187
32223493-8	2020	Furthermore, osteophyte size in the MC was negatively correlated with the inflammatory markers C-reactive protein (r = -0.492, p = 0.0027) and erythrocyte sedimentation rate (r = -0.529, p = 0.0016), whereas that in the LC was negatively correlated with disease activity (r = -0.589, p = 0.0023).	Methylcholanthrene	36-38	C-reactive protein	Homo sapiens	95-113
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	21-41	cytochrome P450 1A1	Bos taurus	81-105
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	21-41	cytochrome P450 1A2	Bos taurus	107-113
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	21-41	cytochrome P450 1B1	Bos taurus	119-125
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	43-47	cytochrome P450 1A1	Bos taurus	81-105
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	43-47	cytochrome P450 1A2	Bos taurus	107-113
31722089-5	2020	A potent carcinogen, 3-methylcholanthrene (3-MC), upregulated gene expression of cytochrome P450 (CYP)1A1, CYP1A2, and CYP1B1 in BH4 and BH5, but only to levels less than one-fifteenth of those in primary cultured bovine hepatocytes.	Methylcholanthrene	43-47	cytochrome P450 1B1	Bos taurus	119-125
31888209-4	2019	Inhibiting LSD1 and UTX, MC3324 induces significant growth arrest and apoptosis in hormone-responsive breast cancer model accompanied by a robust increase in H3K4me2 and H3K27me3.	Methylcholanthrene	25-31	lysine (K)-specific demethylase 1A	Mus musculus	11-15
31888209-4	2019	Inhibiting LSD1 and UTX, MC3324 induces significant growth arrest and apoptosis in hormone-responsive breast cancer model accompanied by a robust increase in H3K4me2 and H3K27me3.	Methylcholanthrene	25-31	lysine (K)-specific demethylase 6A	Mus musculus	20-23
31888209-5	2019	MC3324 down-regulates ERalpha in breast cancer at both transcriptional and non-transcriptional levels, mimicking the action of a selective endocrine receptor disruptor.	Methylcholanthrene	0-6	estrogen receptor 1 (alpha)	Mus musculus	22-29
31888209-6	2019	MC3324 alters the histone methylation of ERalpha-regulated promoters, thereby affecting the transcription of genes involved in cell surveillance, hormone response, and death.	Methylcholanthrene	0-6	estrogen receptor 1 (alpha)	Mus musculus	41-48
31757214-10	2019	However, SULT2B1 deletion or SULT2B1 knockdown suppressed PI3K/AKT signaling, epithelial cell epithelization, and wound healing and induced gastric epithelial cell malignant transition upon 3-MCA induction.	Methylcholanthrene	190-195	sulfotransferase family, cytosolic, 2B, member 1	Mus musculus	9-16
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	interleukin 6	Homo sapiens	159-172
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	interleukin 6	Homo sapiens	174-178
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	C-C motif chemokine ligand 2	Homo sapiens	181-215
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	C-C motif chemokine ligand 2	Homo sapiens	217-222
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	tumor necrosis factor	Homo sapiens	225-256
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	transforming growth factor alpha	Homo sapiens	258-266
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	vascular cell adhesion molecule 1	Homo sapiens	269-302
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	vascular cell adhesion molecule 1	Homo sapiens	304-310
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	vascular endothelial growth factor A	Homo sapiens	316-350
32203941-5	2019	Exposure of MC to the studied dialysates caused intracellular oxidative stress and significantly increased expression of the genes regulating the synthesis of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), vascular cell adhesion molecule 1 (VCAM-1) and vascular endothelial growth factor (VEGF).	Methylcholanthrene	12-14	vascular endothelial growth factor A	Homo sapiens	352-356
32203941-6	2019	Secretion of the studied molecules from MC treated with dialysates was increased: by 96% for IL-6 (P < 0.01), 34% for MCP-1(P < 0.01), 24% for TGF-beta (P < 0.01), 27% for VCAM-1 (P < 0.01), and by 15% for VEGF (P < 0.01).	Methylcholanthrene	40-42	interleukin 6	Homo sapiens	93-97
32203941-6	2019	Secretion of the studied molecules from MC treated with dialysates was increased: by 96% for IL-6 (P < 0.01), 34% for MCP-1(P < 0.01), 24% for TGF-beta (P < 0.01), 27% for VCAM-1 (P < 0.01), and by 15% for VEGF (P < 0.01).	Methylcholanthrene	40-42	C-C motif chemokine ligand 2	Homo sapiens	118-123
32203941-6	2019	Secretion of the studied molecules from MC treated with dialysates was increased: by 96% for IL-6 (P < 0.01), 34% for MCP-1(P < 0.01), 24% for TGF-beta (P < 0.01), 27% for VCAM-1 (P < 0.01), and by 15% for VEGF (P < 0.01).	Methylcholanthrene	40-42	transforming growth factor alpha	Homo sapiens	143-151
32203941-6	2019	Secretion of the studied molecules from MC treated with dialysates was increased: by 96% for IL-6 (P < 0.01), 34% for MCP-1(P < 0.01), 24% for TGF-beta (P < 0.01), 27% for VCAM-1 (P < 0.01), and by 15% for VEGF (P < 0.01).	Methylcholanthrene	40-42	vascular cell adhesion molecule 1	Homo sapiens	172-178
32203941-6	2019	Secretion of the studied molecules from MC treated with dialysates was increased: by 96% for IL-6 (P < 0.01), 34% for MCP-1(P < 0.01), 24% for TGF-beta (P < 0.01), 27% for VCAM-1 (P < 0.01), and by 15% for VEGF (P < 0.01).	Methylcholanthrene	40-42	vascular endothelial growth factor A	Homo sapiens	206-210
31619002-6	2019	We not only demonstrated that AA pre-exposure MCA stimulus tumorigenic cells have more behaviors of cell migration and invasion by enhancing the metalloproteinases (MMP) activity, which is compatible with clinical findings of AA-related UTUC, but we also validated that AA pre-exposure MCA stimulus tumorigeniccells could be activated through the mitogen-activated protein kinases (MAPK) pathway.	Methylcholanthrene	46-49	mitogen-activated protein kinase 1	Homo sapiens	382-386
31266358-5	2019	We verified the substantial production of the anti-CD25/IL-10 protein from the MC in vitro and in vivo.	Methylcholanthrene	79-81	interleukin 2 receptor, alpha chain	Mus musculus	51-55
31411880-6	2019	For this target, we propose a scheme called ABC2 to automatically select an active space for MC-PDFT calculations and MS-CASPT2 calculations; the scheme uses high-spin-state unrestricted Hartree-Fock (UHF) natural orbitals as guess orbitals.	Methylcholanthrene	93-95	ATP binding cassette subfamily A member 2	Homo sapiens	44-48
31326865-10	2019	The MC component was positive for synaptophysin in 6, CK5/6 in 4, and beta-catenin in 3 cases.	Methylcholanthrene	4-6	synaptophysin	Homo sapiens	34-47
31326865-10	2019	The MC component was positive for synaptophysin in 6, CK5/6 in 4, and beta-catenin in 3 cases.	Methylcholanthrene	4-6	keratin 5	Homo sapiens	54-59
31326865-10	2019	The MC component was positive for synaptophysin in 6, CK5/6 in 4, and beta-catenin in 3 cases.	Methylcholanthrene	4-6	catenin beta 1	Homo sapiens	70-82
31326865-15	2019	Frequent co-expression of CK5/6 and beta-catenin in MC combined with common co-existence of squamous morule in the same polyp suggests shared pathogenesis of MC in CIAM and squamous morule, likely representing altered Wnt/beta-catenin signaling pathway.	Methylcholanthrene	52-54	keratin 5	Homo sapiens	26-31
31326865-15	2019	Frequent co-expression of CK5/6 and beta-catenin in MC combined with common co-existence of squamous morule in the same polyp suggests shared pathogenesis of MC in CIAM and squamous morule, likely representing altered Wnt/beta-catenin signaling pathway.	Methylcholanthrene	52-54	catenin beta 1	Homo sapiens	36-48
31326865-15	2019	Frequent co-expression of CK5/6 and beta-catenin in MC combined with common co-existence of squamous morule in the same polyp suggests shared pathogenesis of MC in CIAM and squamous morule, likely representing altered Wnt/beta-catenin signaling pathway.	Methylcholanthrene	158-160	keratin 5	Homo sapiens	26-31
31400563-8	2019	In response to a 10-ppb increase in NO2 exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively.	Methylcholanthrene	72-74	nitric oxide synthase 2	Homo sapiens	50-55
31266358-5	2019	We verified the substantial production of the anti-CD25/IL-10 protein from the MC in vitro and in vivo.	Methylcholanthrene	79-81	interleukin 10	Mus musculus	56-61
31266358-6	2019	The therapeutic effect of MC-derived anti-CD25/IL-10 was evaluated in a skin allograft mouse model by single intravenous infusion.	Methylcholanthrene	26-28	interleukin 2 receptor, alpha chain	Mus musculus	42-46
31266358-6	2019	The therapeutic effect of MC-derived anti-CD25/IL-10 was evaluated in a skin allograft mouse model by single intravenous infusion.	Methylcholanthrene	26-28	interleukin 10	Mus musculus	47-52
31266358-7	2019	Mice treated with the MC encoding anti-CD25/IL-10 exhibited prolonged skin allograft survival times accompanied by improved histologic changes and immunologic regulation.	Methylcholanthrene	22-24	interleukin 2 receptor, alpha chain	Mus musculus	39-43
31266358-7	2019	Mice treated with the MC encoding anti-CD25/IL-10 exhibited prolonged skin allograft survival times accompanied by improved histologic changes and immunologic regulation.	Methylcholanthrene	22-24	interleukin 10	Mus musculus	44-49
31266358-8	2019	These findings indicate that the anti-CD25/IL-10 protein drug obtained by MC technology is functionally active and relevant for reducing allograft rejection.	Methylcholanthrene	74-76	interleukin 2 receptor, alpha chain	Mus musculus	38-42
31266358-8	2019	These findings indicate that the anti-CD25/IL-10 protein drug obtained by MC technology is functionally active and relevant for reducing allograft rejection.	Methylcholanthrene	74-76	interleukin 10	Mus musculus	43-48
31400926-10	2019	KRAS mutation was significantly less prevalent in SRC/SRCC compared to the number of KRAS mutations in MC (12/17, 70.6%) and CON (9/12, 75.0%) (p = 0.015 and 0.01, respectively).	Methylcholanthrene	103-105	KRAS proto-oncogene, GTPase	Homo sapiens	85-89
31358547-7	2019	In the mouse epidermis, inducible expression of the Artn gene by the AhR agonist 3-methylcholanthrene was substantially suppressed compared with that in wild-type mice.	Methylcholanthrene	81-101	artemin	Mus musculus	52-56
31232479-6	2019	The differences of values between MC and LC and between MC and GSC were significantly positive (higher values for MC compared to LC and GSC) for total motility, progressive, rapid movement, VCL, VSL, VAP, STR and hyperactive, thus indicating a systematic effect.	Methylcholanthrene	34-36	vinculin	Homo sapiens	190-193
31232479-6	2019	The differences of values between MC and LC and between MC and GSC were significantly positive (higher values for MC compared to LC and GSC) for total motility, progressive, rapid movement, VCL, VSL, VAP, STR and hyperactive, thus indicating a systematic effect.	Methylcholanthrene	56-58	vinculin	Homo sapiens	190-193
31232479-6	2019	The differences of values between MC and LC and between MC and GSC were significantly positive (higher values for MC compared to LC and GSC) for total motility, progressive, rapid movement, VCL, VSL, VAP, STR and hyperactive, thus indicating a systematic effect.	Methylcholanthrene	56-58	vinculin	Homo sapiens	190-193
31358547-7	2019	In the mouse epidermis, inducible expression of the Artn gene by the AhR agonist 3-methylcholanthrene was substantially suppressed compared with that in wild-type mice.	Methylcholanthrene	81-101	aryl-hydrocarbon receptor	Mus musculus	69-72
31091122-6	2019	MC sheets and HGF-tg MC sheets produced HGF protein and significantly improved acute renal dysfunction, acute tubular necrosis, and survival rate.	Methylcholanthrene	0-2	hepatocyte growth factor	Homo sapiens	40-43
31511218-7	2019	Compared with those in MC group, the expressions of beta-tubulin III, MAP2 and GFAP protein in NLXT group and Y-27632 group were significantly increased on days 3 (P &amp;lt; 0.01) and 7 (P &amp;lt; 0.05).	Methylcholanthrene	23-25	glial fibrillary acidic protein	Mus musculus	79-83
31474836-7	2019	Opn3 and Opn5 were found to be expressed in primary MC cultures prepared at E8 and kept for 2 weeks.	Methylcholanthrene	52-54	opsin 3	Gallus gallus	0-4
31474836-7	2019	Opn3 and Opn5 were found to be expressed in primary MC cultures prepared at E8 and kept for 2 weeks.	Methylcholanthrene	52-54	opsin 5	Gallus gallus	9-13
30816327-4	2019	Robust activity of MC-enhanced CAR-T cells was associated with cachexia in animal models that corresponded with high levels of human cytokine production.	Methylcholanthrene	19-21	nuclear receptor subfamily 1 group I member 3	Homo sapiens	31-34
31091122-6	2019	MC sheets and HGF-tg MC sheets produced HGF protein and significantly improved acute renal dysfunction, acute tubular necrosis, and survival rate.	Methylcholanthrene	21-23	hepatocyte growth factor	Homo sapiens	14-17
31091122-6	2019	MC sheets and HGF-tg MC sheets produced HGF protein and significantly improved acute renal dysfunction, acute tubular necrosis, and survival rate.	Methylcholanthrene	21-23	hepatocyte growth factor	Homo sapiens	40-43
31091122-8	2019	Expression of alpha-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets.	Methylcholanthrene	122-124	hepatocyte growth factor	Homo sapiens	249-252
31091122-8	2019	Expression of alpha-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets.	Methylcholanthrene	142-144	hepatocyte growth factor	Homo sapiens	135-138
31091122-8	2019	Expression of alpha-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets.	Methylcholanthrene	142-144	hepatocyte growth factor	Homo sapiens	249-252
31091122-8	2019	Expression of alpha-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets.	Methylcholanthrene	142-144	hepatocyte growth factor	Homo sapiens	135-138
31091122-8	2019	Expression of alpha-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets.	Methylcholanthrene	142-144	hepatocyte growth factor	Homo sapiens	249-252
31366523-1	2019	BACKGROUND/AIM: This study aimed to obtain accurate differential diagnosis (DDx) of multicentric carcinogenesis (MC) and intrahepatic metastasis (IM) in recurrent lesions of hepatocellular carcinoma.	Methylcholanthrene	113-115	aldo-keto reductase family 1 member C3	Homo sapiens	76-79
31218841-8	2019	The results showed that MC using low-dose VP-16 alone demonstrated strong treatment effects in terms of inducing apoptosis, cell senescence, and reducing tumor cell proliferation, and this treatment also led to changes of the cell cycle.	Methylcholanthrene	24-26	host cell factor C1	Homo sapiens	42-47
31370872-0	2019	AHR and GPER mediate the stimulatory effects induced by 3-methylcholanthrene in breast cancer cells and cancer-associated fibroblasts (CAFs).	Methylcholanthrene	56-76	aryl hydrocarbon receptor	Homo sapiens	0-3
31370872-0	2019	AHR and GPER mediate the stimulatory effects induced by 3-methylcholanthrene in breast cancer cells and cancer-associated fibroblasts (CAFs).	Methylcholanthrene	56-76	G protein-coupled estrogen receptor 1	Homo sapiens	8-12
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	36-56	aryl hydrocarbon receptor	Homo sapiens	76-101
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	36-56	aryl hydrocarbon receptor	Homo sapiens	103-106
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	36-56	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	174-180
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	58-61	aryl hydrocarbon receptor	Homo sapiens	76-101
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	58-61	aryl hydrocarbon receptor	Homo sapiens	103-106
31370872-1	2019	BACKGROUND: The chemical carcinogen 3-methylcholanthrene (3MC) binds to the aryl hydrocarbon receptor (AHR) that regulates the expression of cytochrome P450 (CYP) enzymes as CYP1B1, which is involved in the oncogenic activation of environmental pollutants as well as in the estrogen biosynthesis and metabolism.	Methylcholanthrene	58-61	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	174-180
31370872-2	2019	3MC was shown to induce estrogenic responses binding to the estrogen receptor (ER) alpha and stimulating a functional interaction between AHR and ERalpha.	Methylcholanthrene	0-3	estrogen receptor 1	Homo sapiens	60-88
31370872-2	2019	3MC was shown to induce estrogenic responses binding to the estrogen receptor (ER) alpha and stimulating a functional interaction between AHR and ERalpha.	Methylcholanthrene	0-3	aryl hydrocarbon receptor	Homo sapiens	138-141
31370872-2	2019	3MC was shown to induce estrogenic responses binding to the estrogen receptor (ER) alpha and stimulating a functional interaction between AHR and ERalpha.	Methylcholanthrene	0-3	estrogen receptor 1	Homo sapiens	146-153
31370872-11	2019	RESULTS: We first ascertained by docking simulations the ability of 3MC to interact with GPER.	Methylcholanthrene	68-71	G protein-coupled estrogen receptor 1	Homo sapiens	89-93
31370872-12	2019	Thereafter, we established that 3MC activates the EGFR/ERK/c-Fos transduction signaling through both AHR and GPER in SkBr3 cells and CAFs.	Methylcholanthrene	32-35	epidermal growth factor receptor	Homo sapiens	50-54
31370872-12	2019	Thereafter, we established that 3MC activates the EGFR/ERK/c-Fos transduction signaling through both AHR and GPER in SkBr3 cells and CAFs.	Methylcholanthrene	32-35	mitogen-activated protein kinase 1	Homo sapiens	55-58
31370872-12	2019	Thereafter, we established that 3MC activates the EGFR/ERK/c-Fos transduction signaling through both AHR and GPER in SkBr3 cells and CAFs.	Methylcholanthrene	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-64
31370872-12	2019	Thereafter, we established that 3MC activates the EGFR/ERK/c-Fos transduction signaling through both AHR and GPER in SkBr3 cells and CAFs.	Methylcholanthrene	32-35	aryl hydrocarbon receptor	Homo sapiens	101-104
31370872-12	2019	Thereafter, we established that 3MC activates the EGFR/ERK/c-Fos transduction signaling through both AHR and GPER in SkBr3 cells and CAFs.	Methylcholanthrene	32-35	G protein-coupled estrogen receptor 1	Homo sapiens	109-113
31370872-14	2019	CONCLUSIONS: In the present study we have provided novel insights regarding the molecular mechanisms by which 3MC may trigger a physical and functional interaction between AHR and GPER, leading to the stimulation of both SkBr3 breast cancer cells and CAFs.	Methylcholanthrene	110-113	aryl hydrocarbon receptor	Homo sapiens	172-175
31370872-14	2019	CONCLUSIONS: In the present study we have provided novel insights regarding the molecular mechanisms by which 3MC may trigger a physical and functional interaction between AHR and GPER, leading to the stimulation of both SkBr3 breast cancer cells and CAFs.	Methylcholanthrene	110-113	G protein-coupled estrogen receptor 1	Homo sapiens	180-184
31370872-15	2019	Altogether, our results indicate that 3MC may engage both GPER and AHR transduction pathways toward breast cancer progression.	Methylcholanthrene	38-41	G protein-coupled estrogen receptor 1	Homo sapiens	58-62
31370872-15	2019	Altogether, our results indicate that 3MC may engage both GPER and AHR transduction pathways toward breast cancer progression.	Methylcholanthrene	38-41	aryl hydrocarbon receptor	Homo sapiens	67-70
31228946-8	2019	Although IFNAR1-KO mice exhibited increased susceptibility to methylcholanthrene-induced sarcoma, IFNAR1-sufficient tumors also grow significantly faster in IFNAR1-KO mice and in mice with IFNAR1 deficiency only in T cells (IFNAR1-TKO), suggesting that IFN-I functions in T cells to enhance host cancer immunosurveillance.	Methylcholanthrene	62-80	interferon (alpha and beta) receptor 1	Mus musculus	9-15
30808802-9	2019	RESULTS: A locus associated with MC (p&lt;5e-8) was found on chromosome 9 with the lead SNP rs1934268 in an intron of the PTPRD gene.	Methylcholanthrene	33-35	protein tyrosine phosphatase receptor type D	Homo sapiens	122-127
30808802-13	2019	CONCLUSION: PTPRD is a novel candidate gene for MC that may act via the development of cartilage or nervous system; further work is needed to define the mechanisms underlying the pathways leading to development of MC.	Methylcholanthrene	48-50	protein tyrosine phosphatase receptor type D	Homo sapiens	12-17
30808802-13	2019	CONCLUSION: PTPRD is a novel candidate gene for MC that may act via the development of cartilage or nervous system; further work is needed to define the mechanisms underlying the pathways leading to development of MC.	Methylcholanthrene	214-216	protein tyrosine phosphatase receptor type D	Homo sapiens	12-17
31004879-7	2019	Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P &lt; 0.05).	Methylcholanthrene	123-125	tet methylcytosine dioxygenase 1	Mus musculus	33-37
31004879-7	2019	Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P &lt; 0.05).	Methylcholanthrene	123-125	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	182-186
31004879-7	2019	Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P &lt; 0.05).	Methylcholanthrene	123-125	tet methylcytosine dioxygenase 2	Mus musculus	252-256
31004879-7	2019	Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P &lt; 0.05).	Methylcholanthrene	123-125	tet methylcytosine dioxygenase 3	Mus musculus	261-265
30871803-2	2019	We sought to elucidate the outcomes of MitraClip (MC) implantation in patients with symptomatic ischaemic FMR after CABG.	Methylcholanthrene	50-52	CAP-Gly domain containing linker protein 1	Homo sapiens	39-48
31064775-9	2019	Increased proliferation of osteoblasts in the mandible and chondrocytes forming MC was identified in Fgfr2+/S252W embryos at E12.5.	Methylcholanthrene	80-82	fibroblast growth factor receptor 2	Mus musculus	101-106
31062408-4	2019	Plasma and ear IL-23 levels were dose-dependently (0.3-3 mug) increased in MC injected mice and were sustained over the 14-day study duration.	Methylcholanthrene	75-77	interleukin 23, alpha subunit p19	Mus musculus	15-20
31083300-0	2019	3-Methylcholanthrene Induces Chylous Ascites in TCDD-Inducible Poly-ADP-Ribose Polymerase (Tiparp) Knockout Mice.	Methylcholanthrene	0-20	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	48-89
31236413-10	2019	Conclusion: Prophylactic MC by a vaginal approach during mini-TLH is safe, satisfactory, and efficient for apical support without severe morbidity.	Methylcholanthrene	25-27	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	62-65
30624620-7	2019	Treatment of XPC-/- mice with the carcinogen 3-methylcholanthrene followed by the proliferative agent butylated hydroxytoluene resulted in a 2-fold increase in lung adenocarcinoma development.	Methylcholanthrene	45-65	xeroderma pigmentosum, complementation group C	Mus musculus	13-16
30997802-2	2019	The dissolution flux of solid explosives following corrosion of metal munition housings controls the exposure of biological receptors to toxic munition compounds (MC), including TNT: 2,4,6-trinitrotoluene, RDX: 1,3,5-trinitro-1,3,5-triazinane, and DNB: 1,3-dinitrobenzene.	Methylcholanthrene	163-165	chromosome 16 open reading frame 82	Homo sapiens	178-181
30997802-7	2019	In situ dissolution fluxes estimated in the current study were lower than most dissolution rates reported for laboratory experiments, but they clearly demonstrated that MC are released from underwater munitions to the water column in the Baltic Sea.	Methylcholanthrene	169-171	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	245-248
31083300-0	2019	3-Methylcholanthrene Induces Chylous Ascites in TCDD-Inducible Poly-ADP-Ribose Polymerase (Tiparp) Knockout Mice.	Methylcholanthrene	0-20	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	91-97
31083300-4	2019	In this study, we treated male Tiparp-/- or wild type (WT) mice with a single injection of 100 mg/kg 3-methylcholanthrene (3MC).	Methylcholanthrene	101-121	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	31-37
31083300-5	2019	Consistent with TIPARP"s role as a repressor of AHR signaling, 3MC-treated Tiparp-/- mice exhibited increased hepatic Cyp1a1 and Cyp1b1 levels compared with WT mice.	Methylcholanthrene	63-66	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	16-22
31083300-5	2019	Consistent with TIPARP"s role as a repressor of AHR signaling, 3MC-treated Tiparp-/- mice exhibited increased hepatic Cyp1a1 and Cyp1b1 levels compared with WT mice.	Methylcholanthrene	63-66	aryl-hydrocarbon receptor	Mus musculus	48-51
31083300-5	2019	Consistent with TIPARP"s role as a repressor of AHR signaling, 3MC-treated Tiparp-/- mice exhibited increased hepatic Cyp1a1 and Cyp1b1 levels compared with WT mice.	Methylcholanthrene	63-66	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	75-81
31083300-5	2019	Consistent with TIPARP"s role as a repressor of AHR signaling, 3MC-treated Tiparp-/- mice exhibited increased hepatic Cyp1a1 and Cyp1b1 levels compared with WT mice.	Methylcholanthrene	63-66	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	118-124
31083300-5	2019	Consistent with TIPARP"s role as a repressor of AHR signaling, 3MC-treated Tiparp-/- mice exhibited increased hepatic Cyp1a1 and Cyp1b1 levels compared with WT mice.	Methylcholanthrene	63-66	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	129-135
31083300-11	2019	Our study reveals that Tiparp-/- mice have increased sensitivity to 3MC-induced liver toxicity, but unlike with TCDD, lethality is due to chylous ascites rather than wasting syndrome.	Methylcholanthrene	68-71	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	23-29
29753019-5	2019	Comparisons of MC"s structural magnetic resonance imaging (MRI) data to a probabilistic atlas based on controls reveals that MC"s lesions encompass the posterior, lateral, and ventral early visual cortex bilaterally (V1, V2, V3A/B, LO1/2, TO1/2, hV4 and VO1 in both hemispheres) as well as more extensive damage to right parietal (inferior parietal lobule) and left ventral occipitotemporal cortex (VO1, PHC1/2).	Methylcholanthrene	125-127	polyhomeotic homolog 1	Homo sapiens	404-408
30898771-3	2019	MC stimulates rapid pumping through the nicotinic ACh receptor EAT-2, which is tightly localized at the MC NMJ, and eat-2 mutants exhibit a slow pump rate.	Methylcholanthrene	0-2	Neuronal acetylcholine receptor subunit eat-2	Caenorhabditis elegans	63-68
30449009-6	2019	The MC of serum amyloid A was also sig-d in G-E at 0 h PV, weeks 1, 2 and 4 PV (3, 8, 5 and 8 FI respectively).	Methylcholanthrene	4-6	serum amyloid A protein	Bos taurus	10-25
30449009-8	2019	The IgM MC was sig-d in G-B and C at 3 h PV (5 and 6 FI respectively), at 24 h PV (5 and 9 FI respectively), at week 3 PV(2 and 2 FI respectively) and week 4 PV (3 and 4 FI respectively).	Methylcholanthrene	8-10	IgM	Bos taurus	4-7
30852652-4	2019	Therefore, we performed a genome-wide association study (GWAS) of MC in the 1000 Genomes/ GEUVADIS data (n = 457) and identified a solitary genome-wide significant association with single nucleotide polymorphisms (SNPs) in the intronic region of the cadherin 18 (CDH18) gene on chromosome 5 (lead SNP: rs11744487, p = 1.2 x 10- 8).	Methylcholanthrene	66-68	cadherin 18	Homo sapiens	250-261
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	131-134
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	glutamic pyruvic transaminase, soluble	Mus musculus	136-139
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	alopecia, recessive	Mus musculus	150-153
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	interleukin 1 beta	Mus musculus	160-168
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	interleukin 6	Mus musculus	170-174
31178949-6	2019	The results revealed that MC elicited hepatotoxicity and neurotoxicity which was evident due to the significant elevation of serum AST, ALT, gammaGT, ALP, LDH, IL-1beta, IL-6, and TNF-alpha levels.	Methylcholanthrene	26-28	tumor necrosis factor	Mus musculus	180-189
31178949-7	2019	Furthermore, MC markedly increased MDA and NO contents along with reduction of GSH, SOD, CAT, and GSH-Px in liver and brain tissues.	Methylcholanthrene	13-15	catalase	Mus musculus	89-92
30779979-2	2019	The present study sought to fabricate alginate/chitosan microcapsules containing IL-1Ra (Alg/Chi/IL-1Ra MC) via a single-step electrospraying method.	Methylcholanthrene	104-106	interleukin 1 receptor antagonist	Mus musculus	81-87
30779979-2	2019	The present study sought to fabricate alginate/chitosan microcapsules containing IL-1Ra (Alg/Chi/IL-1Ra MC) via a single-step electrospraying method.	Methylcholanthrene	104-106	interleukin 1 receptor antagonist	Mus musculus	97-103
30852652-4	2019	Therefore, we performed a genome-wide association study (GWAS) of MC in the 1000 Genomes/ GEUVADIS data (n = 457) and identified a solitary genome-wide significant association with single nucleotide polymorphisms (SNPs) in the intronic region of the cadherin 18 (CDH18) gene on chromosome 5 (lead SNP: rs11744487, p = 1.2 x 10- 8).	Methylcholanthrene	66-68	cadherin 18	Homo sapiens	263-268
30900111-6	2019	RESULTS: Prior MC was significantly associated with lower hippocampal subfield volumes in MC patients for right and left CA-2/3 (beta = -22.32 [-40.18, -4.45]; p = 0.016 and beta = -20.03 [-39.38, -0.68]; p = 0.043) and right CA-4 (beta = -17.00 [-33.86, 0.12]; p = 0.048).	Methylcholanthrene	15-17	carbonic anhydrase 2	Homo sapiens	121-125
30900111-6	2019	RESULTS: Prior MC was significantly associated with lower hippocampal subfield volumes in MC patients for right and left CA-2/3 (beta = -22.32 [-40.18, -4.45]; p = 0.016 and beta = -20.03 [-39.38, -0.68]; p = 0.043) and right CA-4 (beta = -17.00 [-33.86, 0.12]; p = 0.048).	Methylcholanthrene	15-17	carbonic anhydrase 4	Homo sapiens	226-230
30900111-11	2019	This could indicate specific atrophy of CA-2/3 after MC and should motivate hippocampal subfield assessment in larger cohorts.	Methylcholanthrene	53-55	carbonic anhydrase 2	Homo sapiens	40-44
30900111-6	2019	RESULTS: Prior MC was significantly associated with lower hippocampal subfield volumes in MC patients for right and left CA-2/3 (beta = -22.32 [-40.18, -4.45]; p = 0.016 and beta = -20.03 [-39.38, -0.68]; p = 0.043) and right CA-4 (beta = -17.00 [-33.86, 0.12]; p = 0.048).	Methylcholanthrene	90-92	carbonic anhydrase 2	Homo sapiens	121-125
30872677-0	2019	Simvastatin reduces the carcinogenic effect of 3-methylcholanthrene in renal epithelial cells through histone deacetylase 1 inhibition and RhoA reactivation.	Methylcholanthrene	47-67	histone deacetylase 1	Homo sapiens	102-123
30872677-0	2019	Simvastatin reduces the carcinogenic effect of 3-methylcholanthrene in renal epithelial cells through histone deacetylase 1 inhibition and RhoA reactivation.	Methylcholanthrene	47-67	ras homolog family member A	Homo sapiens	139-143
30872677-2	2019	In this study, the effects of simvastatin on the carcinogenic properties of 3-methylcholanthrene (3MC; an aryl-hydrocarbon receptor [AhR] agonist) in human renal epithelial cells (hRECs) were investigated.	Methylcholanthrene	76-96	aryl hydrocarbon receptor	Homo sapiens	106-131
30872677-6	2019	Simvastatin abolished the detrimental effects of 3MC by reducing HDAC1 expression, with resulting RhoA upregulation, and reactivating RhoA in vitro and in vivo.	Methylcholanthrene	49-52	histone deacetylase 1	Homo sapiens	65-70
30872677-6	2019	Simvastatin abolished the detrimental effects of 3MC by reducing HDAC1 expression, with resulting RhoA upregulation, and reactivating RhoA in vitro and in vivo.	Methylcholanthrene	49-52	ras homolog family member A	Homo sapiens	98-102
30872677-6	2019	Simvastatin abolished the detrimental effects of 3MC by reducing HDAC1 expression, with resulting RhoA upregulation, and reactivating RhoA in vitro and in vivo.	Methylcholanthrene	49-52	ras homolog family member A	Homo sapiens	134-138
30872677-2	2019	In this study, the effects of simvastatin on the carcinogenic properties of 3-methylcholanthrene (3MC; an aryl-hydrocarbon receptor [AhR] agonist) in human renal epithelial cells (hRECs) were investigated.	Methylcholanthrene	76-96	aryl hydrocarbon receptor	Homo sapiens	133-136
30872677-2	2019	In this study, the effects of simvastatin on the carcinogenic properties of 3-methylcholanthrene (3MC; an aryl-hydrocarbon receptor [AhR] agonist) in human renal epithelial cells (hRECs) were investigated.	Methylcholanthrene	98-101	aryl hydrocarbon receptor	Homo sapiens	106-131
30872677-2	2019	In this study, the effects of simvastatin on the carcinogenic properties of 3-methylcholanthrene (3MC; an aryl-hydrocarbon receptor [AhR] agonist) in human renal epithelial cells (hRECs) were investigated.	Methylcholanthrene	98-101	aryl hydrocarbon receptor	Homo sapiens	133-136
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	histone deacetylase 1	Homo sapiens	132-153
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	histone deacetylase 1	Homo sapiens	155-160
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	ras homolog family member A	Homo sapiens	166-170
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	histone deacetylase 1	Homo sapiens	189-194
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	ras homolog family member A	Homo sapiens	209-213
30872677-4	2019	3MC upregulated the epithelial-mesenchymal transition (EMT) and tumor biomarkers; the models exhibited the reciprocal expression of histone deacetylase 1 (HDAC1) and RhoA, namely increased HDAC1 and decreased RhoA expression, through hypoxia-inducible-factor (HIF)- and AhR-dependent mechanisms.	Methylcholanthrene	0-3	aryl hydrocarbon receptor	Homo sapiens	270-273
30872677-5	2019	In addition to inducing EMT biomarkers, 3MC decreased von Hippel-Lindau protein levels (a risk factor for RCC) and increased CD44 expression in hRECs, which were reversed by digoxin (a HIF inhibitor) and HDAC inhibitors (suberoylanilide hydroxamic acid and trichostatin A [TSA]).	Methylcholanthrene	40-43	CD44 molecule (Indian blood group)	Homo sapiens	125-129
30499612-10	2019	MC showed lower AR positivity index at 2 (2.69 +- 0.046 vs. 2.8 +- 0.055**) and 25 (1.34 +- 0.097 vs. 1.56 +- 0.1***) days of life; at 100 days of life, there was a greater number of apoptotic MC in the RG (8.5 +- 0.4 vs. 2.95 +- 1.1***).	Methylcholanthrene	0-2	androgen receptor	Rattus norvegicus	16-18
30573465-0	2019	Suppression of Hepatic CYP3A4 Expression and Activity by 3-Methylcholanthrene in Humanized PXR-CAR-CYP3A4/3A7 Mice.	Methylcholanthrene	57-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
30573465-0	2019	Suppression of Hepatic CYP3A4 Expression and Activity by 3-Methylcholanthrene in Humanized PXR-CAR-CYP3A4/3A7 Mice.	Methylcholanthrene	57-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-105
30573465-3	2019	The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice.	Methylcholanthrene	23-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-112
30573465-3	2019	The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice.	Methylcholanthrene	23-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	203-209
30573465-3	2019	The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice.	Methylcholanthrene	45-47	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-112
30573465-5	2019	As a positive control response, pronounced induction of hepatic Cyp1a1 by MC was confirmed at both time points in males and females at the mRNA, protein, and catalytic activity levels.	Methylcholanthrene	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	64-70
30573465-7	2019	MC treatment suppressed hepatic CYP3A4 in female mice at 72 hours postdosing at the mRNA, protein, and catalytic activity levels.	Methylcholanthrene	0-2	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
30721054-4	2019	In the present work we benchmark the more affordable multiconfiguration pair-density functional theory (MC-PDFT) method whose accuracy has been recently validated for retinal chromophores in the gas phase, indicating that MC-PDFT could potentially be used to analyze large (e.g., few hundreds) sets of rhodopsin proteins.	Methylcholanthrene	104-106	rhodopsin	Homo sapiens	302-311
30621017-7	2019	Serum levels of AXIN1 and ST1A1 were increased in endometriosis compared with MC (p &lt; 0.001) and healthy controls (p = 0.001), whereas CXCL9 levels were decreased.	Methylcholanthrene	78-80	axin 1	Homo sapiens	16-21
30567645-3	2019	Owning to the strong synergistic effect among the metal oxides, mesoporous carbon, and small cavities and open channels of MOF, the as-prepared CeO2/CuOx@mC nanocomposites not only possess good electrochemical activity but also exhibit strong bioaffinity toward the aptamer strands.	Methylcholanthrene	154-156	lysine acetyltransferase 8	Homo sapiens	123-126
30391393-4	2019	Human and rodent studies have suggested that MC is improved by D2 dopamine receptor agonists.	Methylcholanthrene	45-47	dopamine receptor D2	Homo sapiens	63-83
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Methylcholanthrene	28-48	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	102-128
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Methylcholanthrene	28-48	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	133-139
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Methylcholanthrene	28-48	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	141-148
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Methylcholanthrene	28-48	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	150-157
30982029-6	2019	RESULTS: We confirmed the production of Klotho from MC by its significant availability in cells transfected with the MC, as well as in its conditioned medium, compared to that in cells transfected with parent vector.	Methylcholanthrene	52-54	klotho	Homo sapiens	40-46
30982029-10	2019	CONCLUSION: Together, these findings implied that self-generated Klotho protein, using MC technology, is functionally active and relevant as a therapeutic approach in renal injury.	Methylcholanthrene	87-89	klotho	Homo sapiens	65-71
30621017-7	2019	Serum levels of AXIN1 and ST1A1 were increased in endometriosis compared with MC (p &lt; 0.001) and healthy controls (p = 0.001), whereas CXCL9 levels were decreased.	Methylcholanthrene	78-80	sulfotransferase family 1A member 1	Homo sapiens	26-31
30312597-8	2018	Overexpression of NgR restored the regulation effects of miR-10 on MC proliferation and inflammatory cytokine secretion.	Methylcholanthrene	67-69	reticulon 4 receptor	Rattus norvegicus	18-21
31462112-8	2019	Compared with the MC group, the expression of Bcl-2 and COX-2 was obviously decreased by EGLP treatment, whereas the expression of Bax and cleaved caspase-3 was obviously increased.	Methylcholanthrene	18-20	cox2	Ganoderma lucidum	56-61
30362745-5	2018	Using this MC-SCF hybrid simulation, we determined the radial distribution functions of the nodes and structure factors and osmotic compressibilities of the gels.	Methylcholanthrene	11-13	KIT ligand	Homo sapiens	14-17
30521479-6	2018	ATF2 knockdown also resulted in significant inhibition of neoplastic transformation induced by a chemical carcinogen 3-methylcholanthrene, as well as the expression of Bcl-2/cyclin-A2/cyclin-D1/JUN/MMP-2, in immortalized human normal urothelial SVHUC cells stably expressing AR, but not AR-negative SVHUC cells.	Methylcholanthrene	117-137	activating transcription factor 2	Homo sapiens	0-4
30312597-9	2018	In summary, miR-10 can promote MC proliferation and inhibit the inflammatory cytokine secretion via targeting the NgR gene to down-regulate its expression.	Methylcholanthrene	31-33	reticulon 4 receptor	Rattus norvegicus	114-117
30031257-3	2018	Combining the high electron-hole separation rate of Fe2P@mC, fast electron transfer of CoP@mC, and the strong adsorption of mesoporous carbon, the as-prepared CoP/Fe2P@mC catalyst exhibits substantially enhanced photocatalytic activity toward rhodamine B (RhB) degradation under visible light irradiation.	Methylcholanthrene	57-59	caspase recruitment domain family member 16	Homo sapiens	159-162
30270557-6	2018	Different studies have shown that T regulatory type 1 (Tr1) cells, characterized by the coexpression of CD49b and LAG-3 and by their ability to secrete IL-10, have been associated with the presence and maintenance of persistent MC in beta-thalassemic patients after HSCT.	Methylcholanthrene	228-230	taste 1 receptor member 1	Homo sapiens	34-58
30270557-6	2018	Different studies have shown that T regulatory type 1 (Tr1) cells, characterized by the coexpression of CD49b and LAG-3 and by their ability to secrete IL-10, have been associated with the presence and maintenance of persistent MC in beta-thalassemic patients after HSCT.	Methylcholanthrene	228-230	integrin subunit alpha 2	Homo sapiens	104-109
30270557-6	2018	Different studies have shown that T regulatory type 1 (Tr1) cells, characterized by the coexpression of CD49b and LAG-3 and by their ability to secrete IL-10, have been associated with the presence and maintenance of persistent MC in beta-thalassemic patients after HSCT.	Methylcholanthrene	228-230	lymphocyte activating 3	Homo sapiens	114-119
30270557-6	2018	Different studies have shown that T regulatory type 1 (Tr1) cells, characterized by the coexpression of CD49b and LAG-3 and by their ability to secrete IL-10, have been associated with the presence and maintenance of persistent MC in beta-thalassemic patients after HSCT.	Methylcholanthrene	228-230	interleukin 10	Homo sapiens	152-157
30627376-12	2018	Conclusion: The lowering effect of apelin 40 on MC and its non-effectiveness on APJ/KOR dimerization, while augmenting the contractility and reducing the dimerization by apelin 20 implies the APJ/KOR-related effects of apelin on the MC under acute reno-vascular hypertension.	Methylcholanthrene	48-50	apelin	Rattus norvegicus	35-41
30338977-2	2018	Here, we developed a novel method for fabricating an in situ reinforced MC system with nonequilibrium self-assembled nanofibrous structures based on bisphenol A epoxy resin, 4,4"-diaminodiphenylsulfone, bismaleimide, and a polyphenylene ether (PPO) oligomer.	Methylcholanthrene	72-74	protoporphyrinogen oxidase	Homo sapiens	244-247
30513637-9	2018	This was supported by pharmaceutical inhibition of protein kinase A (PKA), the downstream effector of MC-Rs signaling, using H89 abolished the alpha-MSH-mediated suppression of NO release and eNOS/iNOS protein level.	Methylcholanthrene	102-105	proopiomelanocortin	Homo sapiens	143-152
30327325-7	2018	Our genetic analyses show that Taz is essential for MC fate acquisition and subsequent micropyle formation in zebrafish.	Methylcholanthrene	52-54	tafazzin, phospholipid-lysophospholipid transacylase	Danio rerio	31-34
30338977-6	2018	In particular, the obtained MC showed a significant improvement in glass transition temperature and mechanical properties, which were mainly attributed to the restriction of high thermal stability of PPO on the segmental motion of polymer chains, the toughening and reinforcement behaviors of PPO nanofibers on the matrix, and the chemical interaction at the PPO/matrix interface.	Methylcholanthrene	28-30	protoporphyrinogen oxidase	Homo sapiens	200-203
30338977-6	2018	In particular, the obtained MC showed a significant improvement in glass transition temperature and mechanical properties, which were mainly attributed to the restriction of high thermal stability of PPO on the segmental motion of polymer chains, the toughening and reinforcement behaviors of PPO nanofibers on the matrix, and the chemical interaction at the PPO/matrix interface.	Methylcholanthrene	28-30	protoporphyrinogen oxidase	Homo sapiens	293-296
30338977-6	2018	In particular, the obtained MC showed a significant improvement in glass transition temperature and mechanical properties, which were mainly attributed to the restriction of high thermal stability of PPO on the segmental motion of polymer chains, the toughening and reinforcement behaviors of PPO nanofibers on the matrix, and the chemical interaction at the PPO/matrix interface.	Methylcholanthrene	28-30	protoporphyrinogen oxidase	Homo sapiens	293-296
30210070-1	2018	BACKGROUND: The aim of this study was to investigate long-term survival, clinical status, and echocardiographic findings of patients with severe functional mitral regurgitation (FMR) undergoing MitraClip (MC) treatment and to explore the role of baseline features on outcome.	Methylcholanthrene	205-207	CAP-Gly domain containing linker protein 1	Homo sapiens	194-203
30086648-3	2018	Herein, we addressed the hypothesis that adipose tissue (AT) free fatty acids (FFAs) play a central role in the initiation of hepatic DC/MC accumulation, using a number of mouse models of altered FFA supply to the liver.	Methylcholanthrene	137-139	WD and tetratricopeptide repeats 1	Mus musculus	41-48
30555747-4	2018	In SVHUC-AR cells exposed to a chemical carcinogen 3-methylcholanthrene, silodosin significantly reduced the expression levels of oncogenes (e.g. c-Fos, Jun, Myc), as well as phospho-p38 MAPK and phospho-ERK proteins, and increased those of tumor suppressor genes (e.g. p53, PTEN, UGT1A).	Methylcholanthrene	51-71	androgen receptor	Mus musculus	3-11
30555747-4	2018	In SVHUC-AR cells exposed to a chemical carcinogen 3-methylcholanthrene, silodosin significantly reduced the expression levels of oncogenes (e.g. c-Fos, Jun, Myc), as well as phospho-p38 MAPK and phospho-ERK proteins, and increased those of tumor suppressor genes (e.g. p53, PTEN, UGT1A).	Methylcholanthrene	51-71	FBJ osteosarcoma oncogene	Mus musculus	146-151
30555747-4	2018	In SVHUC-AR cells exposed to a chemical carcinogen 3-methylcholanthrene, silodosin significantly reduced the expression levels of oncogenes (e.g. c-Fos, Jun, Myc), as well as phospho-p38 MAPK and phospho-ERK proteins, and increased those of tumor suppressor genes (e.g. p53, PTEN, UGT1A).	Methylcholanthrene	51-71	myelocytomatosis oncogene	Mus musculus	158-161
30555747-5	2018	ELK1 suppression via ELK1-short hairpin RNA virus infection or silodosin treatment also resulted in significant inhibition in 3-methylcholanthrene-induced neoplastic transformation of SVHUC-AR cells, but not that of SVHUC-vector cells.	Methylcholanthrene	126-146	ELK1, member of ETS oncogene family	Mus musculus	0-4
30555747-5	2018	ELK1 suppression via ELK1-short hairpin RNA virus infection or silodosin treatment also resulted in significant inhibition in 3-methylcholanthrene-induced neoplastic transformation of SVHUC-AR cells, but not that of SVHUC-vector cells.	Methylcholanthrene	126-146	ELK1, member of ETS oncogene family	Mus musculus	21-25
30555747-5	2018	ELK1 suppression via ELK1-short hairpin RNA virus infection or silodosin treatment also resulted in significant inhibition in 3-methylcholanthrene-induced neoplastic transformation of SVHUC-AR cells, but not that of SVHUC-vector cells.	Methylcholanthrene	126-146	androgen receptor	Mus musculus	184-192
30081205-8	2018	The relative proteins (PTEN, PI3K, AKT and P53) expressions of MC group were significantly differences (P &lt; 0.05, respectively) compared with those of NC groups in vitro and vivo studies.	Methylcholanthrene	63-65	AKT serine/threonine kinase 1	Rattus norvegicus	35-38
30081205-8	2018	The relative proteins (PTEN, PI3K, AKT and P53) expressions of MC group were significantly differences (P &lt; 0.05, respectively) compared with those of NC groups in vitro and vivo studies.	Methylcholanthrene	63-65	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	43-46
30081205-9	2018	However, with miRNA-23a infection, the cell apoptosis of miRNA group were significantly suppressed compared with MC groups, and the relative proteins (PTEN, PI3K, AKT and P53) of miRNA group were also significantly differences compared with MC groups in vitro and vivo studies (P &lt; 0.05, respectively).	Methylcholanthrene	113-115	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	171-174
30081205-9	2018	However, with miRNA-23a infection, the cell apoptosis of miRNA group were significantly suppressed compared with MC groups, and the relative proteins (PTEN, PI3K, AKT and P53) of miRNA group were also significantly differences compared with MC groups in vitro and vivo studies (P &lt; 0.05, respectively).	Methylcholanthrene	241-243	AKT serine/threonine kinase 1	Rattus norvegicus	163-166
30081205-9	2018	However, with miRNA-23a infection, the cell apoptosis of miRNA group were significantly suppressed compared with MC groups, and the relative proteins (PTEN, PI3K, AKT and P53) of miRNA group were also significantly differences compared with MC groups in vitro and vivo studies (P &lt; 0.05, respectively).	Methylcholanthrene	241-243	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	171-174
30314280-8	2018	This effect was inhibited by the AhR agonists indole-3-carbinol (I3C) and 3-methylcholanthrene (3MC).	Methylcholanthrene	74-94	aryl-hydrocarbon receptor	Mus musculus	33-36
30314280-8	2018	This effect was inhibited by the AhR agonists indole-3-carbinol (I3C) and 3-methylcholanthrene (3MC).	Methylcholanthrene	96-99	aryl-hydrocarbon receptor	Mus musculus	33-36
29960248-3	2018	Therefore, the present in vitro study aimed to evaluate the influence of thermal and mechanical cycling (TC and MC) on retentive strength of CAD/CAM resin-based crowns in relation to microscale expansion and contraction caused by fatigue.	Methylcholanthrene	112-114	calmodulin 3	Homo sapiens	145-148
30178760-4	2018	According to this rule, we propose the first class of potential ferroelectric-like elemental polar metals in a distorted alpha-La-like structure with a polar space group P63 mc in which two inequivalent Wyckoff positions 2a (0, 0, z) and 2b (1/3, 2/3, z) are occupied by group-V elements (phosphorus, arsenic, antimony, and bismuth).	Methylcholanthrene	174-176	tumor protein p63	Homo sapiens	170-173
30145136-9	2018	GSTs play major role in the detoxification of reactive metabolites of methylcholanthrene by mediating catalytic binding with GSH to form a highly soluble detoxified complex which is then eliminated.	Methylcholanthrene	70-88	glutathione S-transferase kappa 1	Homo sapiens	0-4
30129247-4	2018	The purpose of this study is the evaluation of multiplex RQ-PCR for MC assessment (six biallelic genetic systems and Y-specific locus), allowing the amplification and detection of target gene of interest and glyceraldehyde-3-phosphate dehydrogenase reference housekeeping gene in a single microtube.	Methylcholanthrene	68-70	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	208-248
29940513-6	2018	Analysis of gene expression in zebrafish larvae confirmed the role of Ahr2 in the signaling of 3-MC toxicity.	Methylcholanthrene	95-99	aryl hydrocarbon receptor 2	Danio rerio	70-74
29960248-9	2018	TC and MC significantly reduced the retentive strength of the CAD/CAM resin-based crowns whereas that of the CAD/CAM ceramic crowns was only affected by TC.	Methylcholanthrene	7-9	calmodulin 3	Homo sapiens	66-69
29772423-2	2018	The ball milling process initiated the degradation of BDE209 on beta-MnO2, yielding a nearly complete degradation and debromination of BDE209 within 2 h. The use of beta-MnO2 exhibited much higher MC debromination efficiency than that by using birnessite (delta-MnO2, 40.2%), Bi2O3 (45.6%), CaO (65.3%), and persulfate (81.9%).	Methylcholanthrene	197-199	homeobox D13	Homo sapiens	54-57
30249733-3	2018	Herein, we report a case of a 3-year-old boy with MC-EDS in whom a novel mutation in the CHST14 gene was discovered.	Methylcholanthrene	50-52	carbohydrate sulfotransferase 14	Homo sapiens	89-95
29772423-3	2018	It was demonstrated that the oxidative degradation of BDE209 was promoted by the redox half reactions of both Mn4+  Mn3+ and Mn3+  Mn2+, but naturally existed Mn3+ centers on the surface of beta-MnO2 functioned as dominant reactive species at the initial stage of the MC degradation (often before the degradation efficiency of BDE209 achieved 50%).	Methylcholanthrene	268-270	homeobox D13	Homo sapiens	54-57
29980579-5	2018	CYP1A1 mRNA levels were determined after treatment with varying concentrations of 3-methylcholanthrene (3MC).	Methylcholanthrene	82-102	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
29843042-14	2018	CONCLUSION: These results validate the anti-cancer potential of TAX in DMBA-induced MC through LXR-mTOR/Maf1/PTEN axis.	Methylcholanthrene	84-86	mechanistic target of rapamycin kinase	Rattus norvegicus	99-103
29843042-14	2018	CONCLUSION: These results validate the anti-cancer potential of TAX in DMBA-induced MC through LXR-mTOR/Maf1/PTEN axis.	Methylcholanthrene	84-86	MAF1 homolog, negative regulator of RNA polymerase III	Rattus norvegicus	104-108
29843042-14	2018	CONCLUSION: These results validate the anti-cancer potential of TAX in DMBA-induced MC through LXR-mTOR/Maf1/PTEN axis.	Methylcholanthrene	84-86	phosphatase and tensin homolog	Rattus norvegicus	109-113
29980579-5	2018	CYP1A1 mRNA levels were determined after treatment with varying concentrations of 3-methylcholanthrene (3MC).	Methylcholanthrene	104-107	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
29980579-7	2018	LCLs with the AA genotype displayed significantly higher AHR-XRE binding and CYP1A1 mRNA expression after 3MC treatment than did those with the GG genotype.	Methylcholanthrene	106-109	aryl hydrocarbon receptor	Homo sapiens	57-60
29980579-7	2018	LCLs with the AA genotype displayed significantly higher AHR-XRE binding and CYP1A1 mRNA expression after 3MC treatment than did those with the GG genotype.	Methylcholanthrene	106-109	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	77-83
29980579-8	2018	Electrophoretic mobility shift assay (EMSA) showed that oligonucleotides with the AA genotype displayed higher LCL nuclear extract binding after 3MC treatment than did those with the GG genotype, and mass spectrometric analysis of EMSA protein-DNA complex bands identified three candidate proteins, two of which were co-immunoprecipitated with AHR.	Methylcholanthrene	145-148	aryl hydrocarbon receptor	Homo sapiens	344-347
29980579-9	2018	In conclusion, we have demonstrated that the rs2470893 SNP, which maps 196 bp from a CYP1A1 promoter XRE, is associated with variations in 3MC-dependent AHR binding and CYP1A1 expression.	Methylcholanthrene	139-142	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	85-91
29980579-9	2018	In conclusion, we have demonstrated that the rs2470893 SNP, which maps 196 bp from a CYP1A1 promoter XRE, is associated with variations in 3MC-dependent AHR binding and CYP1A1 expression.	Methylcholanthrene	139-142	aryl hydrocarbon receptor	Homo sapiens	153-156
30593307-6	2018	RESULTS: Compared to C group, MC group rats PAI-1, ox-LDL, e NOS showed increased in serum( P &lt; 0.	Methylcholanthrene	30-32	serpin family E member 1	Rattus norvegicus	44-49
30593307-6	2018	RESULTS: Compared to C group, MC group rats PAI-1, ox-LDL, e NOS showed increased in serum( P &lt; 0.	Methylcholanthrene	30-32	nitric oxide synthase 3	Rattus norvegicus	59-64
30158921-6	2018	Male Mc was quantified by DYS14 real-time PCR in blood samples from 58 women who had previously given birth to at least one male child.	Methylcholanthrene	5-7	testis specific protein Y-linked 1	Homo sapiens	26-31
30103743-5	2018	A highly significant down-regulation of genes involved in hepatic lipogenesis including acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), malic enzyme (ME), and lipoprotein lipase (LPL) was observed in the liver of chickens fed MC.	Methylcholanthrene	235-237	fatty acid synthase	Gallus gallus	118-137
30103743-5	2018	A highly significant down-regulation of genes involved in hepatic lipogenesis including acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), malic enzyme (ME), and lipoprotein lipase (LPL) was observed in the liver of chickens fed MC.	Methylcholanthrene	235-237	lipoprotein lipase	Gallus gallus	168-186
30103743-5	2018	A highly significant down-regulation of genes involved in hepatic lipogenesis including acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), malic enzyme (ME), and lipoprotein lipase (LPL) was observed in the liver of chickens fed MC.	Methylcholanthrene	235-237	lipoprotein lipase	Gallus gallus	188-191
29649551-3	2018	Mc-RACK1 shared typical RACK1 domains containing WD repeats, PKC phosphorylation sites, N-myristoylation sites, PKC activation sites, TK phosphorylation site and WD motifs.	Methylcholanthrene	0-2	receptor for activated C kinase 1	Homo sapiens	3-8
29649551-3	2018	Mc-RACK1 shared typical RACK1 domains containing WD repeats, PKC phosphorylation sites, N-myristoylation sites, PKC activation sites, TK phosphorylation site and WD motifs.	Methylcholanthrene	0-2	receptor for activated C kinase 1	Homo sapiens	24-29
29331029-5	2018	RESULTS: ISM patients showed higher percentages of both BM and PB MC-committed CD34+ HPC vs controls, particularly among ISM cases with MC-restricted KIT mutation (ISMMC ); this was associated with progressive blockade of maturation of CD34+ HPC to the neutrophil lineage from ISMMC to multilineage KIT-mutated cases (ISMML ).	Methylcholanthrene	66-68	CD34 molecule	Homo sapiens	79-83
29627420-10	2018	MC group showed decreased protein levels of p-eNOS, as compared with the YC group.	Methylcholanthrene	0-2	nitric oxide synthase 3	Rattus norvegicus	46-50
30005075-8	2018	In addition, expression of hsa-miR-200a-5p showed negative correlation to that of TPO (rs = - 0.734; **: P &lt; 0.01) and CD56 (rs = - 0.570; **: P &lt; 0.01), but positive correlation to that of Galectin-3 (rs = 0.601; **: P &lt; 0.01), MC (rs = 0.508; **: P &lt; 0.01), CK19 (rs = 0.712; **: P &lt; 0.01) and B-raf (rs = 0.378; **: P &lt; 0.01).	Methylcholanthrene	238-240	membrane associated ring-CH-type finger 8	Homo sapiens	31-34
30005075-8	2018	In addition, expression of hsa-miR-200a-5p showed negative correlation to that of TPO (rs = - 0.734; **: P &lt; 0.01) and CD56 (rs = - 0.570; **: P &lt; 0.01), but positive correlation to that of Galectin-3 (rs = 0.601; **: P &lt; 0.01), MC (rs = 0.508; **: P &lt; 0.01), CK19 (rs = 0.712; **: P &lt; 0.01) and B-raf (rs = 0.378; **: P &lt; 0.01).	Methylcholanthrene	238-240	thyroid peroxidase	Homo sapiens	82-85
29978166-2	2018	In this article PID-s has been investigated by applying high voltage stress on mc-Si solar cells for their degradation and recovery and results have been explained on the basis of DC and AC characterization.	Methylcholanthrene	79-81	metastasis associated 1 family member 2	Homo sapiens	16-19
29978166-5	2018	Observed negative capacitance behaviour in impedance spectra of mc-Si solar cells after PID-s has been attributed to structural deformation caused by potential induced migration of sodium ions (Na+) into mc-Si.	Methylcholanthrene	64-66	metastasis associated 1 family member 2	Homo sapiens	88-91
29978166-5	2018	Observed negative capacitance behaviour in impedance spectra of mc-Si solar cells after PID-s has been attributed to structural deformation caused by potential induced migration of sodium ions (Na+) into mc-Si.	Methylcholanthrene	204-206	metastasis associated 1 family member 2	Homo sapiens	88-91
29968763-8	2018	The univariate unweighted Cox regression showed a 42% reduction in death risk for patients on MC (95%CI: 0.370-0.906; p = 0.017).	Methylcholanthrene	94-96	cytochrome c oxidase subunit 8A	Homo sapiens	26-29
29672918-6	2018	Finally, there are more MC cells in the epidermis of p53-/- mice after IR exposure as compared to wild-type mice.	Methylcholanthrene	24-26	transformation related protein 53, pseudogene	Mus musculus	53-56
30381121-12	2018	Compared with the MC group, the expression of PKC, NF-kappaBp65 and Rac-1 decreased in the XFC group.	Methylcholanthrene	18-20	protein kinase C, gamma	Rattus norvegicus	46-49
30381121-12	2018	Compared with the MC group, the expression of PKC, NF-kappaBp65 and Rac-1 decreased in the XFC group.	Methylcholanthrene	18-20	Rac family small GTPase 1	Rattus norvegicus	68-73
29848709-6	2018	RESULTS: UEA and MC-I subtypes exhibited horizontally continuous, strong nuclear p16 immunoreactivity in the tumor cells, whereas none of the MC-G cases showed diffuse and strong nuclear immunoreactivity for p16 in the tumor cells.	Methylcholanthrene	17-19	cyclin dependent kinase inhibitor 2A	Homo sapiens	81-84
29848709-11	2018	CONCLUSION: Stromal p16 expression of MC-G was significantly higher than that of normal cervix and other histological subtypes of adenocarcinoma and was associated with advanced stage, parametrial invasion, and lymphovascular invasion, reflecting the aggressive behavior of MC-G.	Methylcholanthrene	38-41	cyclin dependent kinase inhibitor 2A	Homo sapiens	20-23
29848712-9	2018	There is a highly significant inverse correlation between the individual values of the NAD24 and plasma SOD1 values postoperatively in LC and MC patients (r=-0.335, p=0.011).	Methylcholanthrene	142-144	superoxide dismutase 1	Homo sapiens	104-108
29331029-5	2018	RESULTS: ISM patients showed higher percentages of both BM and PB MC-committed CD34+ HPC vs controls, particularly among ISM cases with MC-restricted KIT mutation (ISMMC ); this was associated with progressive blockade of maturation of CD34+ HPC to the neutrophil lineage from ISMMC to multilineage KIT-mutated cases (ISMML ).	Methylcholanthrene	136-138	CD34 molecule	Homo sapiens	79-83
29331029-5	2018	RESULTS: ISM patients showed higher percentages of both BM and PB MC-committed CD34+ HPC vs controls, particularly among ISM cases with MC-restricted KIT mutation (ISMMC ); this was associated with progressive blockade of maturation of CD34+ HPC to the neutrophil lineage from ISMMC to multilineage KIT-mutated cases (ISMML ).	Methylcholanthrene	136-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-153
29665133-5	2018	A cell lineage-tracing study revealed that upon differentiation, MC-derived HSCs or perivascular mesenchymal cells express ITGA8 during liver development.	Methylcholanthrene	65-67	integrin alpha 8	Mus musculus	123-128
29867031-8	2018	Compared with the NC group, the MC group had significantly increased serum peptide YY (PYY) and cholecystokinin (CCK) levels.	Methylcholanthrene	32-34	peptide YY	Sus scrofa	75-85
29867031-8	2018	Compared with the NC group, the MC group had significantly increased serum peptide YY (PYY) and cholecystokinin (CCK) levels.	Methylcholanthrene	32-34	peptide YY	Sus scrofa	87-90
29867031-8	2018	Compared with the NC group, the MC group had significantly increased serum peptide YY (PYY) and cholecystokinin (CCK) levels.	Methylcholanthrene	32-34	cholecystokinin	Sus scrofa	96-111
29867031-8	2018	Compared with the NC group, the MC group had significantly increased serum peptide YY (PYY) and cholecystokinin (CCK) levels.	Methylcholanthrene	32-34	cholecystokinin	Sus scrofa	113-116
29665133-6	2018	Using anti-ITGA8 antibodies, we succeeded in isolating MC-derived HSCs and perivascular mesenchymal cells from embryonic livers.	Methylcholanthrene	55-57	integrin alpha 8	Mus musculus	11-16
29665133-10	2018	CONCLUSIONS: ITGA8 is a specific cell surface marker of MC-derived HSCs and perivascular mesenchymal cells in the developing liver.	Methylcholanthrene	56-58	integrin alpha 8	Mus musculus	13-18
29669576-8	2018	The incidence rates of MC were 0, 0.3, 0.6, 0.9, 0.7, and 0.2%, respectively, in different intervertebral disc segments C2-3, C3-4, C4-5, C5-6, C6-7, and C7T1.	Methylcholanthrene	23-25	nucleolin	Homo sapiens	120-124
29512156-11	2018	Remarkably, in the other (~70%) CA1 PCs, although no responses could be detected at resting potentials, clear excitatory MP or MC responses to the same flash stimulus were observed at depolarizing potentials, and these responses were further found to depend on NMDA receptors.	Methylcholanthrene	127-129	carbonic anhydrase 1	Homo sapiens	32-35
29592878-5	2018	In immortalized human normal urothelial SVHUC cells stably expressing AR, NF-kappaB activators and inhibitors accelerated and prevented, respectively, their neoplastic transformation induced by a chemical carcinogen 3-methylcholanthrene.	Methylcholanthrene	216-236	androgen receptor	Homo sapiens	70-72
29592878-5	2018	In immortalized human normal urothelial SVHUC cells stably expressing AR, NF-kappaB activators and inhibitors accelerated and prevented, respectively, their neoplastic transformation induced by a chemical carcinogen 3-methylcholanthrene.	Methylcholanthrene	216-236	nuclear factor kappa B subunit 1	Homo sapiens	74-83
29396895-0	2018	Spin-orbit effects on magnetically induced current densities in the M5- (M = N,P,As,Sb,Bi,Mc) clusters.	Methylcholanthrene	90-92	spindlin 1	Homo sapiens	0-4
29635147-4	2018	Sixteen patients with MC from HER2-BC received IT trastuzumab.	Methylcholanthrene	22-24	erb-b2 receptor tyrosine kinase 2	Homo sapiens	30-34
29635147-12	2018	CONCLUSIONS: The MTD and recommended phase II weekly dose of IT trastuzumab in patients with HER2-BC and MC is 150 mg. A phase II trial using this dose regimen in MC from HER2-BC is ongoing.	Methylcholanthrene	163-165	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-175
29669576-8	2018	The incidence rates of MC were 0, 0.3, 0.6, 0.9, 0.7, and 0.2%, respectively, in different intervertebral disc segments C2-3, C3-4, C4-5, C5-6, C6-7, and C7T1.	Methylcholanthrene	23-25	complement C4A (Rodgers blood group)	Homo sapiens	132-136
29534881-3	2018	In response to microcystin-LR (MC-LR), a time- and concentration-dependent formation of MC-positive protein bands in HL1-hT1 cells was observed.	Methylcholanthrene	31-33	intelectin 1	Homo sapiens	117-120
29516867-5	2018	We observed that MC increases CD206+ staining and IL-10 (M2 macrophages), whereas HA shows cells expressing more CD86 and secreting more TNF-alpha.	Methylcholanthrene	17-19	interleukin 10	Mus musculus	50-55
29534881-5	2018	Accumulation of MC-positive protein bands in HL1-hT1 cells was associated neither with alterations of cell viability and growth, dysregulations of ERK1/2 and p38 kinases, reactive oxygen species formation, induction of double-stranded DNA breaks nor modulations of stress-inducible genes (ATF3, HSP5).	Methylcholanthrene	16-18	intelectin 1	Homo sapiens	45-48
29534881-5	2018	Accumulation of MC-positive protein bands in HL1-hT1 cells was associated neither with alterations of cell viability and growth, dysregulations of ERK1/2 and p38 kinases, reactive oxygen species formation, induction of double-stranded DNA breaks nor modulations of stress-inducible genes (ATF3, HSP5).	Methylcholanthrene	16-18	activating transcription factor 3	Homo sapiens	289-293
29495225-9	2018	The HE staining showed that pulmonary vascular-related and pulmonary alveolar-related developmental indexes in group MC were lower than those in the group NC, and those in the group MT were between the two groups.In addition, immunohistochemical staining showed that the average optical density (AOD) of KLF5 in group NC, MC, MT was 0.194 8+-0.007 4, 0.212 1+-0.004 9 and 0.192 7+-0.001 9, respectively (F=14.53, P=0.002); and AOD of Survivin was 0.185 2+-0.008 7, 0.209 2+-0.003 6 and 0.192 8+-0.007 5, respectively (F=12.31, P=0.003).	Methylcholanthrene	117-119	Kruppel-like factor 5	Rattus norvegicus	304-308
29702993-5	2018	Sequencing validation revealed other mutations in the 4 samples in which no mutation was detected by the ARMS-MC method.ARMS-MC provides a rapid, simple, inexpensive, and accurate screening method for detecting the most common G6PD mutations in Chinese people.	Methylcholanthrene	110-112	glucose-6-phosphate dehydrogenase	Homo sapiens	227-231
29301088-2	2018	Here, we investigate how the MC-PDFT total energy and its components depend on the active space choice in the case of the H2 and N2 molecules.	Methylcholanthrene	29-31	relaxin 2	Homo sapiens	122-131
29282578-9	2018	These findings indicate that miR-21-mediated inhibition of MC degranulation is involved in the anti-ACD effect of berberine via inhibiting p38 pathway, which provide a new insight into the immunopharmacological role of berberine and suggest its potential application for the treatment of allergic inflammation, such as ACD.	Methylcholanthrene	59-61	microRNA 21	Rattus norvegicus	29-35
29282578-9	2018	These findings indicate that miR-21-mediated inhibition of MC degranulation is involved in the anti-ACD effect of berberine via inhibiting p38 pathway, which provide a new insight into the immunopharmacological role of berberine and suggest its potential application for the treatment of allergic inflammation, such as ACD.	Methylcholanthrene	59-61	mitogen activated protein kinase 14	Rattus norvegicus	139-142
29491387-0	2018	Understanding the Structure, Multimerization, Subcellular Localization and mC Selectivity of a Genomic Mutator and Anti-HIV Factor APOBEC3H.	Methylcholanthrene	75-77	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	131-139
29123257-5	2018	In SVHUC cells, exposure to a chemical carcinogen 3-methylcholanthrene considerably increased and decreased the expression of EP2/EP4 and phosphatase and tensin homologue (PTEN), respectively.	Methylcholanthrene	50-70	prostaglandin E receptor 2	Homo sapiens	126-129
29094188-8	2018	Co-treatment with alpha-naphthoflavone (alphaNF), a specific antagonist of AhR, prevented almost every 3MC-induced changes.	Methylcholanthrene	103-106	aryl hydrocarbon receptor	Rattus norvegicus	75-78
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	nuclear factor kappa B subunit 1	Homo sapiens	101-110
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	RELA proto-oncogene, NF-kB subunit	Homo sapiens	111-114
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	116-121
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	nitric oxide synthase 2	Homo sapiens	123-127
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	tumor necrosis factor	Homo sapiens	129-138
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	interleukin 1 beta	Homo sapiens	140-148
29117589-6	2018	Additionally, long-term exposure of MC-LR at low concentration remarkably promoted the expression of NF-kappaB p65, COX-2, iNOS, TNF-alpha, IL-1beta, and IL-6 in the cells, suggesting that long-term MC-LR exposure at low concentration can induce inflammatory reaction to HepG2 cells, which might account for MC-induced human hepatitis.	Methylcholanthrene	36-38	interleukin 6	Homo sapiens	154-158
29123257-5	2018	In SVHUC cells, exposure to a chemical carcinogen 3-methylcholanthrene considerably increased and decreased the expression of EP2/EP4 and phosphatase and tensin homologue (PTEN), respectively.	Methylcholanthrene	50-70	prostaglandin E receptor 4	Homo sapiens	130-133
29123257-5	2018	In SVHUC cells, exposure to a chemical carcinogen 3-methylcholanthrene considerably increased and decreased the expression of EP2/EP4 and phosphatase and tensin homologue (PTEN), respectively.	Methylcholanthrene	50-70	phosphatase and tensin homolog	Homo sapiens	138-170
29123257-5	2018	In SVHUC cells, exposure to a chemical carcinogen 3-methylcholanthrene considerably increased and decreased the expression of EP2/EP4 and phosphatase and tensin homologue (PTEN), respectively.	Methylcholanthrene	50-70	phosphatase and tensin homolog	Homo sapiens	172-176
29123257-6	2018	Treatment with selective EP2/EP4 antagonist or celecoxib also resulted in prevention in 3-methylcholanthrene-induced neoplastic transformation of SVHUC cells.	Methylcholanthrene	88-108	prostaglandin E receptor 2	Homo sapiens	25-28
29123257-6	2018	Treatment with selective EP2/EP4 antagonist or celecoxib also resulted in prevention in 3-methylcholanthrene-induced neoplastic transformation of SVHUC cells.	Methylcholanthrene	88-108	prostaglandin E receptor 4	Homo sapiens	29-32
30130987-4	2018	Group I included patients with MC which was defined as being composed of &gt;50% extracellular mucin.	Methylcholanthrene	31-33	LOC100508689	Homo sapiens	95-100
28464341-4	2018	Novel open field exposure in both CC and MC resulted in a marked increase in Fos expression in the anterior and posterior parts of the basolateral amygdaloid nucleus, basomedial nucleus, and medial nucleus, whereas these increases in expression were not observed in CR.	Methylcholanthrene	41-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
28643424-5	2017	Here, we explore whether MDM2 is involved in podocyte MC during hyperglycaemia.	Methylcholanthrene	54-56	MDM2 proto-oncogene	Homo sapiens	25-29
30372685-10	2018	Results show that the levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and the chemokine (C-C motif) ligand 2 (CCL2) were lesser in the brains of GMF-KO mice and MC-KO mice when compared to Wt mice brain after MPTP administration.	Methylcholanthrene	194-196	chemokine (C-C motif) ligand 2	Mus musculus	143-147
30430930-10	2018	In summary, data indicate that the MC-LR-induced alterations in lncRNA may be associated with hepatotoxicity and that upregulation of LINC00847, MIR22HG and LNC_00027 may play important roles in the observed MC-mediated liver damage.	Methylcholanthrene	35-37	MIR22 host gene	Homo sapiens	145-152
30430930-10	2018	In summary, data indicate that the MC-LR-induced alterations in lncRNA may be associated with hepatotoxicity and that upregulation of LINC00847, MIR22HG and LNC_00027 may play important roles in the observed MC-mediated liver damage.	Methylcholanthrene	208-210	long intergenic non-protein coding RNA 847	Homo sapiens	134-143
30430930-10	2018	In summary, data indicate that the MC-LR-induced alterations in lncRNA may be associated with hepatotoxicity and that upregulation of LINC00847, MIR22HG and LNC_00027 may play important roles in the observed MC-mediated liver damage.	Methylcholanthrene	208-210	MIR22 host gene	Homo sapiens	145-152
28833704-8	2017	Notably, LPS-induced desensitization of MCs was short term with MC sensitivity to IgE reconstituted within 48 hours, which was associated with recapitulation of FcepsilonRI expression on the MCs.	Methylcholanthrene	40-42	Fc receptor, IgE, high affinity I, gamma polypeptide	Mus musculus	161-172
28643424-14	2017	Notch1 signalling is an essential downstream pathway of MDM2 in mediating HG-induced MC in podocytes.	Methylcholanthrene	85-87	notch receptor 1	Homo sapiens	0-6
28643424-14	2017	Notch1 signalling is an essential downstream pathway of MDM2 in mediating HG-induced MC in podocytes.	Methylcholanthrene	85-87	MDM2 proto-oncogene	Homo sapiens	56-60
28795445-3	2017	Adsorption experiments at pH 6.8 with 2 mg ZnO@MC as adsorbent illustrated an adsorption efficiency of 92.3 % in 5 mL hemoglobin (Hb) solution with a concentration of 100 mg L-1 .	Methylcholanthrene	47-49	immunoglobulin kappa variable 1-16	Homo sapiens	174-177
29109414-5	2017	We show that autophagy suppression in Atg 13 knockout non-small cell lung carcinoma cells lead to the dramatic decrease of MC rate.	Methylcholanthrene	123-125	autophagy related 13	Homo sapiens	38-44
29109414-6	2017	Furthermore, mitochondria-linked anti-apoptotic proteins Mcl-1 and Bcl-xL play a crucial role in the duration of MC and a cross-talk between autophagy and apoptosis.	Methylcholanthrene	113-115	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	57-62
29109414-6	2017	Furthermore, mitochondria-linked anti-apoptotic proteins Mcl-1 and Bcl-xL play a crucial role in the duration of MC and a cross-talk between autophagy and apoptosis.	Methylcholanthrene	113-115	BCL2 like 1	Homo sapiens	67-73
29109414-7	2017	Thus, the suppression of apoptosis by overexpression of Mcl-1 or Bcl-xL affected MC and lead to a significant induction of autophagy in HCT116 wt and HCT116 14-3-3sigma-/- cells.	Methylcholanthrene	81-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	56-61
29109414-7	2017	Thus, the suppression of apoptosis by overexpression of Mcl-1 or Bcl-xL affected MC and lead to a significant induction of autophagy in HCT116 wt and HCT116 14-3-3sigma-/- cells.	Methylcholanthrene	81-83	BCL2 like 1	Homo sapiens	65-71
28472685-2	2017	The proof of adsorption of Pb(II) ions onto NCS/SA/MC beads was identified from FT-IR and EDX-SEM Studies.	Methylcholanthrene	51-53	submaxillary gland androgen regulated protein 3B	Homo sapiens	27-33
28972393-2	2017	In the present study, LNCaP cells were knocked down of AhR by siRNA, or treated with the AhR agonist 3-methylcholanthrene (3MC).	Methylcholanthrene	101-121	aryl hydrocarbon receptor	Homo sapiens	89-92
28972393-2	2017	In the present study, LNCaP cells were knocked down of AhR by siRNA, or treated with the AhR agonist 3-methylcholanthrene (3MC).	Methylcholanthrene	123-126	aryl hydrocarbon receptor	Homo sapiens	89-92
28972393-8	2017	Activation of AhR by 3MC treatment, further aggravated these changes of LNCaP cells on oxidative stress.	Methylcholanthrene	21-24	aryl hydrocarbon receptor	Homo sapiens	14-17
28472685-5	2017	The desorption studies reveals that the recovery of Pb(II) from NCS/SA/MC bead was found to be effective by using 0.1M HCl solution.	Methylcholanthrene	71-73	submaxillary gland androgen regulated protein 3B	Homo sapiens	52-58
28472685-6	2017	From the results it was evident that the NCS/SA/MC bead showed better Pb(II) uptake performance and regeneration for further use and hence it was found to be an efficient biosorbent for treating industrial effluent.	Methylcholanthrene	48-50	submaxillary gland androgen regulated protein 3B	Homo sapiens	70-76
30023533-5	2017	The fabricated ZrHCF@mFe3O4@mC-based aptasensor exhibited not only high selectivity because of the formation of aptamer-MUC1 complex but also good stability, acceptable reproducibility, and applicability.	Methylcholanthrene	28-30	mucin 1, cell surface associated	Homo sapiens	120-124
28978808-7	2017	MM patients with EBNA-1-specific mc IgG (14.0%) showed substantially greater bone marrow plasma cell infiltration and higher beta2-microglobulin and inflammation/infection-linked cytokine levels compared with other smoldering myeloma/MM patients.	Methylcholanthrene	33-35	beta-2-microglobulin	Homo sapiens	125-144
29065866-10	2017	RESULTS: Serum vaspin concentrations were significantly higher in the T2DM group than in the T2DM + MC group (F = 13.122, P &lt; 0.01).	Methylcholanthrene	100-102	serpin family A member 12	Homo sapiens	15-21
29039776-7	2017	Results of microarray and subsequent PCR analysis did reveal that estrogen metabolizing and synthesizing enzymes, such as CYP1B1 and aromatase, were increased by 3-MC in hFOB and osteosarcoma cell line, MG-63.	Methylcholanthrene	162-166	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	122-128
29039776-10	2017	The status of cell proliferation in both hFOB and MG-63 cells was stimulated by 3-MC and testosterone treatment, which was also inhibited by an estrogen blocker, aromatase inhibitor, or AhR antagonist.	Methylcholanthrene	80-84	aryl hydrocarbon receptor	Homo sapiens	186-189
29039776-1	2017	Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and beta-naphthoflavone (beta-NF).	Methylcholanthrene	144-164	aryl hydrocarbon receptor	Homo sapiens	0-25
29039776-1	2017	Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and beta-naphthoflavone (beta-NF).	Methylcholanthrene	144-164	aryl hydrocarbon receptor	Homo sapiens	27-30
29039776-1	2017	Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and beta-naphthoflavone (beta-NF).	Methylcholanthrene	166-170	aryl hydrocarbon receptor	Homo sapiens	0-25
29039776-1	2017	Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and beta-naphthoflavone (beta-NF).	Methylcholanthrene	166-170	aryl hydrocarbon receptor	Homo sapiens	27-30
28826232-5	2017	c-Met-targeted, tyrosine trimer-containing polyplexes were optimized into compacted rod structures with a size of 65-100 nm for pDNA and 35-40 nm for MC.	Methylcholanthrene	150-152	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
28744936-3	2017	In complement to the usual SB, we applied MC in a large cohort of 586 individuals with clinical FSHD.	Methylcholanthrene	42-44	FSHMD1A	Homo sapiens	96-100
28826232-6	2017	Notably, these MC polyplexes display a lack of cell cycle dependence of transfection and a ~200-fold enhanced gene transfer efficiency in c-Met-positive DU145 prostate carcinoma cultures over their tyrosine-free pDNA analogues.	Methylcholanthrene	15-17	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-143
28831024-8	2017	In addition, the serum levels of IL-6 and TNF-alpha were higher in the MC group than those in the NC group.	Methylcholanthrene	71-73	interleukin 6	Rattus norvegicus	33-37
28831024-8	2017	In addition, the serum levels of IL-6 and TNF-alpha were higher in the MC group than those in the NC group.	Methylcholanthrene	71-73	tumor necrosis factor	Rattus norvegicus	42-51
28831024-9	2017	The expression of MMP-9 protein in the AMs from rats was higher, and TIMP1 protein was lower in the MC group compared with the NC group.	Methylcholanthrene	100-102	matrix metallopeptidase 9	Rattus norvegicus	18-23
28831024-9	2017	The expression of MMP-9 protein in the AMs from rats was higher, and TIMP1 protein was lower in the MC group compared with the NC group.	Methylcholanthrene	100-102	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	69-74
28817805-4	2017	Here, we report that MC-GC synapses undergo a presynaptic, NMDA-receptor-independent form of long-term potentiation (LTP) that requires postsynaptic brain-derived neurotrophic factor (BDNF)/TrkB and presynaptic cyclic AMP (cAMP)/PKA signaling.	Methylcholanthrene	21-23	brain derived neurotrophic factor	Homo sapiens	149-182
28817805-4	2017	Here, we report that MC-GC synapses undergo a presynaptic, NMDA-receptor-independent form of long-term potentiation (LTP) that requires postsynaptic brain-derived neurotrophic factor (BDNF)/TrkB and presynaptic cyclic AMP (cAMP)/PKA signaling.	Methylcholanthrene	21-23	brain derived neurotrophic factor	Homo sapiens	184-188
28817805-4	2017	Here, we report that MC-GC synapses undergo a presynaptic, NMDA-receptor-independent form of long-term potentiation (LTP) that requires postsynaptic brain-derived neurotrophic factor (BDNF)/TrkB and presynaptic cyclic AMP (cAMP)/PKA signaling.	Methylcholanthrene	21-23	neurotrophic receptor tyrosine kinase 2	Homo sapiens	190-194
27997510-13	2017	CONCLUSION: We have identified two novel candidate genes, MAML1 and HSPG2, associating with MC.	Methylcholanthrene	92-94	mastermind like transcriptional coactivator 1	Homo sapiens	58-63
27997510-13	2017	CONCLUSION: We have identified two novel candidate genes, MAML1 and HSPG2, associating with MC.	Methylcholanthrene	92-94	heparan sulfate proteoglycan 2	Homo sapiens	68-73
28479091-3	2017	Activation-induced cytidine deaminase, one of the APOBEC members, was reported to deaminate methylated cytosine (mC) on DNA, and this mC deamination was proposed to be involved in the demethylation of mC for epigenetic regulation.	Methylcholanthrene	113-115	activation induced cytidine deaminase	Homo sapiens	0-37
28747761-5	2017	BMP2 covalently immobilized on an MC hydrogel (MC-BMP2) was prepared quantitatively by a simple biorthogonal reaction between alkyne groups on BMP2-OpgY and azide groups on MC-N3 via a Cu(I)-catalyzed click reaction.	Methylcholanthrene	34-36	bone morphogenetic protein 2	Homo sapiens	0-4
28747761-5	2017	BMP2 covalently immobilized on an MC hydrogel (MC-BMP2) was prepared quantitatively by a simple biorthogonal reaction between alkyne groups on BMP2-OpgY and azide groups on MC-N3 via a Cu(I)-catalyzed click reaction.	Methylcholanthrene	34-36	bone morphogenetic protein 2	Homo sapiens	50-54
28747761-5	2017	BMP2 covalently immobilized on an MC hydrogel (MC-BMP2) was prepared quantitatively by a simple biorthogonal reaction between alkyne groups on BMP2-OpgY and azide groups on MC-N3 via a Cu(I)-catalyzed click reaction.	Methylcholanthrene	34-36	bone morphogenetic protein 2	Homo sapiens	50-54
28731029-5	2017	In the MC-specific Nrp2 knockout mice, circuit formation of Nrp2+ MCs and odour-induced attractive social responses are impaired.	Methylcholanthrene	7-9	neuropilin 2	Mus musculus	19-23
28731029-5	2017	In the MC-specific Nrp2 knockout mice, circuit formation of Nrp2+ MCs and odour-induced attractive social responses are impaired.	Methylcholanthrene	7-9	neuropilin 2	Mus musculus	60-64
28686201-5	2017	In spleen, MC-and HGPC-fed dams had higher proportions of cytotoxic (CD8+) T cells expressing CD27, CD71 and CD127, total B cells (CD45RA+) and dendritic cells (OX6+OX62+), and produced less IL-6 and IFN-gamma after ConA than Control-fed dams (p &lt; 0.05).	Methylcholanthrene	11-13	CD27 molecule	Rattus norvegicus	94-98
28686201-5	2017	In spleen, MC-and HGPC-fed dams had higher proportions of cytotoxic (CD8+) T cells expressing CD27, CD71 and CD127, total B cells (CD45RA+) and dendritic cells (OX6+OX62+), and produced less IL-6 and IFN-gamma after ConA than Control-fed dams (p &lt; 0.05).	Methylcholanthrene	11-13	interleukin 6	Rattus norvegicus	191-195
28686201-5	2017	In spleen, MC-and HGPC-fed dams had higher proportions of cytotoxic (CD8+) T cells expressing CD27, CD71 and CD127, total B cells (CD45RA+) and dendritic cells (OX6+OX62+), and produced less IL-6 and IFN-gamma after ConA than Control-fed dams (p &lt; 0.05).	Methylcholanthrene	11-13	interferon gamma	Rattus norvegicus	200-209
28686201-6	2017	MC and HGPC LPS-stimulated splenocytes produced less IL-1beta and IL-6 than Control.	Methylcholanthrene	0-2	interleukin 1 beta	Rattus norvegicus	53-61
28686201-6	2017	MC and HGPC LPS-stimulated splenocytes produced less IL-1beta and IL-6 than Control.	Methylcholanthrene	0-2	interleukin 6	Rattus norvegicus	66-70
28658292-6	2017	RESULTS: Moderate to strong significant correlations (0.49 &lt; r &lt; 0.73) were found between MC and HRF, for both sexes, and correlation values were stable across the age groups.	Methylcholanthrene	96-98	tumor protein, translationally-controlled 1	Homo sapiens	103-106
28658292-7	2017	The MC model explained 74% of the HRF variance, with the locomotor component being the highest predictor for the entire sample (beta = .302; p &lt; .001).	Methylcholanthrene	4-6	tumor protein, translationally-controlled 1	Homo sapiens	34-37
28658292-11	2017	CONCLUSION: These results support the idea that: (1) the relationship between overall MC and HRF is strong and stable across childhood and early adolescence; (2) when accounting for the different MC components, boys and girls show different relationship patterns with HFR across age.	Methylcholanthrene	86-88	tumor protein, translationally-controlled 1	Homo sapiens	93-96
28479091-8	2017	A3A and A3H showed distinctively high deaminase activities on C and mC with relatively high selectivity for mC, whereas six other APOBEC members showed relatively low deaminase activity and selectivity for mC.	Methylcholanthrene	68-70	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	8-11
28479091-8	2017	A3A and A3H showed distinctively high deaminase activities on C and mC with relatively high selectivity for mC, whereas six other APOBEC members showed relatively low deaminase activity and selectivity for mC.	Methylcholanthrene	108-110	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	8-11
28799130-3	2017	In order to detect MC, the proposed method majorly includes pre-processing by colour correction, colour transformation followed by near-set based segmentation and post-processing for delineating only mucin regions from the histological images at 40x.	Methylcholanthrene	19-21	LOC100508689	Homo sapiens	200-205
28799130-10	2017	In addition, computation of percentage of mucin present in a histological image is provided for understanding the alteration of such diagnostic indicator in MC detection.	Methylcholanthrene	157-159	LOC100508689	Homo sapiens	42-47
28702904-5	2017	Therefore, the MC technology was modified for treatment of the PCB and PBDE containing soil including an efficient cooling system which could prevent the formation of PXDD/F during the destruction of PCBs and PBDEs.	Methylcholanthrene	15-17	pyruvate carboxylase	Homo sapiens	63-66
28634398-8	2017	Surprisingly, we found that the N51A hAID mutant, with no detectable activity on C, efficiently deaminated 5 mC, which may suggest different requirements for C and 5 mC deamination.	Methylcholanthrene	109-111	activation induced cytidine deaminase	Homo sapiens	37-41
28634398-10	2017	Consequently, we have proposed mechanisms that explain why wild type hAID more efficiently deaminates C than 5 mC in vitro and why 5 hmC is not deaminated.	Methylcholanthrene	111-113	activation induced cytidine deaminase	Homo sapiens	69-73
28479091-3	2017	Activation-induced cytidine deaminase, one of the APOBEC members, was reported to deaminate methylated cytosine (mC) on DNA, and this mC deamination was proposed to be involved in the demethylation of mC for epigenetic regulation.	Methylcholanthrene	134-136	activation induced cytidine deaminase	Homo sapiens	0-37
28479091-3	2017	Activation-induced cytidine deaminase, one of the APOBEC members, was reported to deaminate methylated cytosine (mC) on DNA, and this mC deamination was proposed to be involved in the demethylation of mC for epigenetic regulation.	Methylcholanthrene	134-136	activation induced cytidine deaminase	Homo sapiens	0-37
28479091-4	2017	The mC deamination activity is later demonstrated for APOBEC3A (A3A) and more recently for APOBEC3B and APOBEC3H (A3H).	Methylcholanthrene	4-6	apolipoprotein B mRNA editing enzyme catalytic subunit 3A	Homo sapiens	54-62
28479091-4	2017	The mC deamination activity is later demonstrated for APOBEC3A (A3A) and more recently for APOBEC3B and APOBEC3H (A3H).	Methylcholanthrene	4-6	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	91-99
28479091-4	2017	The mC deamination activity is later demonstrated for APOBEC3A (A3A) and more recently for APOBEC3B and APOBEC3H (A3H).	Methylcholanthrene	4-6	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	104-112
28479091-4	2017	The mC deamination activity is later demonstrated for APOBEC3A (A3A) and more recently for APOBEC3B and APOBEC3H (A3H).	Methylcholanthrene	4-6	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	114-117
28384415-5	2017	MC strongly induced CYP1A1 mRNA levels and markedly downregulated CYP2C8 mRNA levels in HepaRG cells.	Methylcholanthrene	0-2	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	20-26
28574475-5	2017	At 3 weeks, MC and HGPC pups were heavier and their splenocytes had a higher proportion of helper T cells expressing CD25 and CD28 and produced less interferon gamma (IFN-gamma) and tumor-necrosis factor-alpha (TNF-alpha) after Concanavalin A stimulation vs. Control pups (p &lt; 0.05).	Methylcholanthrene	12-14	Cd28 molecule	Rattus norvegicus	126-130
28574475-5	2017	At 3 weeks, MC and HGPC pups were heavier and their splenocytes had a higher proportion of helper T cells expressing CD25 and CD28 and produced less interferon gamma (IFN-gamma) and tumor-necrosis factor-alpha (TNF-alpha) after Concanavalin A stimulation vs. Control pups (p &lt; 0.05).	Methylcholanthrene	12-14	interferon gamma	Rattus norvegicus	149-176
28574475-5	2017	At 3 weeks, MC and HGPC pups were heavier and their splenocytes had a higher proportion of helper T cells expressing CD25 and CD28 and produced less interferon gamma (IFN-gamma) and tumor-necrosis factor-alpha (TNF-alpha) after Concanavalin A stimulation vs. Control pups (p &lt; 0.05).	Methylcholanthrene	12-14	tumor necrosis factor	Rattus norvegicus	211-220
28574475-6	2017	At 10 weeks, MC and HGPC offspring had a lower proportion of macrophages and dendritic cells and produced less interleukin (IL)-1beta but more IL-10 after lipopolysaccharide stimulation vs. Control pups (p &lt; 0.05).	Methylcholanthrene	13-15	interleukin 1 beta	Rattus norvegicus	111-133
28574475-6	2017	At 10 weeks, MC and HGPC offspring had a lower proportion of macrophages and dendritic cells and produced less interleukin (IL)-1beta but more IL-10 after lipopolysaccharide stimulation vs. Control pups (p &lt; 0.05).	Methylcholanthrene	13-15	interleukin 10	Rattus norvegicus	143-148
28384415-0	2017	Downregulation of cytochrome P450 2C8 by 3-methylcholanthrene in human hepatocellular carcinoma cell lines.	Methylcholanthrene	41-61	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	18-37
28384415-5	2017	MC strongly induced CYP1A1 mRNA levels and markedly downregulated CYP2C8 mRNA levels in HepaRG cells.	Methylcholanthrene	0-2	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	66-72
28384415-1	2017	The marked induction of cytochromes P450 such as CYP1A1 caused by polycyclic aromatic hydrocarbons (PAHs) like 3-methylcholanthrene (MC) is often accompanied by suppression of other hepatic P450s.	Methylcholanthrene	111-131	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-40
28384415-1	2017	The marked induction of cytochromes P450 such as CYP1A1 caused by polycyclic aromatic hydrocarbons (PAHs) like 3-methylcholanthrene (MC) is often accompanied by suppression of other hepatic P450s.	Methylcholanthrene	111-131	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	49-55
28384415-1	2017	The marked induction of cytochromes P450 such as CYP1A1 caused by polycyclic aromatic hydrocarbons (PAHs) like 3-methylcholanthrene (MC) is often accompanied by suppression of other hepatic P450s.	Methylcholanthrene	133-135	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-40
28384415-1	2017	The marked induction of cytochromes P450 such as CYP1A1 caused by polycyclic aromatic hydrocarbons (PAHs) like 3-methylcholanthrene (MC) is often accompanied by suppression of other hepatic P450s.	Methylcholanthrene	133-135	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	49-55
28384415-3	2017	MC suppresses mRNA levels for CYP2C8, an important human P450, in cultured human hepatocytes.	Methylcholanthrene	0-2	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	30-36
28384415-6	2017	Although MC also suppressed CYP2C8 mRNA levels in the HepG2 human hepatocellular carcinoma cell line, basal CYP2C8 expression was extremely low.	Methylcholanthrene	9-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	28-34
28384415-3	2017	MC suppresses mRNA levels for CYP2C8, an important human P450, in cultured human hepatocytes.	Methylcholanthrene	0-2	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	57-61
28247413-6	2017	MC-derived CAFs showed activation of Smad-dependent TGF-beta signalling, which was disrupted in OvCa cells, despite their elevated TGF-beta production.	Methylcholanthrene	0-2	transforming growth factor, beta 1	Mus musculus	52-60
28384415-4	2017	To avoid hepatocyte lot-to-lot variability, we assessed CYP2C8 regulation by MC in HepaRG cells, a terminally differentiated human hepatocellular carcinoma cell line that maintains high P450 expression.	Methylcholanthrene	77-79	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	56-62
28247413-6	2017	MC-derived CAFs showed activation of Smad-dependent TGF-beta signalling, which was disrupted in OvCa cells, despite their elevated TGF-beta production.	Methylcholanthrene	0-2	transforming growth factor, beta 1	Mus musculus	131-139
28247413-8	2017	Together, these results indicate that bidirectional communication between OvCa cells and MC-derived CAFs, via TGF-beta-mediated MMT, seems to be crucial to form a suitable metastatic niche.	Methylcholanthrene	89-91	transforming growth factor, beta 1	Mus musculus	110-118
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	thymoma viral proto-oncogene 1	Mus musculus	309-313
28525768-2	2017	(2017) identify mitochondrial chaperonin HSP60 as a direct target of myrtucommulone (MC), a nonprenylated acylphloroglucinol that is well known for its apoptotic activity in cancer cells.	Methylcholanthrene	85-87	heat shock protein family D (Hsp60) member 1	Homo sapiens	41-46
28525768-3	2017	The authors propose MC as a chemical probe to study HSP60 biology and a potential chemotherapeutic agent in treating cancer and other HSP60-associated diseases.	Methylcholanthrene	20-22	heat shock protein family D (Hsp60) member 1	Homo sapiens	52-57
28525768-3	2017	The authors propose MC as a chemical probe to study HSP60 biology and a potential chemotherapeutic agent in treating cancer and other HSP60-associated diseases.	Methylcholanthrene	20-22	heat shock protein family D (Hsp60) member 1	Homo sapiens	134-139
28138783-14	2017	This provides insight into the pain generator at MC levels and informs novel therapeutic targets for treatment of MC-associated LBP.	Methylcholanthrene	114-116	lipopolysaccharide binding protein	Homo sapiens	128-131
28229459-11	2017	Albeit located in parallel partitions of the olfactory system, 5-HT largely elicited MC excitation in the MOB while it evoked two different kinetic rates of MC inhibition in the AOB.	Methylcholanthrene	85-87	sphingomyelin synthase 1	Mus musculus	106-109
28229459-12	2017	Using a combination of pharmacological agents, we found that the MC excitatory responses in the MOB were mediated by 5-HT2A receptors through a direct activation.	Methylcholanthrene	65-67	sphingomyelin synthase 1	Mus musculus	96-99
28229459-12	2017	Using a combination of pharmacological agents, we found that the MC excitatory responses in the MOB were mediated by 5-HT2A receptors through a direct activation.	Methylcholanthrene	65-67	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	117-123
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	28-48	aryl-hydrocarbon receptor	Mus musculus	69-94
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	28-48	aryl-hydrocarbon receptor	Mus musculus	96-99
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	28-48	thymoma viral proto-oncogene 1	Mus musculus	118-121
27442426-7	2017	Coimmunoprecipitation assay results indicated that 3-MC significantly reduced the interaction between eNOS and its regulatory proteins, including Akt1 and HSP90, but increased the interaction between eNOS and caveolin-1.	Methylcholanthrene	51-55	nitric oxide synthase 3, endothelial cell	Mus musculus	102-106
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	50-53	aryl-hydrocarbon receptor	Mus musculus	69-94
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	50-53	aryl-hydrocarbon receptor	Mus musculus	96-99
27442426-2	2017	We previously reported that 3-methylcholanthrene (3MC) activates the aryl hydrocarbon receptor (AhR) and reduces PI3K/Akt phosphorylation.	Methylcholanthrene	50-53	thymoma viral proto-oncogene 1	Mus musculus	118-121
27442426-3	2017	This study investigated the mechanism underlying the downregulatory effects of 3-MC on nitric oxide (NO) production occurring through the AhR/RhoA/Akt-mediated mechanism.	Methylcholanthrene	79-83	aryl-hydrocarbon receptor	Mus musculus	138-141
27442426-7	2017	Coimmunoprecipitation assay results indicated that 3-MC significantly reduced the interaction between eNOS and its regulatory proteins, including Akt1 and HSP90, but increased the interaction between eNOS and caveolin-1.	Methylcholanthrene	51-55	thymoma viral proto-oncogene 1	Mus musculus	146-150
27442426-7	2017	Coimmunoprecipitation assay results indicated that 3-MC significantly reduced the interaction between eNOS and its regulatory proteins, including Akt1 and HSP90, but increased the interaction between eNOS and caveolin-1.	Methylcholanthrene	51-55	heat shock protein, 3	Mus musculus	155-160
27442426-3	2017	This study investigated the mechanism underlying the downregulatory effects of 3-MC on nitric oxide (NO) production occurring through the AhR/RhoA/Akt-mediated mechanism.	Methylcholanthrene	79-83	ras homolog family member A	Mus musculus	142-146
27442426-3	2017	This study investigated the mechanism underlying the downregulatory effects of 3-MC on nitric oxide (NO) production occurring through the AhR/RhoA/Akt-mediated mechanism.	Methylcholanthrene	79-83	thymoma viral proto-oncogene 1	Mus musculus	147-150
27442426-4	2017	The mechanism underlying the effects of 3-MC on eNOS activity and blood pressure was examined in vitro and in vivo through genetic and pharmacological approaches.	Methylcholanthrene	40-44	nitric oxide synthase 3, endothelial cell	Mus musculus	48-52
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	heat shock protein, 3	Mus musculus	37-58
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	heat shock protein, 3	Mus musculus	60-65
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	caveolin 1, caveolae protein	Mus musculus	68-78
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	nitric oxide synthase 3, endothelial cell	Mus musculus	92-96
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	aryl-hydrocarbon receptor	Mus musculus	137-140
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	ras homolog family member A	Mus musculus	141-145
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	nitric oxide synthase 3, endothelial cell	Mus musculus	242-246
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	aryl-hydrocarbon receptor	Mus musculus	275-278
27442426-5	2017	Results indicated that 3-MC modified heat shock protein 90 (HSP90), caveolin-1, dynein, and eNOS mRNA and protein expression through the AhR/RhoA-dependent mechanism in mouse cerebral vascular endothelial cells (MCVECs) and that 3-MC reduced eNOS phosphorylation through the AhR/RhoA-mediated inactivation of Akt1.	Methylcholanthrene	23-27	ras homolog family member A	Mus musculus	279-283
27442426-7	2017	Coimmunoprecipitation assay results indicated that 3-MC significantly reduced the interaction between eNOS and its regulatory proteins, including Akt1 and HSP90, but increased the interaction between eNOS and caveolin-1.	Methylcholanthrene	51-55	nitric oxide synthase 3, endothelial cell	Mus musculus	200-204
27442426-7	2017	Coimmunoprecipitation assay results indicated that 3-MC significantly reduced the interaction between eNOS and its regulatory proteins, including Akt1 and HSP90, but increased the interaction between eNOS and caveolin-1.	Methylcholanthrene	51-55	caveolin 1, caveolae protein	Mus musculus	209-219
27442426-8	2017	Immunofluorescence and Western blot analysis revealed that 3-MC reduced the amount of membrane-bound activated eNOS, and a modified Griess assay revealed that 3-MC concomitantly reduced NO production.	Methylcholanthrene	59-63	nitric oxide synthase 3, endothelial cell	Mus musculus	111-115
28380363-5	2017	We demonstrate that this spatial control of MC remodeling depends on the antagonist activity of the Hox genes abdominal-A and Abdominal-B.	Methylcholanthrene	44-46	tinman	Drosophila melanogaster	100-103
28216549-2	2017	Most candidates for MC have severe heart failure (HF) with increased N-terminal pro-B-type natriuretic peptide (NT-pro BNP) levels.	Methylcholanthrene	20-22	natriuretic peptide B	Homo sapiens	119-122
28216549-5	2017	NT-pro BNP responders were defined as patients whose NT-pro BNP levels decreased by &gt; 30% at 6 months after MC.	Methylcholanthrene	111-113	natriuretic peptide B	Homo sapiens	7-10
28216549-12	2017	In conclusion, NT-pro BNP levels significantly decreased after MC.	Methylcholanthrene	63-65	natriuretic peptide B	Homo sapiens	22-25
28216549-13	2017	DM and RVSD were determinants of NT-pro BNP nonresponse after the MC procedure.	Methylcholanthrene	66-68	natriuretic peptide B	Homo sapiens	40-43
28380363-5	2017	We demonstrate that this spatial control of MC remodeling depends on the antagonist activity of the Hox genes abdominal-A and Abdominal-B.	Methylcholanthrene	44-46	abdominal A	Drosophila melanogaster	110-121
28380363-5	2017	We demonstrate that this spatial control of MC remodeling depends on the antagonist activity of the Hox genes abdominal-A and Abdominal-B.	Methylcholanthrene	44-46	Abdominal B	Drosophila melanogaster	126-137
28192119-4	2017	The toxicity profiles of the classical AhR ligands such as 3-methylcholanthrene and dioxins limit their use as a therapeutic agent in humans.	Methylcholanthrene	59-79	aryl hydrocarbon receptor	Homo sapiens	39-42
28160151-8	2017	When compared with the PD group without MC, both PD with MC and PARK2 showed a markedly smaller size of NM-rich SNc area.	Methylcholanthrene	40-42	parkin RBR E3 ubiquitin protein ligase	Homo sapiens	64-69
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	146-151
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	153-158
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	160-165
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-172
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	NRAS proto-oncogene, GTPase	Homo sapiens	178-183
28062358-3	2017	The results of qPCR and Western blotting showed that MC-LR-exposure at non- or sub-cytotoxic concentrations promoted the expressions of oncogenes c-fos, c-jun, c-myc, c-met, and N-ras while suppressed tumor-suppressor gene PTEN in HepG2 cells at both transcription and protein levels.	Methylcholanthrene	53-55	phosphatase and tensin homolog	Homo sapiens	223-227
28132505-5	2017	Evidence for a strong spin-selection in the chiral semiconductors is presented by magnetic conducting (mc-)AFM measurements, in which chiral and achiral Zn-porphyrins are compared.	Methylcholanthrene	103-105	spindlin 1	Homo sapiens	22-26
28323876-12	2017	Success of PIM1 delivery and integration into mCPCs in vitro and cardiomyocytes in vivo by MC highlights the possibility of a non-cell based therapeutic approach for treatment of ischemic heart disease and MI.	Methylcholanthrene	91-93	proviral integration site 1	Mus musculus	11-15
28298363-9	2017	Taken together, these results suggest that the EC-MC interaction potentiates BMP9 signaling both in ECs and MCs and plays a critical role in the maintenance of proper vessel functions.	Methylcholanthrene	50-52	growth differentiation factor 2	Homo sapiens	77-81
28241520-3	2017	The modified MC-FTS allows us to measure the wavelength dependence of the GP and thus that of the optical rotation angle due to the sample.	Methylcholanthrene	13-15	AKT interacting protein	Homo sapiens	16-19
28179517-4	2017	Specifically, we link increases in cellular apoptosis and TGF-BR2 signalling to MC breakdown in opossums.	Methylcholanthrene	80-82	transforming growth factor beta receptor 2	Homo sapiens	58-65
28344878-3	2017	Cish-deficient mice were highly resistant to methylcholanthrene-induced sarcoma formation and protected from lung metastasis of B16F10 melanoma and RM-1 prostate carcinoma cells.	Methylcholanthrene	45-63	cytokine inducible SH2-containing protein	Mus musculus	0-4
28112929-2	2017	This replication is initiated by the recognition of hemimethylated CpG sites and further flipping of methylated cytosines (mC) by the Set and Ring Associated (SRA) domain of UHRF1.	Methylcholanthrene	123-125	macrophage scavenger receptor 1	Homo sapiens	159-162
28112929-2	2017	This replication is initiated by the recognition of hemimethylated CpG sites and further flipping of methylated cytosines (mC) by the Set and Ring Associated (SRA) domain of UHRF1.	Methylcholanthrene	123-125	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	174-179
28112929-3	2017	Although crystallography has shed light on the mechanism of mC flipping by SRA, tools are required to monitor in real time how SRA reads DNA and flips the modified nucleobase.	Methylcholanthrene	60-62	macrophage scavenger receptor 1	Homo sapiens	75-78
28179517-5	2017	We demonstrate that a simple change in TGF-beta signalling is sufficient to inhibit MC breakdown during opossum development, indicating that changes in TGF-beta signalling might be key during mammalian evolution.	Methylcholanthrene	84-86	transforming growth factor beta 1	Homo sapiens	39-47
28179517-5	2017	We demonstrate that a simple change in TGF-beta signalling is sufficient to inhibit MC breakdown during opossum development, indicating that changes in TGF-beta signalling might be key during mammalian evolution.	Methylcholanthrene	84-86	transforming growth factor beta 1	Homo sapiens	152-160
28217242-5	2017	Here this is tested via FRET to mC arising from the association of glutathione (GSH) and glutathione S-transferase (GST) with an intrinsically homogeneous and more mobile donor Oregon Green 488 (OG).	Methylcholanthrene	32-34	glutathione S-transferase kappa 1	Homo sapiens	89-114
27802782-5	2017	More importantly, it was demonstrated that delivery of 5 mug of MC.CD20 to mouse liver via hydrodynamic injection resulted in both the expression of a therapeutic level of anti-CD3/CD20 throughout the 32-day experiment and effective anticancer activity in a B-cell lymphoma xenograft mouse model.	Methylcholanthrene	64-66	membrane-spanning 4-domains, subfamily A, member 1	Mus musculus	67-71
27802782-5	2017	More importantly, it was demonstrated that delivery of 5 mug of MC.CD20 to mouse liver via hydrodynamic injection resulted in both the expression of a therapeutic level of anti-CD3/CD20 throughout the 32-day experiment and effective anticancer activity in a B-cell lymphoma xenograft mouse model.	Methylcholanthrene	64-66	CD3 antigen, epsilon polypeptide	Mus musculus	177-180
27802782-5	2017	More importantly, it was demonstrated that delivery of 5 mug of MC.CD20 to mouse liver via hydrodynamic injection resulted in both the expression of a therapeutic level of anti-CD3/CD20 throughout the 32-day experiment and effective anticancer activity in a B-cell lymphoma xenograft mouse model.	Methylcholanthrene	64-66	membrane-spanning 4-domains, subfamily A, member 1	Mus musculus	181-185
29957982-12	2017	The proteinsof TLR4, MyD88, IRAK1, TRAF6, NF-kappaB, TNF-alpha were highly expressed in MC group, and those proteinsdeclined in high and moderate dose XFC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	88-90	toll-like receptor 4	Rattus norvegicus	15-19
29957982-12	2017	The proteinsof TLR4, MyD88, IRAK1, TRAF6, NF-kappaB, TNF-alpha were highly expressed in MC group, and those proteinsdeclined in high and moderate dose XFC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	88-90	MYD88, innate immune signal transduction adaptor	Rattus norvegicus	21-26
29957982-12	2017	The proteinsof TLR4, MyD88, IRAK1, TRAF6, NF-kappaB, TNF-alpha were highly expressed in MC group, and those proteinsdeclined in high and moderate dose XFC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	88-90	interleukin-1 receptor-associated kinase 1	Rattus norvegicus	28-33
29957982-12	2017	The proteinsof TLR4, MyD88, IRAK1, TRAF6, NF-kappaB, TNF-alpha were highly expressed in MC group, and those proteinsdeclined in high and moderate dose XFC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	88-90	TNF receptor associated factor 6	Rattus norvegicus	35-40
29957982-12	2017	The proteinsof TLR4, MyD88, IRAK1, TRAF6, NF-kappaB, TNF-alpha were highly expressed in MC group, and those proteinsdeclined in high and moderate dose XFC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	88-90	tumor necrosis factor	Rattus norvegicus	53-62
28217242-5	2017	Here this is tested via FRET to mC arising from the association of glutathione (GSH) and glutathione S-transferase (GST) with an intrinsically homogeneous and more mobile donor Oregon Green 488 (OG).	Methylcholanthrene	32-34	glutathione S-transferase kappa 1	Homo sapiens	116-119
26917494-8	2017	In the OTM + MC group on day 7 of tooth movement, the expression of TGF-beta1 and VEGF was significantly reduced whereas the expression of bFGF was increased in PL.	Methylcholanthrene	13-15	transforming growth factor, beta 1	Rattus norvegicus	68-77
27039926-7	2017	Genes involved in positive regulation of apoptosis, negative regulator of apoptosis, death-like, mitochondrial apoptotic signaling, induction of apoptosis through DR3 and DR4/5 death receptors, and anti-apoptosis were highly affected in MC-A+cisplatin or MC-A+epirubicin combinations compared to each agent only.	Methylcholanthrene	237-241	tumor necrosis factor receptor superfamily, member 25	Mus musculus	163-166
29061058-11	2017	Comparing with MC group, the PI3K, Akt and mTOR gene and protein expression of miRNA group were significantly up-regulated and the P53 expression was significantly down-regulated (p&lt;0.05, respectively).	Methylcholanthrene	15-17	AKT serine/threonine kinase 1	Homo sapiens	35-38
29061058-11	2017	Comparing with MC group, the PI3K, Akt and mTOR gene and protein expression of miRNA group were significantly up-regulated and the P53 expression was significantly down-regulated (p&lt;0.05, respectively).	Methylcholanthrene	15-17	mechanistic target of rapamycin kinase	Homo sapiens	43-47
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	Janus kinase 1	Rattus norvegicus	30-34
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	Janus kinase 2	Rattus norvegicus	36-40
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	signal transducer and activator of transcription 1	Rattus norvegicus	42-47
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	signal transducer and activator of transcription 3	Rattus norvegicus	49-54
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	signal transducer and activator of transcription 5A	Rattus norvegicus	59-64
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	suppressor of cytokine signaling 1	Rattus norvegicus	95-100
28950251-9	2017	The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group.	Methylcholanthrene	129-131	suppressor of cytokine signaling 3	Rattus norvegicus	105-110
27055685-9	2017	Other AhR ligands (3-methylcholanthrene and PCB 126) decreased ADH1B, 4 and 6 mRNAs by more than 78 and 55 %, respectively (p &lt; 0.01).	Methylcholanthrene	19-39	aryl hydrocarbon receptor	Homo sapiens	6-9
27055685-9	2017	Other AhR ligands (3-methylcholanthrene and PCB 126) decreased ADH1B, 4 and 6 mRNAs by more than 78 and 55 %, respectively (p &lt; 0.01).	Methylcholanthrene	19-39	alcohol dehydrogenase 1B (class I), beta polypeptide	Homo sapiens	63-68
26917494-8	2017	In the OTM + MC group on day 7 of tooth movement, the expression of TGF-beta1 and VEGF was significantly reduced whereas the expression of bFGF was increased in PL.	Methylcholanthrene	13-15	vascular endothelial growth factor A	Rattus norvegicus	82-86
26917494-8	2017	In the OTM + MC group on day 7 of tooth movement, the expression of TGF-beta1 and VEGF was significantly reduced whereas the expression of bFGF was increased in PL.	Methylcholanthrene	13-15	fibroblast growth factor 2	Rattus norvegicus	139-143
27973371-4	2016	MC was the biofilm carrier selected due to allowing the development of larger aerobic and anaerobic layers in the biofilm (896 and 1,058 mum, respectively).	Methylcholanthrene	0-2	latexin	Homo sapiens	137-140
29403536-7	2017	The serum SCF level was lower in the MC group than in the NC group; this effect was ameliorated in the YRD-treated mice.	Methylcholanthrene	37-39	kit ligand	Mus musculus	10-13
27491640-4	2017	We analyzed genomic distribution of SB and LV integrations and show that a significantly higher proportion of MC-derived CAR transposons compared with LV integrants had occurred outside of highly expressed and cancer-related genes into genomic safe harbor loci that are not expected to cause mutagenesis or genotoxicity.	Methylcholanthrene	110-112	nuclear receptor subfamily 1 group I member 3	Homo sapiens	121-124
27435790-7	2016	However, there was a statistically significant correlation between the individual values of the plasma 8-OHdG (PRE) versus IL-10 (PRE) for the MC and LC patients (r = 0.214, p = 0.037).	Methylcholanthrene	143-145	interleukin 10	Homo sapiens	123-128
27435790-8	2016	There was also a statistically significant correlation between the individual values of the plasma 8-OHdG (POP2) versus IL-1beta (POP2) for the MC and LC patients (r = 0.25, p = 0.01).	Methylcholanthrene	144-146	pyrin domain containing 2	Homo sapiens	107-111
27435790-8	2016	There was also a statistically significant correlation between the individual values of the plasma 8-OHdG (POP2) versus IL-1beta (POP2) for the MC and LC patients (r = 0.25, p = 0.01).	Methylcholanthrene	144-146	interleukin 1 beta	Homo sapiens	120-128
27435790-8	2016	There was also a statistically significant correlation between the individual values of the plasma 8-OHdG (POP2) versus IL-1beta (POP2) for the MC and LC patients (r = 0.25, p = 0.01).	Methylcholanthrene	144-146	pyrin domain containing 2	Homo sapiens	130-134
27806426-7	2017	In the over-MC group, a subgroup of patients with AFP level &lt;115 ng/ml and PET-negative status (n = 22) had a significantly lower 5-year recurrence rate than the other patients (n = 27, 19% vs. 53%, P = 0.019).	Methylcholanthrene	12-14	alpha fetoprotein	Homo sapiens	50-53
27534815-0	2016	Biochemical Characterization of APOBEC3H Variants: Implications for Their HIV-1 Restriction Activity and mC Modification.	Methylcholanthrene	105-107	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	32-40
27897179-3	2016	Here we show by means of optogenetics that MC in layers II/III of the mouse primary somatosensory cortex are inhibited by both parvalbumin (PV)- and vasoactive intestinal polypeptide (VIP)-expressing cells.	Methylcholanthrene	43-45	parvalbumin	Mus musculus	127-138
27897179-3	2016	Here we show by means of optogenetics that MC in layers II/III of the mouse primary somatosensory cortex are inhibited by both parvalbumin (PV)- and vasoactive intestinal polypeptide (VIP)-expressing cells.	Methylcholanthrene	43-45	vasoactive intestinal polypeptide	Mus musculus	149-182
27897179-3	2016	Here we show by means of optogenetics that MC in layers II/III of the mouse primary somatosensory cortex are inhibited by both parvalbumin (PV)- and vasoactive intestinal polypeptide (VIP)-expressing cells.	Methylcholanthrene	43-45	vasoactive intestinal polypeptide	Mus musculus	184-187
27534815-9	2016	Moreover, mC deamination of A3H displayed a strong preference for the sequence motif of T-mCpG-C/G, which may suggest a potential role in genomic mC modification at the characteristic "CpG" island motif.	Methylcholanthrene	10-12	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	28-31
27534815-9	2016	Moreover, mC deamination of A3H displayed a strong preference for the sequence motif of T-mCpG-C/G, which may suggest a potential role in genomic mC modification at the characteristic "CpG" island motif.	Methylcholanthrene	90-92	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	28-31
27792226-5	2016	The MC curves at low temperature exhibited a complex line shape, which indicated that intersystem crossing, TPtI, TtPI, and TCI occurred simultaneously in the device.	Methylcholanthrene	4-6	latexin	Homo sapiens	124-127
27857218-4	2016	Focal knockdown of spinal Tet1 expression decreased Tet1 binding and 5 hmC enrichment, further increased 5 mC enrichment at CpG sites in the bdnf promoter and decreased spinal BDNF expression accompanied by the alleviation of the developed allodynia.	Methylcholanthrene	72-74	tet methylcytosine dioxygenase 1	Rattus norvegicus	26-30
27620500-10	2016	Nematode Cdc37, which does not require the N-terminal Hsp90 domain for binding, can form a ternary complex with the MC construct of Hsp90, which lacks the aggregation propensity of sB-Raf.	Methylcholanthrene	116-118	cell division cycle 37, HSP90 cochaperone	Homo sapiens	9-14
27603089-6	2016	In consequence, an MC-MP2/cc-pVDZ calculation of a benzene dimer is 2700 times faster on 256 GPUs (using 2048 electron pairs) than on two CPUs, each with 8 cores (which can use only up to 256 pairs effectively).	Methylcholanthrene	19-21	tryptase pseudogene 1	Homo sapiens	22-25
27872682-10	2016	However, most patients with recurrent HCC considered for SLT are untransplantable cases due to HCC recurrence beyond MC or comorbidity.	Methylcholanthrene	117-119	HCC	Homo sapiens	38-41
26526840-5	2016	In this study, PARP1 and poly-ADP-ribose (PAR) were highly expressed in GO-treated MCs, and this was accompanied by loss of MC viability, excessive generation of reactive oxygen species (ROS), collapse of mitochondria membrane potential (DeltaPsim), and redistribution of the mitochondrial downstream pathway-related molecules Bax and cytochrome c, eventually causing MC death.	Methylcholanthrene	83-85	poly (ADP-ribose) polymerase 1	Rattus norvegicus	15-20
26526840-5	2016	In this study, PARP1 and poly-ADP-ribose (PAR) were highly expressed in GO-treated MCs, and this was accompanied by loss of MC viability, excessive generation of reactive oxygen species (ROS), collapse of mitochondria membrane potential (DeltaPsim), and redistribution of the mitochondrial downstream pathway-related molecules Bax and cytochrome c, eventually causing MC death.	Methylcholanthrene	124-126	poly (ADP-ribose) polymerase 1	Rattus norvegicus	15-20
26526840-9	2016	We conclude that GO treatment induces activation of PARP1, which causes MC damage via mitochondrial mediation.	Methylcholanthrene	72-74	poly (ADP-ribose) polymerase 1	Rattus norvegicus	52-57
26526840-10	2016	PARP1 plays a pivotal role in GO-induced MC death, at least in part, via the caspase-3 cascade.	Methylcholanthrene	41-43	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-5
26526840-10	2016	PARP1 plays a pivotal role in GO-induced MC death, at least in part, via the caspase-3 cascade.	Methylcholanthrene	41-43	caspase 3	Rattus norvegicus	77-86
27356039-3	2016	MeCP2-MBD binds to mC-containing variants of double stranded CpG stronger than any other cytosine modified CpG with the strongest affinity to mC/mC.	Methylcholanthrene	19-21	methyl-CpG binding protein 2	Homo sapiens	0-5
27356039-3	2016	MeCP2-MBD binds to mC-containing variants of double stranded CpG stronger than any other cytosine modified CpG with the strongest affinity to mC/mC.	Methylcholanthrene	142-144	methyl-CpG binding protein 2	Homo sapiens	0-5
27356039-3	2016	MeCP2-MBD binds to mC-containing variants of double stranded CpG stronger than any other cytosine modified CpG with the strongest affinity to mC/mC.	Methylcholanthrene	142-144	methyl-CpG binding protein 2	Homo sapiens	0-5
27741278-4	2016	When incorporated into a DNA vaccine, signaling by the MC adjuvant increased antigen-specific CD8+ T cells and promoted elimination of pre-established tumors.	Methylcholanthrene	55-57	CD8a molecule	Homo sapiens	94-97
27741278-6	2016	In particular, MC adjuvant-modified keratinocytes increased inflammatory cytokine secretion, upregulated surface MHC class I, and were able to increase in vitro and in vivo priming of antigen-specific CD8+ T cells.	Methylcholanthrene	15-17	CD8a molecule	Homo sapiens	201-204
27741278-8	2016	Altogether, our data support a mechanism by which MC signaling activates an inflammatory phenotype in atypical antigen-presenting cells within the cutaneous vaccination site, leading to an enhanced CD8+ T cell response against DNA vaccine-encoded antigens, through both CD8alpha+/CD103+ dendritic cell-dependent and independent pathways.	Methylcholanthrene	50-52	CD8a molecule	Homo sapiens	198-201
27741278-8	2016	Altogether, our data support a mechanism by which MC signaling activates an inflammatory phenotype in atypical antigen-presenting cells within the cutaneous vaccination site, leading to an enhanced CD8+ T cell response against DNA vaccine-encoded antigens, through both CD8alpha+/CD103+ dendritic cell-dependent and independent pathways.	Methylcholanthrene	50-52	CD8a molecule	Homo sapiens	270-278
27620500-10	2016	Nematode Cdc37, which does not require the N-terminal Hsp90 domain for binding, can form a ternary complex with the MC construct of Hsp90, which lacks the aggregation propensity of sB-Raf.	Methylcholanthrene	116-118	heat shock protein 90 alpha family class A member 1	Homo sapiens	132-137
27620500-10	2016	Nematode Cdc37, which does not require the N-terminal Hsp90 domain for binding, can form a ternary complex with the MC construct of Hsp90, which lacks the aggregation propensity of sB-Raf.	Methylcholanthrene	116-118	zinc fingers and homeoboxes 2	Homo sapiens	184-187
27295070-6	2016	Delivered beta-galactosidase, inactive within the MC complex, became enzymatically active within cells to convert a prodrug.	Methylcholanthrene	50-52	galactosidase beta 1	Homo sapiens	10-28
27193975-5	2016	In line with this, the MC could be transferred to the level of immunofluorescence stainings for iNOS and CCL27 protein on paraffin-embedded sections, where patients were diagnosed with sensitivity and specificity &gt;88%.	Methylcholanthrene	23-25	nitric oxide synthase 2	Homo sapiens	96-100
27193975-5	2016	In line with this, the MC could be transferred to the level of immunofluorescence stainings for iNOS and CCL27 protein on paraffin-embedded sections, where patients were diagnosed with sensitivity and specificity &gt;88%.	Methylcholanthrene	23-25	C-C motif chemokine ligand 27	Homo sapiens	105-110
27478537-5	2016	HCC that presents beyond MC initially can be downstaged with locoregional therapy (LRT).	Methylcholanthrene	25-27	HCC	Homo sapiens	0-3
27711870-2	2016	Three potential surrogates for HGL; Rhizopus Oryzae Lipase (ROL), Rabbit Gastric Lipase (RGL) and recombinant HGL (rHGL), were used to catalyze the in vitro digestion of two infant formulas (a medium-chain triacylglyceride enriched formula (MC-IF) and a predominantly long-chain triacylglyceride formula (LC-IF)).	Methylcholanthrene	241-243	lipase F, gastric type	Homo sapiens	110-113
27711870-8	2016	Digestion of a MC-IF by HGL in vivo showed that MC-FAs are preferentially released, but some LC-FAs are also released.	Methylcholanthrene	15-17	lipase F, gastric type	Homo sapiens	24-27
27666706-1	2016	Objective: To investigate the effect of interleukin-4 (IL-4) stimulation on the expression of FcepsilonRIalpha and NK-1R on mature mast cells(MC) cultured and differentiated from mouse bone marrow stem cells, and then to study if these MC also respond to substance P (SP) both in FcepsilonRIalpha and NK-1R dependent manners.	Methylcholanthrene	142-144	interleukin 4	Mus musculus	40-53
27666706-1	2016	Objective: To investigate the effect of interleukin-4 (IL-4) stimulation on the expression of FcepsilonRIalpha and NK-1R on mature mast cells(MC) cultured and differentiated from mouse bone marrow stem cells, and then to study if these MC also respond to substance P (SP) both in FcepsilonRIalpha and NK-1R dependent manners.	Methylcholanthrene	142-144	interleukin 4	Mus musculus	55-59
27666706-1	2016	Objective: To investigate the effect of interleukin-4 (IL-4) stimulation on the expression of FcepsilonRIalpha and NK-1R on mature mast cells(MC) cultured and differentiated from mouse bone marrow stem cells, and then to study if these MC also respond to substance P (SP) both in FcepsilonRIalpha and NK-1R dependent manners.	Methylcholanthrene	142-144	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	94-110
27666706-1	2016	Objective: To investigate the effect of interleukin-4 (IL-4) stimulation on the expression of FcepsilonRIalpha and NK-1R on mature mast cells(MC) cultured and differentiated from mouse bone marrow stem cells, and then to study if these MC also respond to substance P (SP) both in FcepsilonRIalpha and NK-1R dependent manners.	Methylcholanthrene	142-144	tachykinin receptor 1	Mus musculus	115-120
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	12-14	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	60-76
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	12-14	tachykinin receptor 1	Mus musculus	81-86
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	12-14	interleukin 4	Mus musculus	110-114
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	165-167	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	60-76
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	165-167	interleukin 4	Mus musculus	110-114
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	165-167	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	60-76
27666706-13	2016	Bone marrow MC were shown to have the highest expression of FcepsilonRIalpha and NK-1R in culture of 20 mug/L IL-4 by the detection of Western blot, meanwhile these MC could be activated to degranulate by a lower concentration of SP (0.01 mg/L), with the release rate of histamine from MC showing a positive correlation with SP concentrations.	Methylcholanthrene	165-167	interleukin 4	Mus musculus	110-114
27666706-14	2016	On the other hand, MC with high expression of FcepsilonRIalpha and little expression of NK-1R cultured with 0 mug/L IL-4, could also be activated by a much higher concentration of SP (1.0 mg/L).	Methylcholanthrene	19-21	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	46-62
27666706-14	2016	On the other hand, MC with high expression of FcepsilonRIalpha and little expression of NK-1R cultured with 0 mug/L IL-4, could also be activated by a much higher concentration of SP (1.0 mg/L).	Methylcholanthrene	19-21	tachykinin receptor 1	Mus musculus	88-93
27666706-14	2016	On the other hand, MC with high expression of FcepsilonRIalpha and little expression of NK-1R cultured with 0 mug/L IL-4, could also be activated by a much higher concentration of SP (1.0 mg/L).	Methylcholanthrene	19-21	interleukin 4	Mus musculus	116-120
27666706-15	2016	Conclusions: Bone marrow mast cells were shown to be successfully differentiated and to express NK-1R and FcepsilonRIalpha upon co-culture with SCF and IL-3 or SCF, IL-3 and IL-4.When IL-4 was added into RPMI 1640, bone marrow MC could highly produce FcepsilonRIalpha and NK-1R, thus building a better model of MC degranulation regulated by SP.	Methylcholanthrene	227-229	interleukin 4	Mus musculus	184-188
27584787-7	2016	In addition, we show that PARP1 is not an exclusive marker for late apoptosis but is also involved in MC.	Methylcholanthrene	102-104	poly(ADP-ribose) polymerase 1	Homo sapiens	26-31
27478537-2	2016	After initially dismal outcomes, the Milan criteria (MC) (single HCC &lt;= 5 cm or up to 3 HCCs &lt;= 3 cm) have been adopted worldwide to select HCC patients for LT, however cumulative experience has shown that MC can be too strict.	Methylcholanthrene	53-55	HCC	Homo sapiens	65-68
27449295-2	2016	Momordin Iotac (Mc), a natural pentacyclic triterpenoid, inhibited SENP1 in vitro, as reflected by reduced SENP1C-induced cleavage of SUMO2-DeltaRanGAP1.	Methylcholanthrene	16-18	SUMO specific peptidase 1	Homo sapiens	67-72
27449295-2	2016	Momordin Iotac (Mc), a natural pentacyclic triterpenoid, inhibited SENP1 in vitro, as reflected by reduced SENP1C-induced cleavage of SUMO2-DeltaRanGAP1.	Methylcholanthrene	16-18	small ubiquitin like modifier 2	Homo sapiens	134-139
27449295-3	2016	Mc also altered the thermal stability of SENP1 in a newly developed cellular thermal shift assay, indicating that Mc directly interacts with SENP1 in PCa cells.	Methylcholanthrene	0-2	SUMO specific peptidase 1	Homo sapiens	41-46
27449295-3	2016	Mc also altered the thermal stability of SENP1 in a newly developed cellular thermal shift assay, indicating that Mc directly interacts with SENP1 in PCa cells.	Methylcholanthrene	0-2	SUMO specific peptidase 1	Homo sapiens	141-146
27449295-3	2016	Mc also altered the thermal stability of SENP1 in a newly developed cellular thermal shift assay, indicating that Mc directly interacts with SENP1 in PCa cells.	Methylcholanthrene	114-116	SUMO specific peptidase 1	Homo sapiens	41-46
27449295-3	2016	Mc also altered the thermal stability of SENP1 in a newly developed cellular thermal shift assay, indicating that Mc directly interacts with SENP1 in PCa cells.	Methylcholanthrene	114-116	SUMO specific peptidase 1	Homo sapiens	141-146
27449295-4	2016	Consistent with SENP1 inhibition, Mc increased SUMOylated protein levels, which was further confirmed by the accumulation of two known SUMOylated proteins, hypoxia inducible factor-1a and nucleus accumbens associated protein 1 in PC3 cells.	Methylcholanthrene	34-36	SUMO specific peptidase 1	Homo sapiens	16-21
27449295-4	2016	Consistent with SENP1 inhibition, Mc increased SUMOylated protein levels, which was further confirmed by the accumulation of two known SUMOylated proteins, hypoxia inducible factor-1a and nucleus accumbens associated protein 1 in PC3 cells.	Methylcholanthrene	34-36	hypoxia inducible factor 1 subunit alpha	Homo sapiens	156-183
27449295-4	2016	Consistent with SENP1 inhibition, Mc increased SUMOylated protein levels, which was further confirmed by the accumulation of two known SUMOylated proteins, hypoxia inducible factor-1a and nucleus accumbens associated protein 1 in PC3 cells.	Methylcholanthrene	34-36	nucleus accumbens associated 1	Homo sapiens	188-226
27449295-4	2016	Consistent with SENP1 inhibition, Mc increased SUMOylated protein levels, which was further confirmed by the accumulation of two known SUMOylated proteins, hypoxia inducible factor-1a and nucleus accumbens associated protein 1 in PC3 cells.	Methylcholanthrene	34-36	BTG anti-proliferation factor 2	Homo sapiens	230-233
27449295-5	2016	Compared to LNCaP and normal prostate epithelial RWPE-1 cells, PC3 cells had higher levels of SENP1 mRNA and were more sensitive to Mc-induced growth inhibition.	Methylcholanthrene	132-134	BTG anti-proliferation factor 2	Homo sapiens	63-66
27449295-6	2016	Mc also reduced SENP1 mRNA levels in PCa cells.	Methylcholanthrene	0-2	SUMO specific peptidase 1	Homo sapiens	16-21
27449295-7	2016	Overexpression of SENP1 rescued PC3 cells from Mc-induced apoptosis.	Methylcholanthrene	47-49	SUMO specific peptidase 1	Homo sapiens	18-23
27449295-7	2016	Overexpression of SENP1 rescued PC3 cells from Mc-induced apoptosis.	Methylcholanthrene	47-49	BTG anti-proliferation factor 2	Homo sapiens	32-35
27449295-8	2016	Finally, Mc suppressed cell proliferation and induced cell death in vivo in a xenograft PC3 tumor mouse model.	Methylcholanthrene	9-11	BTG anti-proliferation factor 2	Mus musculus	88-91
27449295-9	2016	These findings demonstrate that Mc is a novel SENP1 inhibitor with potential therapeutic value for PCa.	Methylcholanthrene	32-34	SUMO specific peptidase 1	Homo sapiens	46-51
27666706-15	2016	Conclusions: Bone marrow mast cells were shown to be successfully differentiated and to express NK-1R and FcepsilonRIalpha upon co-culture with SCF and IL-3 or SCF, IL-3 and IL-4.When IL-4 was added into RPMI 1640, bone marrow MC could highly produce FcepsilonRIalpha and NK-1R, thus building a better model of MC degranulation regulated by SP.	Methylcholanthrene	311-313	interleukin 4	Mus musculus	184-188
27666706-16	2016	And SP-controlled MC degranulation may be mediated through both FcepsilonRIalpha (immunologically) and NK-1R (non-IgE mediated or non-immunologically) pathway.	Methylcholanthrene	18-20	Fc receptor, IgE, high affinity I, alpha polypeptide	Mus musculus	64-80
27666706-16	2016	And SP-controlled MC degranulation may be mediated through both FcepsilonRIalpha (immunologically) and NK-1R (non-IgE mediated or non-immunologically) pathway.	Methylcholanthrene	18-20	tachykinin receptor 1	Mus musculus	103-108
27898890-3	2016	The MC supplied (analyzed values) 5,397 U of xylanase, 162 U of beta-glucanase, and 2,000 U of protease per kg of diet, and guaranteed minimum activities of 1,000 U of alpha-amylase and 25 U of pectinase per kg of diet.	Methylcholanthrene	4-6	LOW QUALITY PROTEIN: pancreatic alpha-amylase	Sus scrofa	168-181
27898914-5	2016	The MC supplied (analyzed values) 5,397 U of xylanase, 162 U of beta-glucanase, and 2,000 U of protease and guaranteed minimum activities of 1,000 U of alpha-amylase and 25 U of pectinase per kg of diet.	Methylcholanthrene	4-6	LOW QUALITY PROTEIN: pancreatic alpha-amylase	Sus scrofa	152-165
27302415-9	2016	Compared to the control group, the MC group had significantly lower expressions of TIMP-1 and TIMP-2 (p &lt; 0.05).	Methylcholanthrene	35-37	metalloproteinase inhibitor 1	Oryctolagus cuniculus	83-89
27302415-9	2016	Compared to the control group, the MC group had significantly lower expressions of TIMP-1 and TIMP-2 (p &lt; 0.05).	Methylcholanthrene	35-37	metalloproteinase inhibitor 2	Oryctolagus cuniculus	94-100
27183589-10	2016	Reconstitution of MC-deficient Wsh mice with Fyn(-/-) MCs produced greater LPS-dependent production of TNF in the peritoneal cavity.	Methylcholanthrene	18-20	Fyn proto-oncogene	Mus musculus	45-48
27455316-7	2016	Additionally, the acute inflammatory response (IL-6) was attenuated in the MC group.	Methylcholanthrene	75-77	interleukin 6	Homo sapiens	47-51
27514062-1	2016	The use of intra/inter-cellular calcium ion (Ca2+) signaling for molecular communication (MC) is investigated in this paper.	Methylcholanthrene	90-92	carbonic anhydrase 2	Homo sapiens	45-48
27503160-11	2016	However, on POD 1, the IL-6 levels were observed to be significantly greater in the MC group than in the PSD group (P &lt; 0.005).	Methylcholanthrene	84-86	interleukin-6	Sus scrofa	23-27
27421067-9	2016	Our results show that thrombin dose-dependently stimulates MC proliferation by 44%, with a calculated Ec50 of 0.86 nM.	Methylcholanthrene	59-61	coagulation factor II, thrombin	Homo sapiens	22-30
27421067-11	2016	We demonstrate that thrombin induces MC cell proliferation through the Ras-independent activation of the Raf/MEK/ERK cascade, under the control of protein kinase C (PKC)-zeta.	Methylcholanthrene	37-39	coagulation factor II, thrombin	Homo sapiens	20-28
27421067-11	2016	We demonstrate that thrombin induces MC cell proliferation through the Ras-independent activation of the Raf/MEK/ERK cascade, under the control of protein kinase C (PKC)-zeta.	Methylcholanthrene	37-39	zinc fingers and homeoboxes 2	Homo sapiens	105-108
27421067-11	2016	We demonstrate that thrombin induces MC cell proliferation through the Ras-independent activation of the Raf/MEK/ERK cascade, under the control of protein kinase C (PKC)-zeta.	Methylcholanthrene	37-39	mitogen-activated protein kinase kinase 7	Homo sapiens	109-112
27421067-11	2016	We demonstrate that thrombin induces MC cell proliferation through the Ras-independent activation of the Raf/MEK/ERK cascade, under the control of protein kinase C (PKC)-zeta.	Methylcholanthrene	37-39	mitogen-activated protein kinase 1	Homo sapiens	113-116
27421067-11	2016	We demonstrate that thrombin induces MC cell proliferation through the Ras-independent activation of the Raf/MEK/ERK cascade, under the control of protein kinase C (PKC)-zeta.	Methylcholanthrene	37-39	protein kinase C zeta	Homo sapiens	147-174
27183589-10	2016	Reconstitution of MC-deficient Wsh mice with Fyn(-/-) MCs produced greater LPS-dependent production of TNF in the peritoneal cavity.	Methylcholanthrene	18-20	tumor necrosis factor	Mus musculus	103-106
27058733-6	2016	This investigation confirms the expectation that the MC-srDFT method is accurate for a broad range of excitations and comparable to accurate wave function methods such as CASPT2, NEVPT2, and the coupled cluster based CC2 and CC3.	Methylcholanthrene	53-55	C-C motif chemokine ligand 14	Homo sapiens	225-228
27272789-6	2016	In addition, MPS1 inhibition altered cell-cycle progression and exacerbated centrosome abnormalities, resulting in enhanced MC induced by etoposide but not by IR.	Methylcholanthrene	124-126	Ttk protein kinase	Mus musculus	13-17
27774272-8	2016	In our in vivo study, MC down-regulated MMP-2, MMP-9, and TIMP-4 and increased TIMP-3 in young SHR.	Methylcholanthrene	22-24	matrix metallopeptidase 2	Homo sapiens	40-45
27774272-8	2016	In our in vivo study, MC down-regulated MMP-2, MMP-9, and TIMP-4 and increased TIMP-3 in young SHR.	Methylcholanthrene	22-24	matrix metallopeptidase 9	Homo sapiens	47-52
27774272-8	2016	In our in vivo study, MC down-regulated MMP-2, MMP-9, and TIMP-4 and increased TIMP-3 in young SHR.	Methylcholanthrene	22-24	TIMP metallopeptidase inhibitor 4	Homo sapiens	58-64
27774272-8	2016	In our in vivo study, MC down-regulated MMP-2, MMP-9, and TIMP-4 and increased TIMP-3 in young SHR.	Methylcholanthrene	22-24	TIMP metallopeptidase inhibitor 3	Homo sapiens	79-85
27774272-10	2016	CONCLUSIONS: Our data indicate that treatment of MC can modulate the expression of MMPs and TIMPs in vitro and in vivo in SHR.	Methylcholanthrene	49-51	matrix metallopeptidase 2	Homo sapiens	83-87
26854997-11	2016	Moreover, PC and MC (1 mM) decreased KCNQ1 protein expression (relative density: 0.58 +- 0.08 and 0.16 +- 0.05; P &lt; .01).	Methylcholanthrene	17-19	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	37-42
26931093-9	2016	A MC target for the peptide was determined using GLP-1 receptor binding assays, immunocytochemistry for the receptor and injection of fluorescence-labelled GLP-1 analogue exendin-4.	Methylcholanthrene	2-4	glucagon-like peptide 1 receptor	Mus musculus	49-63
26931093-9	2016	A MC target for the peptide was determined using GLP-1 receptor binding assays, immunocytochemistry for the receptor and injection of fluorescence-labelled GLP-1 analogue exendin-4.	Methylcholanthrene	2-4	glucagon	Mus musculus	49-54
26970402-6	2016	Three of the 12mer peptides (namely 11-3, 1-7, and 7-3) suppressed the 3MC-induced, CYP1A1-dependent EROD activity and the ROS production caused by benzo[a]pyrene.	Methylcholanthrene	71-74	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	84-90
26842656-8	2016	RESULTS: C4 GCN analysis showed that fewer MC patients had more than 2 copies of the C4A gene as well as a lower C4A gene-copy index (1.90 +- 0.54 vs. 2.21 +- 0.78) as compared to healthy controls.	Methylcholanthrene	43-45	complement C4A (Rodgers blood group)	Homo sapiens	85-88
26842656-8	2016	RESULTS: C4 GCN analysis showed that fewer MC patients had more than 2 copies of the C4A gene as well as a lower C4A gene-copy index (1.90 +- 0.54 vs. 2.21 +- 0.78) as compared to healthy controls.	Methylcholanthrene	43-45	complement C4A (Rodgers blood group)	Homo sapiens	113-116
26914287-9	2016	Simultaneous loss of SETDB1 and caspase activity resulted in further increase in MC, indicating that the two components work cooperatively.	Methylcholanthrene	81-83	eggless	Drosophila melanogaster	21-27
26513738-4	2016	RESULTS: 3-methylcholanthrene induced fibrosarcoma in wild-type, Nox1y/-, Nox2y/- and Nox4-/- mice.	Methylcholanthrene	9-29	NADPH oxidase 1	Mus musculus	65-69
26513738-4	2016	RESULTS: 3-methylcholanthrene induced fibrosarcoma in wild-type, Nox1y/-, Nox2y/- and Nox4-/- mice.	Methylcholanthrene	9-29	NADPH oxidase 4	Mus musculus	86-90
26372666-2	2016	OBJECTIVES: We investigated the influence of the AHR ligand 3-methylcholanthrene (3-MC) on ER-mediated signaling in mammary gland tissue of ovariectomized (ovx) rats.	Methylcholanthrene	60-80	aryl hydrocarbon receptor	Rattus norvegicus	49-52
26372666-2	2016	OBJECTIVES: We investigated the influence of the AHR ligand 3-methylcholanthrene (3-MC) on ER-mediated signaling in mammary gland tissue of ovariectomized (ovx) rats.	Methylcholanthrene	60-80	estrogen receptor 1	Rattus norvegicus	91-93
26372666-2	2016	OBJECTIVES: We investigated the influence of the AHR ligand 3-methylcholanthrene (3-MC) on ER-mediated signaling in mammary gland tissue of ovariectomized (ovx) rats.	Methylcholanthrene	82-86	estrogen receptor 1	Rattus norvegicus	91-93
26372666-8	2016	This inhibitory effect of 3-MC was partially mirrored when 8-PN was used as an ER ligand.	Methylcholanthrene	26-30	estrogen receptor 1	Rattus norvegicus	79-81
26706492-5	2016	RESULTS: There was a difference in the percentage of immunoreactive cells of GLUT-1 and GLUT-3 in MC components among lesions and in the intensity of GLUT-1 in MCG and MC components, GLUT-3 in MGC components, and M-CSF in MC components.	Methylcholanthrene	98-100	solute carrier family 2 member 1	Homo sapiens	77-83
26706492-5	2016	RESULTS: There was a difference in the percentage of immunoreactive cells of GLUT-1 and GLUT-3 in MC components among lesions and in the intensity of GLUT-1 in MCG and MC components, GLUT-3 in MGC components, and M-CSF in MC components.	Methylcholanthrene	98-100	solute carrier family 2 member 3	Homo sapiens	88-94
26706492-5	2016	RESULTS: There was a difference in the percentage of immunoreactive cells of GLUT-1 and GLUT-3 in MC components among lesions and in the intensity of GLUT-1 in MCG and MC components, GLUT-3 in MGC components, and M-CSF in MC components.	Methylcholanthrene	160-162	solute carrier family 2 member 1	Homo sapiens	150-156
26706492-5	2016	RESULTS: There was a difference in the percentage of immunoreactive cells of GLUT-1 and GLUT-3 in MC components among lesions and in the intensity of GLUT-1 in MCG and MC components, GLUT-3 in MGC components, and M-CSF in MC components.	Methylcholanthrene	160-162	solute carrier family 2 member 1	Homo sapiens	150-156
27163632-7	2016	Also, 3MC inhibited the ovulation rate and induced an overexpression of both the Cyp1a1 and Cyp1b1 genes, measured by chromatin immunoprecipitation assay.	Methylcholanthrene	6-9	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-87
27163632-7	2016	Also, 3MC inhibited the ovulation rate and induced an overexpression of both the Cyp1a1 and Cyp1b1 genes, measured by chromatin immunoprecipitation assay.	Methylcholanthrene	6-9	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	92-98
27163632-9	2016	Moreover, the alphaNF treatment prevented completely not only the 3MC-induced decrease in all types of follicles but also the 3MC-induced overexpression of Cyp enzymes and the genetic damage in bone marrow cells and oocytes.	Methylcholanthrene	126-129	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	156-159
26914287-9	2016	Simultaneous loss of SETDB1 and caspase activity resulted in further increase in MC, indicating that the two components work cooperatively.	Methylcholanthrene	81-83	Death caspase-1	Drosophila melanogaster	32-39
27036881-9	2016	MC-eNOS vectors showed higher transfection efficiency (21 +- 3 %) compared to P-eNOS (9 +- 1 %) and also generated higher NO levels.	Methylcholanthrene	0-2	nitric oxide synthase 3	Homo sapiens	3-7
27036881-10	2016	In vitro capillary tubule formation assays showed both MC-eNOS and P-eNOS gene-modified rBMSCs formed longer (14.66 +- 0.55 mm and 13.58 +- 0.68 mm, respectively) and a greater number of tubules (56.33 +- 3.51 and 51 +- 4, respectively) compared to controls, which was reduced with the NOS inhibitor L-NAME.	Methylcholanthrene	55-57	nitric oxide synthase 3	Homo sapiens	58-62
27036881-11	2016	In an in vitro wound healing assay, MC-eNOS transfected cells showed greater migration which was also reversed by L-NAME treatment.	Methylcholanthrene	36-38	nitric oxide synthase 3	Homo sapiens	39-43
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	fibroblast growth factor 2	Homo sapiens	172-177
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	nitric oxide synthase 3	Homo sapiens	40-44
26864197-12	2016	One of the MC specific miRNA, miR-34a, was selected for further analysis.	Methylcholanthrene	11-13	microRNA 34a	Bos taurus	30-37
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	platelet and endothelial cell adhesion molecule 1	Homo sapiens	130-134
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	vascular endothelial growth factor A	Homo sapiens	162-167
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	platelet derived growth factor receptor alpha	Homo sapiens	212-222
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	fibroblast growth factor receptor 2	Homo sapiens	227-232
27642645-6	2016	The temperature dependence of the domain configuration revealed that the volume fraction of the MC phase decreases with temperature accompanied by the reduction of [Formula: see text], d31, and k31 due to the substantially smaller intrinsic properties of the T phase.	Methylcholanthrene	96-98	keratin 31	Homo sapiens	194-197
26787258-4	2016	The largest paramagnetic contribution, which originates from the coupling of alkylidene sigma(MC) and pi*(MC) orbitals under the action of the magnetic field, is analogous to that resulting from coupling sigma(CC) and pi*(CC) in ethylene; thus, delta11 is in the MCH plane and is perpendicular to the MC internuclear direction.	Methylcholanthrene	94-96	pro-melanin concentrating hormone	Homo sapiens	263-266
26818732-3	2016	Here we show that mutations in the SEUSS (SEU) gene led to a higher frequency of MC formation.	Methylcholanthrene	81-83	SEUSS transcriptional co-regulator	Arabidopsis thaliana	35-40
26818732-3	2016	Here we show that mutations in the SEUSS (SEU) gene led to a higher frequency of MC formation.	Methylcholanthrene	81-83	SEUSS transcriptional co-regulator	Arabidopsis thaliana	35-38
26818732-5	2016	Our results further indicate that SEU physically associates with upstream regulatory sequences of SHR, SCR, and SCL3; and that SEU has distinct genetic interactions with these genes in the control of MC formation, with SCL3 being epistatic to SEU.	Methylcholanthrene	200-202	SEUSS transcriptional co-regulator	Arabidopsis thaliana	127-130
26818732-5	2016	Our results further indicate that SEU physically associates with upstream regulatory sequences of SHR, SCR, and SCL3; and that SEU has distinct genetic interactions with these genes in the control of MC formation, with SCL3 being epistatic to SEU.	Methylcholanthrene	200-202	scarecrow-like 3	Arabidopsis thaliana	219-223
26818732-5	2016	Our results further indicate that SEU physically associates with upstream regulatory sequences of SHR, SCR, and SCL3; and that SEU has distinct genetic interactions with these genes in the control of MC formation, with SCL3 being epistatic to SEU.	Methylcholanthrene	200-202	SEUSS transcriptional co-regulator	Arabidopsis thaliana	127-130
26818732-6	2016	Similar to SCL3, SEU was repressed by the phytohormone GA and induced by the GA biosynthesis inhibitor paclobutrazol, suggesting that SEU acts downstream of GA signaling to regulate MC formation.	Methylcholanthrene	182-184	scarecrow-like 3	Arabidopsis thaliana	11-15
26818732-6	2016	Similar to SCL3, SEU was repressed by the phytohormone GA and induced by the GA biosynthesis inhibitor paclobutrazol, suggesting that SEU acts downstream of GA signaling to regulate MC formation.	Methylcholanthrene	182-184	SEUSS transcriptional co-regulator	Arabidopsis thaliana	17-20
26818732-6	2016	Similar to SCL3, SEU was repressed by the phytohormone GA and induced by the GA biosynthesis inhibitor paclobutrazol, suggesting that SEU acts downstream of GA signaling to regulate MC formation.	Methylcholanthrene	182-184	SEUSS transcriptional co-regulator	Arabidopsis thaliana	134-137
26818732-8	2016	Together, our study identifies SEU as a new critical player that integrates GA signaling with transcriptional inputs from the SHR-SCR-SCL3 module to regulate MC formation in the Arabidopsis root.	Methylcholanthrene	158-160	SEUSS transcriptional co-regulator	Arabidopsis thaliana	31-34
26818732-8	2016	Together, our study identifies SEU as a new critical player that integrates GA signaling with transcriptional inputs from the SHR-SCR-SCL3 module to regulate MC formation in the Arabidopsis root.	Methylcholanthrene	158-160	GRAS family transcription factor	Arabidopsis thaliana	130-133
26818732-8	2016	Together, our study identifies SEU as a new critical player that integrates GA signaling with transcriptional inputs from the SHR-SCR-SCL3 module to regulate MC formation in the Arabidopsis root.	Methylcholanthrene	158-160	scarecrow-like 3	Arabidopsis thaliana	134-138
26704294-3	2016	To penetrate through the plasma membrane, MC-LR needs specific transporters such the organic anion-transporting polypeptides (OATP) that are highly expressed on the hepatocytes.	Methylcholanthrene	42-44	solute carrier organic anion transporter family member 1A2	Homo sapiens	85-124
26704294-3	2016	To penetrate through the plasma membrane, MC-LR needs specific transporters such the organic anion-transporting polypeptides (OATP) that are highly expressed on the hepatocytes.	Methylcholanthrene	42-44	solute carrier organic anion transporter family member 1A2	Homo sapiens	126-130
27082035-8	2016	RESULTS: Neurological deficit scores, perihematomal PPARgamma levels, and BBB permeability were all significantly increased in the MC group compared to the NC group.	Methylcholanthrene	131-133	peroxisome proliferator-activated receptor gamma	Oryctolagus cuniculus	52-61
26911935-6	2016	GAPDH associated proteins in EAC cells and 3-methylcholanthrene (3MC) induced mouse tumor tissue were detected by mass spectrometry analysis and immunoprecipitation (IP) experiment, respectively.	Methylcholanthrene	65-68	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	0-5
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	173-193	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	29-34
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	173-193	glucose-6-phosphate isomerase 1	Mus musculus	85-88
26702136-6	2016	After BDL and CCl4 treatment, MC-derived HSCs and myofibroblasts were distributed near the liver surface and the thickness of collagen was increased in Glisson"s capsule beneath the liver surface.	Methylcholanthrene	30-32	C-C motif chemokine ligand 4	Homo sapiens	14-18
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	173-193	pyruvate kinase, muscle	Mus musculus	114-118
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	195-198	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	29-34
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	195-198	glucose-6-phosphate isomerase 1	Mus musculus	54-83
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	195-198	glucose-6-phosphate isomerase 1	Mus musculus	85-88
26911935-9	2016	RESULT: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue.	Methylcholanthrene	195-198	pyruvate kinase, muscle	Mus musculus	114-118
26702136-9	2016	During regression of CCl4-induced fibrosis, 20% of MC-derived myofibroblasts survived in the liver and deactivated to vitamin A-poor HSCs.	Methylcholanthrene	51-53	C-C motif chemokine ligand 4	Homo sapiens	21-25
26373698-3	2016	Thirty-one and three patients have been reported with MC-EDS so far with bi-allelic mutations identified in CHST14 and DSE, respectively, encoding two enzymes necessary for dermatan sulfate (DS) biosynthesis.	Methylcholanthrene	54-56	carbohydrate sulfotransferase 14	Homo sapiens	108-114
26648448-5	2016	However, the expression of CCR2 was significantly upregulated in the GES-1 cells following pretreatment with the chemical carcinogen, N-methyl-N-nitro-N"-nitrosoguanidine (MNNG), for 12 h or transformed with MNNG (MC cells).	Methylcholanthrene	214-216	C-C motif chemokine receptor 2	Homo sapiens	27-31
25813008-2	2016	Inflammation is considered as a key factor that triggers symptoms in especially type I MC, but so far of the potential inflammatory candidates only TNFalpha has been linked to MC.	Methylcholanthrene	176-178	tumor necrosis factor	Homo sapiens	148-156
28118619-11	2016	In contrast, DCX+ neurons were scarce in the DMC but highly numerous in the MC, particularly in the granular cell layer.	Methylcholanthrene	46-48	doublecortin	Homo sapiens	13-16
25381005-7	2016	We hypothesized that AMPA-R phosphorylation may also be a key plastic process for supporting MC because it occurs in a few minutes, and potentiates AMPA-R ion channel function.	Methylcholanthrene	93-95	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	21-27
25381005-8	2016	Here, we show that knock-in mutant mice that specifically lack both of S845 and S831 phosphorylation sites on the GluA1 subunit had reduced MC in two different behavioral tasks specifically designed to assess MC in mice.	Methylcholanthrene	140-142	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	114-119
25381005-8	2016	Here, we show that knock-in mutant mice that specifically lack both of S845 and S831 phosphorylation sites on the GluA1 subunit had reduced MC in two different behavioral tasks specifically designed to assess MC in mice.	Methylcholanthrene	209-211	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	114-119
25381005-9	2016	This demonstrated a causal link between AMPA-R phosphorylation and MC.	Methylcholanthrene	67-69	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	40-46
25813008-8	2016	Of the multiple genes tested, statistically significant associations were observed for M-CSF1 (p = 0.028), RANKL (p = 0.035), RUNX1 (p = 0.032), and RUNX2 (p = 0.047) that were increased in "Type II MC," while OSCAR (p = 0.042) was increased in "Type I MC" group compared to "No MC."	Methylcholanthrene	199-201	TNF superfamily member 11	Homo sapiens	107-112
25813008-8	2016	Of the multiple genes tested, statistically significant associations were observed for M-CSF1 (p = 0.028), RANKL (p = 0.035), RUNX1 (p = 0.032), and RUNX2 (p = 0.047) that were increased in "Type II MC," while OSCAR (p = 0.042) was increased in "Type I MC" group compared to "No MC."	Methylcholanthrene	199-201	RUNX family transcription factor 1	Homo sapiens	126-131
25813008-8	2016	Of the multiple genes tested, statistically significant associations were observed for M-CSF1 (p = 0.028), RANKL (p = 0.035), RUNX1 (p = 0.032), and RUNX2 (p = 0.047) that were increased in "Type II MC," while OSCAR (p = 0.042) was increased in "Type I MC" group compared to "No MC."	Methylcholanthrene	199-201	RUNX family transcription factor 2	Homo sapiens	149-154
26522070-10	2015	Endothelial VCAM-1 targeted delivery of the CCR2 antagonist resulted in inhibition of pulmonary metastases both in a murine (MC-38GFP cells) and a human xenograft (patient-derived cells) model.	Methylcholanthrene	125-127	vascular cell adhesion molecule 1	Mus musculus	12-18
26758677-8	2016	The patients in the MC group had higher elevation of the CRP mean values post-operatively (p = 0.01).	Methylcholanthrene	20-22	C-reactive protein	Homo sapiens	57-60
26758677-9	2016	However, the patients in the MC group had higher elevation of the IL-1ra mean values post-operatively, the mean pre-/post-operative IL-1ra values being 299/614 pg/ml in the MC group versus 379/439 pg/ml in the LC group (p = 0.003).	Methylcholanthrene	29-31	interleukin 1 receptor antagonist	Homo sapiens	66-72
26758677-9	2016	However, the patients in the MC group had higher elevation of the IL-1ra mean values post-operatively, the mean pre-/post-operative IL-1ra values being 299/614 pg/ml in the MC group versus 379/439 pg/ml in the LC group (p = 0.003).	Methylcholanthrene	29-31	interleukin 1 receptor antagonist	Homo sapiens	132-138
26758677-11	2016	However, the patients in the MC group had higher IL-6 mean values six hours post-operatively (POP2), the mean IL-6 values being 27.6 pg/ml in the MC group versus 14.8 pg/ml in the LC group (p = 0.037).	Methylcholanthrene	29-31	interleukin 6	Homo sapiens	49-53
28101686-5	2016	We have recently developed a strategy for MC-based SB transposition of chimeric antigen receptor (CAR) transgenes that enable improved transposition rates compared to conventional plasmids and rapid manufacturing of therapeutic CAR T cell doses (Monjezi et al.	Methylcholanthrene	42-44	nuclear receptor subfamily 1 group I member 3	Homo sapiens	71-96
28101686-5	2016	We have recently developed a strategy for MC-based SB transposition of chimeric antigen receptor (CAR) transgenes that enable improved transposition rates compared to conventional plasmids and rapid manufacturing of therapeutic CAR T cell doses (Monjezi et al.	Methylcholanthrene	42-44	nuclear receptor subfamily 1 group I member 3	Homo sapiens	98-101
28101686-5	2016	We have recently developed a strategy for MC-based SB transposition of chimeric antigen receptor (CAR) transgenes that enable improved transposition rates compared to conventional plasmids and rapid manufacturing of therapeutic CAR T cell doses (Monjezi et al.	Methylcholanthrene	42-44	nuclear receptor subfamily 1 group I member 3	Homo sapiens	228-231
28101686-7	2016	This advance enables manufacturing CAR T cells in a virus-free process that relies on SB-mediated transposition from MC DNA to accomplish gene-transfer.	Methylcholanthrene	117-119	nuclear receptor subfamily 1 group I member 3	Homo sapiens	35-38
28101686-8	2016	Advantages of this approach include a strong safety profile due to the nature of the MC itself and the genomic insertion pattern of MC-derived CAR transposons.	Methylcholanthrene	132-134	nuclear receptor subfamily 1 group I member 3	Homo sapiens	143-146
28101686-10	2016	In this chapter, we will review our experience in MC-based CAR T cell engineering and discuss our recent advances in MC manufacturing to accelerate both pre-clinical and clinical implementation.	Methylcholanthrene	50-52	nuclear receptor subfamily 1 group I member 3	Homo sapiens	59-62
26529501-5	2016	Microarray analysis showed that MC was conducive to express osteogenesis-related genes, such as BMP-2, COL1A1, and CTSK, and stimulate osteogenic differentiation, such as osteoblast differentiation pathway and skeletal system development pathway.	Methylcholanthrene	32-34	bone morphogenetic protein 2	Homo sapiens	96-101
26529501-5	2016	Microarray analysis showed that MC was conducive to express osteogenesis-related genes, such as BMP-2, COL1A1, and CTSK, and stimulate osteogenic differentiation, such as osteoblast differentiation pathway and skeletal system development pathway.	Methylcholanthrene	32-34	collagen type I alpha 1 chain	Homo sapiens	103-109
26529501-5	2016	Microarray analysis showed that MC was conducive to express osteogenesis-related genes, such as BMP-2, COL1A1, and CTSK, and stimulate osteogenic differentiation, such as osteoblast differentiation pathway and skeletal system development pathway.	Methylcholanthrene	32-34	cathepsin K	Homo sapiens	115-119
26758677-11	2016	However, the patients in the MC group had higher IL-6 mean values six hours post-operatively (POP2), the mean IL-6 values being 27.6 pg/ml in the MC group versus 14.8 pg/ml in the LC group (p = 0.037).	Methylcholanthrene	29-31	pyrin domain containing 2	Homo sapiens	94-98
26522070-10	2015	Endothelial VCAM-1 targeted delivery of the CCR2 antagonist resulted in inhibition of pulmonary metastases both in a murine (MC-38GFP cells) and a human xenograft (patient-derived cells) model.	Methylcholanthrene	125-127	chemokine (C-C motif) receptor 2	Mus musculus	44-48
26758677-11	2016	However, the patients in the MC group had higher IL-6 mean values six hours post-operatively (POP2), the mean IL-6 values being 27.6 pg/ml in the MC group versus 14.8 pg/ml in the LC group (p = 0.037).	Methylcholanthrene	29-31	interleukin 6	Homo sapiens	110-114
26758677-12	2016	In addition, the patients in the MC group had higher elevation of the IL-6 mean values post-operatively, the mean pre-/post-operative IL-6 values being 4.1/27.6 pg/ml in the MC group versus 3.8/14.8 pg/ml in the LC group (p = 0.04).	Methylcholanthrene	33-35	interleukin 6	Homo sapiens	70-74
26275838-5	2015	Moreover, the results of differentiation experiments indicated that hMSCs cultured on MC substrates displayed high level of osteogenic differentiation marker expression, alkaline phosphatase activity and osteocalcin secretion, suggesting that the MC scaffolds can direct hMSC differentiation toward osteoblasts without inducer treatment and cross-linking density of MC scaffolds have stimulatory effect on inducing differentiation.	Methylcholanthrene	86-88	bone gamma-carboxyglutamate protein	Homo sapiens	204-215
26758677-12	2016	In addition, the patients in the MC group had higher elevation of the IL-6 mean values post-operatively, the mean pre-/post-operative IL-6 values being 4.1/27.6 pg/ml in the MC group versus 3.8/14.8 pg/ml in the LC group (p = 0.04).	Methylcholanthrene	33-35	interleukin 6	Homo sapiens	134-138
26758677-12	2016	In addition, the patients in the MC group had higher elevation of the IL-6 mean values post-operatively, the mean pre-/post-operative IL-6 values being 4.1/27.6 pg/ml in the MC group versus 3.8/14.8 pg/ml in the LC group (p = 0.04).	Methylcholanthrene	174-176	interleukin 6	Homo sapiens	134-138
26758677-15	2016	A new finding with possible clinical relevance in the present work is higher relative elevation of the IL-1ra and IL-6 mean values post-operatively in the MC group.	Methylcholanthrene	155-157	interleukin 1 receptor antagonist	Homo sapiens	103-109
26758677-15	2016	A new finding with possible clinical relevance in the present work is higher relative elevation of the IL-1ra and IL-6 mean values post-operatively in the MC group.	Methylcholanthrene	155-157	interleukin 6	Homo sapiens	114-118
25902363-8	2015	MS revealed that phycocyanin and the core-membrane linker peptide are the responsible allergens, and MC(-) extracts containing these proteins induced beta-hexosaminidase release in rat basophil leukemia cells.	Methylcholanthrene	101-104	O-GlcNAcase	Rattus norvegicus	150-169
26417045-4	2015	Although the effects of the classic AhR ligands such as 3-methylcholanthrene and dioxins on phase 1 enzymes are well studied in rodent lung, liver, and other organs, the toxicity profiles limit their use as therapeutic agents in humans.	Methylcholanthrene	56-76	aryl hydrocarbon receptor	Homo sapiens	36-39
26275838-5	2015	Moreover, the results of differentiation experiments indicated that hMSCs cultured on MC substrates displayed high level of osteogenic differentiation marker expression, alkaline phosphatase activity and osteocalcin secretion, suggesting that the MC scaffolds can direct hMSC differentiation toward osteoblasts without inducer treatment and cross-linking density of MC scaffolds have stimulatory effect on inducing differentiation.	Methylcholanthrene	247-249	bone gamma-carboxyglutamate protein	Homo sapiens	204-215
26275838-5	2015	Moreover, the results of differentiation experiments indicated that hMSCs cultured on MC substrates displayed high level of osteogenic differentiation marker expression, alkaline phosphatase activity and osteocalcin secretion, suggesting that the MC scaffolds can direct hMSC differentiation toward osteoblasts without inducer treatment and cross-linking density of MC scaffolds have stimulatory effect on inducing differentiation.	Methylcholanthrene	247-249	bone gamma-carboxyglutamate protein	Homo sapiens	204-215
26296470-0	2015	Caffeic acid phenethyl ester inhibits 3-MC-induced CYP1A1 expression through induction of hypoxia-inducible factor-1alpha.	Methylcholanthrene	38-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	51-57
26528143-7	2015	Lastly, we have also implemented a disinhibitory pathway mediated by another interneuron type (VIP interneurons), which inhibits MC and abolishes surround suppression.	Methylcholanthrene	129-131	vasoactive intestinal peptide	Homo sapiens	95-98
26296470-7	2015	CAPE-mediated HIF-1alpha reduced 3-MC-inducible CYP1A1 protein expression.	Methylcholanthrene	33-37	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-24
26300425-6	2015	Furthermore, HSD17B13 were only down-regulated in MC group while HK2 were only up-regulated in SC group among these dysregulated proteins.	Methylcholanthrene	50-52	hydroxysteroid 17-beta dehydrogenase 13	Homo sapiens	13-21
26195824-6	2015	We also reveal that both A3B and A3BCD2 can deaminate methylcytosine (mC).	Methylcholanthrene	70-72	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	25-28
26195824-6	2015	We also reveal that both A3B and A3BCD2 can deaminate methylcytosine (mC).	Methylcholanthrene	70-72	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	33-39
26195824-7	2015	Guided by structural and functional analysis, we successfully engineered A3BCD2 to gain over two orders of magnitude higher activity for mC deamination.	Methylcholanthrene	137-139	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	73-79
26195824-8	2015	Important determinants that contribute to the activity and selectivity for mC deamination have been identified, which reveals that multiple elements, rather than single ones, contribute to the mC deamination activity and selectivity in A3BCD2 and possibly other APOBECs.	Methylcholanthrene	75-77	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	236-242
26195824-8	2015	Important determinants that contribute to the activity and selectivity for mC deamination have been identified, which reveals that multiple elements, rather than single ones, contribute to the mC deamination activity and selectivity in A3BCD2 and possibly other APOBECs.	Methylcholanthrene	193-195	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	236-242
26296470-7	2015	CAPE-mediated HIF-1alpha reduced 3-MC-inducible CYP1A1 protein expression.	Methylcholanthrene	33-37	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	48-54
26296470-0	2015	Caffeic acid phenethyl ester inhibits 3-MC-induced CYP1A1 expression through induction of hypoxia-inducible factor-1alpha.	Methylcholanthrene	38-42	hypoxia inducible factor 1 subunit alpha	Homo sapiens	90-121
26296470-8	2015	Taken together, CAPE decreases 3-MC-mediated CYP1A1 expression, and this inhibitory response is associated with inhibition of AhR and HIF-1alpha induction.	Methylcholanthrene	31-35	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	45-51
26296470-2	2015	In this study, we examined the effects of CAPE on 3-methylcholanthrene (3-MC)-induced CYP1A1 expression and activities.	Methylcholanthrene	50-70	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	86-92
26296470-2	2015	In this study, we examined the effects of CAPE on 3-methylcholanthrene (3-MC)-induced CYP1A1 expression and activities.	Methylcholanthrene	72-76	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	86-92
26296470-4	2015	Moreover, CAPE inhibited 3-MC-induced CYP1A1 activity, mRNA expression, protein level, and promoter activity.	Methylcholanthrene	25-29	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	38-44
26716343-5	2015	MC adsorbed FDH less than KB, but enzyme activity was higher on MC per FDH.	Methylcholanthrene	0-2	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	12-15
25867055-5	2015	Further, the double level selectivity studies of MC using different metal ions [CoII, NiII, CuII, ZnII] and a number of simple bidentate chelating ligands shows the selective formation of PRT1 that justifies the self-sorting nature of the system.	Methylcholanthrene	49-51	eukaryotic translation initiation factor 3 subunit B	Homo sapiens	188-192
26716343-5	2015	MC adsorbed FDH less than KB, but enzyme activity was higher on MC per FDH.	Methylcholanthrene	64-66	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	71-74
25940678-2	2015	As a first example, a microporous polymer network was formed from macrocycle MC via acid-catalysed cyclotrimerization yielding a BET surface area of ca.	Methylcholanthrene	77-79	delta/notch like EGF repeat containing	Homo sapiens	129-132
26711077-11	2015	(2) Methylation of CpG island in LCHAD gene promoter region: (1) Methylation of CpG island in LC-FFA and MC-FFA groups showed rising trend with the time: Methylation level of LC-FFA group at 72 h (0.55+-0.08) was significantly higher than that of 48 h (0.35+-0.12) and 24 h (0.31+-0.04) (P&lt;0.05).	Methylcholanthrene	105-107	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha	Homo sapiens	33-38
26546041-4	2015	Here we show that GADD45a physically interacts--and functionally cooperates with TET1 in methylcytosine (mC) processing.	Methylcholanthrene	105-107	growth arrest and DNA damage inducible alpha	Homo sapiens	18-25
26546041-4	2015	Here we show that GADD45a physically interacts--and functionally cooperates with TET1 in methylcytosine (mC) processing.	Methylcholanthrene	105-107	tet methylcytosine dioxygenase 1	Homo sapiens	81-85
26546041-7	2015	Likewise, in global analysis GADD45a positively regulates TET1 mediated mC oxidation and enhances fC/caC removal.	Methylcholanthrene	72-74	growth arrest and DNA damage inducible alpha	Homo sapiens	29-36
26546041-7	2015	Likewise, in global analysis GADD45a positively regulates TET1 mediated mC oxidation and enhances fC/caC removal.	Methylcholanthrene	72-74	tet methylcytosine dioxygenase 1	Homo sapiens	58-62
26098772-8	2015	Further, MC-induced invasion was significantly reduced by anti-CSF-1 treatment while microglia-induced invasion was reduced to a lower extend.	Methylcholanthrene	9-11	colony stimulating factor 1	Homo sapiens	63-68
26076008-0	2015	Methylcholanthrene-Induced Sarcomas Develop Independently from NOX2-Derived ROS.	Methylcholanthrene	0-18	cytochrome b-245, beta polypeptide	Mus musculus	63-67
26076008-4	2015	In this study we aimed to decipher the role of NOX2-derived ROS in a chemically (by methylcholanthrene (MCA)) induced sarcoma model.	Methylcholanthrene	84-102	cytochrome b-245, beta polypeptide	Mus musculus	47-51
26076008-4	2015	In this study we aimed to decipher the role of NOX2-derived ROS in a chemically (by methylcholanthrene (MCA)) induced sarcoma model.	Methylcholanthrene	104-107	cytochrome b-245, beta polypeptide	Mus musculus	47-51
26283922-9	2015	Nevertheless, the mature centriole (MC) frequently docked to the plasma membrane in MGE cells migrating on N-cadherin, suggesting that plasma membrane docking is a basic feature of the centrosome in migrating MGE cells.	Methylcholanthrene	36-38	cadherin 2	Homo sapiens	107-117
26174335-3	2015	The aim of this study was to investigate the hepatoprotective activity and possible underlying mechanisms of Micromeria croatica ethanolic extract (MC) using a model of carbon tetrachloride (CCl4)-induced liver injury in mice.	Methylcholanthrene	148-150	chemokine (C-C motif) ligand 4	Mus musculus	191-195
26174335-14	2015	The hepatoprotective activity of MC was accompanied by the increase in nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor-alpha (TNF-alpha) expression, indicating amelioration of hepatic inflammation.	Methylcholanthrene	33-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	71-92
26174335-14	2015	The hepatoprotective activity of MC was accompanied by the increase in nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor-alpha (TNF-alpha) expression, indicating amelioration of hepatic inflammation.	Methylcholanthrene	33-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	94-103
26174335-14	2015	The hepatoprotective activity of MC was accompanied by the increase in nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor-alpha (TNF-alpha) expression, indicating amelioration of hepatic inflammation.	Methylcholanthrene	33-35	tumor necrosis factor	Mus musculus	120-147
26174335-14	2015	The hepatoprotective activity of MC was accompanied by the increase in nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor-alpha (TNF-alpha) expression, indicating amelioration of hepatic inflammation.	Methylcholanthrene	33-35	tumor necrosis factor	Mus musculus	149-158
26174335-15	2015	Additionally, MC prevented tumor growth factor-beta1 (TGF-beta1) and alpha-smooth muscle actin (alpha-SMA) expression, suggesting the potential for suppression of hepatic fibrogenesis.	Methylcholanthrene	14-16	transforming growth factor, beta 1	Mus musculus	54-63
26174335-15	2015	Additionally, MC prevented tumor growth factor-beta1 (TGF-beta1) and alpha-smooth muscle actin (alpha-SMA) expression, suggesting the potential for suppression of hepatic fibrogenesis.	Methylcholanthrene	14-16	actin alpha 2, smooth muscle, aorta	Mus musculus	69-94
26174335-15	2015	Additionally, MC prevented tumor growth factor-beta1 (TGF-beta1) and alpha-smooth muscle actin (alpha-SMA) expression, suggesting the potential for suppression of hepatic fibrogenesis.	Methylcholanthrene	14-16	actin alpha 2, smooth muscle, aorta	Mus musculus	96-105
25690886-3	2015	Activation of AhR by its ligands, formylindolo[3,2-b]carbazole (FICZ) or 3-methylcholanthrene (3MC), attenuated LPS-induced microglial immune responses.	Methylcholanthrene	73-93	aryl-hydrocarbon receptor	Mus musculus	14-17
25690886-3	2015	Activation of AhR by its ligands, formylindolo[3,2-b]carbazole (FICZ) or 3-methylcholanthrene (3MC), attenuated LPS-induced microglial immune responses.	Methylcholanthrene	95-98	aryl-hydrocarbon receptor	Mus musculus	14-17
25582180-2	2015	The suppressive effects of brewed green tea and black tea on 3-methylcholanthrene (MC)-induced AhR activation and its downstream events were examined in the liver of rats.	Methylcholanthrene	61-81	aryl hydrocarbon receptor	Rattus norvegicus	95-98
25571936-5	2015	High levels of CXCL10 in circulation have been found in HCV+MC, especially in patients with clinically active vasculitis.	Methylcholanthrene	60-62	C-X-C motif chemokine ligand 10	Homo sapiens	15-21
25582180-2	2015	The suppressive effects of brewed green tea and black tea on 3-methylcholanthrene (MC)-induced AhR activation and its downstream events were examined in the liver of rats.	Methylcholanthrene	83-85	aryl hydrocarbon receptor	Rattus norvegicus	95-98
25582180-3	2015	Ad-libitum drinking of green tea and black tea suppressed MC-induced AhR activation and elevation of ethoxyresorufin O-deethylase activity in the liver, whereas the teas themselves did not induce them.	Methylcholanthrene	58-60	aryl hydrocarbon receptor	Rattus norvegicus	69-72
26309800-3	2015	Previously, we demonstrated that microcarriers (MCs) coated with mouse laminin-111 (LN111) and positively charged poly-l-lysine (PLL) critically enable the formation and evolution of cells/MC aggregates with high cell yields obtained under agitated conditions.	Methylcholanthrene	48-50	laminin B1	Mus musculus	71-82
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	insulin-like growth factor 1	Rattus norvegicus	23-28
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	insulin-like growth factor binding protein 3	Rattus norvegicus	30-59
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	growth hormone receptor	Rattus norvegicus	73-96
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	growth hormone receptor	Rattus norvegicus	98-101
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	AKT serine/threonine kinase 1	Rattus norvegicus	224-227
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	mechanistic target of rapamycin kinase	Rattus norvegicus	230-234
25909895-8	2015	In the MC group, serum IGF-1, IGF-binding protein (IGFBP)-3, and hepatic growth hormone receptor (GHR) levels were significantly decreased and phosphorylation of the downstream anabolic signaling effectors protein kinase B (Akt), mTOR, and ribosomal protein S6 kinase 1 (S6K1) were significantly lower than in other groups.	Methylcholanthrene	7-9	ribosomal protein S6 kinase B1	Rattus norvegicus	271-275
25794236-6	2015	MVIC (P &lt; 0.05) did not decline in the MC group (vs. PLA) across the 72-h post-trial period and economy (P &lt; 0.05) was improved in the MC group at 24 h. IL-6 (P &lt; 0.001) and hsCRP (P &lt; 0.05) responses to the trial were attenuated with MC (vs. PLA).	Methylcholanthrene	141-143	interleukin 6	Homo sapiens	159-163
25794236-6	2015	MVIC (P &lt; 0.05) did not decline in the MC group (vs. PLA) across the 72-h post-trial period and economy (P &lt; 0.05) was improved in the MC group at 24 h. IL-6 (P &lt; 0.001) and hsCRP (P &lt; 0.05) responses to the trial were attenuated with MC (vs. PLA).	Methylcholanthrene	141-143	interleukin 6	Homo sapiens	159-163
26309800-3	2015	Previously, we demonstrated that microcarriers (MCs) coated with mouse laminin-111 (LN111) and positively charged poly-l-lysine (PLL) critically enable the formation and evolution of cells/MC aggregates with high cell yields obtained under agitated conditions.	Methylcholanthrene	48-50	laminin B1	Mus musculus	84-89
26309800-9	2015	The new LN521-based MC system offers a defined, xeno-free, GMP-compatible, and scalable bioprocessing platform for the production of hPSC with the quantity and quality compliant for clinical applications.	Methylcholanthrene	20-22	PSC	Homo sapiens	133-137
25201259-4	2015	Additionally, MCs express the NK1R, suggesting an adjuvant role for NK1R agonists in FcepsilonRI-MC-mediated pathologies; however, in-depth research addressing this relevant aspect of MC biology is lacking.	Methylcholanthrene	14-16	tachykinin receptor 1	Mus musculus	30-34
25201259-4	2015	Additionally, MCs express the NK1R, suggesting an adjuvant role for NK1R agonists in FcepsilonRI-MC-mediated pathologies; however, in-depth research addressing this relevant aspect of MC biology is lacking.	Methylcholanthrene	14-16	tachykinin receptor 1	Mus musculus	68-72
25201259-10	2015	In a positive signaling loop HK-1 promoted TNF and IL-6 secretion by MC degranulation and protein synthesis, the latter through the phosphoinositide 3-kinase/Akt/nuclear factor kappaB pathways.	Methylcholanthrene	69-71	tumor necrosis factor	Mus musculus	43-46
25201259-10	2015	In a positive signaling loop HK-1 promoted TNF and IL-6 secretion by MC degranulation and protein synthesis, the latter through the phosphoinositide 3-kinase/Akt/nuclear factor kappaB pathways.	Methylcholanthrene	69-71	interleukin 6	Mus musculus	51-55
25201259-12	2015	CONCLUSIONS: FcepsilonRI stimulation of MCs promotes autocrine secretion of HK-1, which signals through NK1R to provide adjuvancy for efficient development of FcepsilonRI-MC-mediated disorders.	Methylcholanthrene	40-42	Fc receptor, IgE, high affinity I, gamma polypeptide	Mus musculus	13-24
25201259-12	2015	CONCLUSIONS: FcepsilonRI stimulation of MCs promotes autocrine secretion of HK-1, which signals through NK1R to provide adjuvancy for efficient development of FcepsilonRI-MC-mediated disorders.	Methylcholanthrene	40-42	tachykinin receptor 1	Mus musculus	104-108
25201259-12	2015	CONCLUSIONS: FcepsilonRI stimulation of MCs promotes autocrine secretion of HK-1, which signals through NK1R to provide adjuvancy for efficient development of FcepsilonRI-MC-mediated disorders.	Methylcholanthrene	40-42	Fc receptor, IgE, high affinity I, gamma polypeptide	Mus musculus	159-170
26021445-8	2015	RESULTS: The Purdy score, perihematomal PPARgamma levels, BBB permeability, and BWC were all significantly increased in the MC group compared to the NC group.	Methylcholanthrene	124-126	peroxisome proliferator-activated receptor gamma	Oryctolagus cuniculus	40-49
25786523-1	2015	The effects of the peroxisome proliferator, dehydroepiandrosterone sulfate (DHEAS), and the typical cytochrome P450 (CYP) inducers phenobarbital (PB) and 3-methylcholanthrene (3-MC) on fatty liver were examined in rats.	Methylcholanthrene	154-174	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-120
25734369-4	2015	(2) Molecular compound (MC) crystals were formed in the mixtures of OOP/OPO and PPO/OOP.	Methylcholanthrene	24-26	protoporphyrinogen oxidase	Homo sapiens	80-83
25734369-7	2015	We determined that specific molecular interactions may cause this different phase behavior (stability of POP/OPO and POP/PPO MC crystals and metastability of OOP/OPO and PPO/OOP MC crystals).	Methylcholanthrene	125-127	protoporphyrinogen oxidase	Homo sapiens	121-124
25377919-4	2015	A 40 mg/kg dose of the Cyp1a1 inducer 3-methylcholanthrene (3MC) eliminated POR expression in both liver and small intestine, whereas treatment at 4 mg/kg led to a more targeted deletion in the liver.	Methylcholanthrene	38-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	23-29
25645457-5	2015	In addition, this report outlines for the first time, the sensitivity of MC-DBP gain to linear transmission line impairments and defines a trade-off between performance and complexity.	Methylcholanthrene	73-75	D-box binding PAR bZIP transcription factor	Homo sapiens	76-79
25377919-4	2015	A 40 mg/kg dose of the Cyp1a1 inducer 3-methylcholanthrene (3MC) eliminated POR expression in both liver and small intestine, whereas treatment at 4 mg/kg led to a more targeted deletion in the liver.	Methylcholanthrene	38-58	cytochrome p450 oxidoreductase	Mus musculus	76-79
25377919-4	2015	A 40 mg/kg dose of the Cyp1a1 inducer 3-methylcholanthrene (3MC) eliminated POR expression in both liver and small intestine, whereas treatment at 4 mg/kg led to a more targeted deletion in the liver.	Methylcholanthrene	60-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	23-29
25377919-4	2015	A 40 mg/kg dose of the Cyp1a1 inducer 3-methylcholanthrene (3MC) eliminated POR expression in both liver and small intestine, whereas treatment at 4 mg/kg led to a more targeted deletion in the liver.	Methylcholanthrene	60-63	cytochrome p450 oxidoreductase	Mus musculus	76-79
25528284-8	2015	When BP-3 was incubated with liver microsomes from untreated rats or phenobarbital-, 3-methylcholanthrene-, or acetone-treated rats in the presence of NADPH, estrogenic activity was increased.	Methylcholanthrene	85-105	Blood pressure QTL 3	Rattus norvegicus	5-9
25615839-5	2015	Control mice treated with 3-methylcholanthrene (3MC), an AhR agonist, exhibited decreased bone mass and increased bone resorption, whereas AhR(CtskDeltaOc/DeltaOc) (Ctsk(Cre/+);AhR(flox/flox)) mice injected with 3MC appeared to have a normal bone phenotype.	Methylcholanthrene	48-51	aryl-hydrocarbon receptor	Mus musculus	57-60
25410648-10	2015	CONCLUSIONS: Both 2-L PEG/Asc and SP/MC had adequate bowel cleansing efficacy to satisfy PDR and ADR as quality indicator and had showed similar tolerability.	Methylcholanthrene	37-39	aldo-keto reductase family 1 member B	Homo sapiens	97-100
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	cadherin 1	Homo sapiens	117-121
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	glutathione S-transferase pi 1	Homo sapiens	123-128
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	phosphatase and tensin homolog	Homo sapiens	130-134
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	APC regulator of WNT signaling pathway	Homo sapiens	136-139
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	RUNX family transcription factor 3	Homo sapiens	141-146
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	O-6-methylguanine-DNA methyltransferase	Homo sapiens	151-155
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	cellular communication network factor 1	Homo sapiens	231-236
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	semaphorin 3C	Homo sapiens	238-244
25784989-4	2015	Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues.	Methylcholanthrene	34-36	prostaglandin-endoperoxide synthase 2	Homo sapiens	249-254
25560632-12	2015	We observe that MC and NCSC are able to increase expression of keratins 8, 14, 19, and vimentin in the co-cultured HPK.	Methylcholanthrene	16-18	vimentin	Homo sapiens	87-95
25384044-0	2014	Increased CD112 expression in methylcholanthrene-induced tumors in CD155-deficient mice.	Methylcholanthrene	30-48	nectin cell adhesion molecule 2	Mus musculus	10-15
26186463-6	2015	Single-nucleotide 5 hmC profiling performed on a genome-wide scale revealed that TET1 overexpression induced 5 mC oxidation without a distribution bias among genetic elements and structures.	Methylcholanthrene	21-23	tet methylcytosine dioxygenase 1	Homo sapiens	81-85
26839242-6	2015	In the study of receptor status of tumors it was observed that 100% of MC cases were estrogen-, progesterone- and HER2/ neu negative.	Methylcholanthrene	71-73	erb-b2 receptor tyrosine kinase 2	Homo sapiens	114-118
26839242-6	2015	In the study of receptor status of tumors it was observed that 100% of MC cases were estrogen-, progesterone- and HER2/ neu negative.	Methylcholanthrene	71-73	erb-b2 receptor tyrosine kinase 2	Homo sapiens	120-123
26105999-1	2015	Hydroxymethylcytosine (hmC) is a natural nucleobase, which is converted from methylcytosine (mC) by tet methylcytosine dioxygenase (TET) family (TET1-3) enzymes.	Methylcholanthrene	24-26	tet methylcytosine dioxygenase 1	Homo sapiens	145-151
23712962-0	2014	Acute exposure to 3-methylcholanthrene induces hepatic oxidative stress via activation of the Nrf2/ARE signaling pathway in mice.	Methylcholanthrene	18-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	94-98
23712962-6	2014	Moreover, the mRNA levels of Nrf2/ARE target genes, including glutathione peroxidase (Gpx), glutathione reductase (GR), glutathione synthetase (GS), NAD(P)H: quinone oxidoreductase 1 (Nqo1), superoxide dismutase 1 (Sod1), and Sod2, increased significantly after treatment with 3MC for 24 hours.	Methylcholanthrene	277-280	nuclear factor, erythroid derived 2, like 2	Mus musculus	29-33
23712962-7	2014	The hepatic levels of NQO1 and the activities of GR and GS were also significantly enhanced at 24 hours after 3MC treatment.	Methylcholanthrene	110-113	NAD(P)H dehydrogenase, quinone 1	Mus musculus	22-26
23712962-7	2014	The hepatic levels of NQO1 and the activities of GR and GS were also significantly enhanced at 24 hours after 3MC treatment.	Methylcholanthrene	110-113	glutathione reductase	Mus musculus	49-51
23712962-8	2014	Because the expression of NQO1 is co-regulated by Nrf2/ARE and AhR/XRE in mammalian tissues, NQO1 may play an important role in protecting against the oxidative stress induced by 3MC.	Methylcholanthrene	179-182	NAD(P)H quinone dehydrogenase 1	Homo sapiens	26-30
23712962-8	2014	Because the expression of NQO1 is co-regulated by Nrf2/ARE and AhR/XRE in mammalian tissues, NQO1 may play an important role in protecting against the oxidative stress induced by 3MC.	Methylcholanthrene	179-182	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
23712962-8	2014	Because the expression of NQO1 is co-regulated by Nrf2/ARE and AhR/XRE in mammalian tissues, NQO1 may play an important role in protecting against the oxidative stress induced by 3MC.	Methylcholanthrene	179-182	aryl hydrocarbon receptor	Homo sapiens	63-66
23712962-8	2014	Because the expression of NQO1 is co-regulated by Nrf2/ARE and AhR/XRE in mammalian tissues, NQO1 may play an important role in protecting against the oxidative stress induced by 3MC.	Methylcholanthrene	179-182	NAD(P)H quinone dehydrogenase 1	Homo sapiens	93-97
23712962-9	2014	Taken together, our findings suggested that acute exposure to 3MC altered the cellular redox balance in hepatocytes to trigger Nrf2-regulated antioxidant responses, which may represent an adaptive cell defense mechanism against the oxidative stress induced by PAHs.	Methylcholanthrene	62-65	nuclear factor, erythroid derived 2, like 2	Mus musculus	127-131
25584145-9	2014	Indeed, we found that 7-day exposure of BNL cells to 3-MC reduced the level of the adhesion molecule and epithelial marker Ecadherin and increased reciprocally the level of the mesenchymal marker vimentin in a dose-dependent manner.	Methylcholanthrene	53-57	cadherin 1	Mus musculus	123-132
25584145-9	2014	Indeed, we found that 7-day exposure of BNL cells to 3-MC reduced the level of the adhesion molecule and epithelial marker Ecadherin and increased reciprocally the level of the mesenchymal marker vimentin in a dose-dependent manner.	Methylcholanthrene	53-57	vimentin	Mus musculus	196-204
25174530-4	2014	Previous studies indicate that the loss of beta-catenin in hepatocytes diminishes the response to the AhR agonists 3-methylcholanthrene (3MC) in vivo and to 2,3,7,8-tetrachlorodibenzo-[p]-dioxin in vitro.	Methylcholanthrene	115-135	catenin (cadherin associated protein), beta 1	Mus musculus	43-55
25174530-4	2014	Previous studies indicate that the loss of beta-catenin in hepatocytes diminishes the response to the AhR agonists 3-methylcholanthrene (3MC) in vivo and to 2,3,7,8-tetrachlorodibenzo-[p]-dioxin in vitro.	Methylcholanthrene	115-135	aryl-hydrocarbon receptor	Mus musculus	102-105
25174530-4	2014	Previous studies indicate that the loss of beta-catenin in hepatocytes diminishes the response to the AhR agonists 3-methylcholanthrene (3MC) in vivo and to 2,3,7,8-tetrachlorodibenzo-[p]-dioxin in vitro.	Methylcholanthrene	137-140	catenin (cadherin associated protein), beta 1	Mus musculus	43-55
25174530-4	2014	Previous studies indicate that the loss of beta-catenin in hepatocytes diminishes the response to the AhR agonists 3-methylcholanthrene (3MC) in vivo and to 2,3,7,8-tetrachlorodibenzo-[p]-dioxin in vitro.	Methylcholanthrene	137-140	aryl-hydrocarbon receptor	Mus musculus	102-105
25482539-2	2015	Using the MC-SCE method in conjunction with backbone variability, we can reliably determine the side chain rotamer populations derived from both room temperature and cryogenically cooled X-ray crystallographic structures for CypA and H-Ras and NMR J-coupling constants for CypA, Eglin-C, and the DHFR product binary complexes E:THF and E:FOL.	Methylcholanthrene	10-12	peptidylprolyl isomerase A	Homo sapiens	225-229
25482539-2	2015	Using the MC-SCE method in conjunction with backbone variability, we can reliably determine the side chain rotamer populations derived from both room temperature and cryogenically cooled X-ray crystallographic structures for CypA and H-Ras and NMR J-coupling constants for CypA, Eglin-C, and the DHFR product binary complexes E:THF and E:FOL.	Methylcholanthrene	10-12	HRas proto-oncogene, GTPase	Homo sapiens	234-239
25482539-2	2015	Using the MC-SCE method in conjunction with backbone variability, we can reliably determine the side chain rotamer populations derived from both room temperature and cryogenically cooled X-ray crystallographic structures for CypA and H-Ras and NMR J-coupling constants for CypA, Eglin-C, and the DHFR product binary complexes E:THF and E:FOL.	Methylcholanthrene	10-12	peptidylprolyl isomerase A	Homo sapiens	273-277
25482539-2	2015	Using the MC-SCE method in conjunction with backbone variability, we can reliably determine the side chain rotamer populations derived from both room temperature and cryogenically cooled X-ray crystallographic structures for CypA and H-Ras and NMR J-coupling constants for CypA, Eglin-C, and the DHFR product binary complexes E:THF and E:FOL.	Methylcholanthrene	10-12	dihydrofolate reductase	Homo sapiens	296-300
25336106-6	2015	Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4.	Methylcholanthrene	84-104	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-65
25336106-6	2015	Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4.	Methylcholanthrene	84-104	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	109-115
25336106-6	2015	Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4.	Methylcholanthrene	84-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	138-144
24768319-8	2015	Indeed, it has been shown that PGE2 prevents human and murine MC activity in vitro through activation of the EP2 receptor, and also that both exogenously administered and endogenous PGE2 inhibit airway MC activity in vivo in mouse models of asthma (likely through an EP2-mediated mechanism as well).	Methylcholanthrene	202-204	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	109-112
25135755-5	2014	The absorption spectra of all complexes are significantly affected by spin-orbit coupling (red-shift and broadening), especially in the non-cyclometalated complexes and characterized by the presence of pure low-lying (3)MC states.	Methylcholanthrene	220-222	spindlin 1	Homo sapiens	70-74
25501021-1	2014	TET2 (Ten Eleven Translocation 2) is a dioxygenase that converts methylcytosine (mC) to hydroxymethylcytosine (hmC).	Methylcholanthrene	81-83	tet methylcytosine dioxygenase 2	Mus musculus	0-4
25501021-1	2014	TET2 (Ten Eleven Translocation 2) is a dioxygenase that converts methylcytosine (mC) to hydroxymethylcytosine (hmC).	Methylcholanthrene	81-83	tet methylcytosine dioxygenase 2	Mus musculus	6-32
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	78-98	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	126-145
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	78-98	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	147-154
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	78-98	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	221-228
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	100-103	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	126-145
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	100-103	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	147-154
25112181-6	2014	In studying the concentration dependent effects of the environmental toxicant 3-methylcholanthrene (3MC) on the activation of cytochrome P450 1A1 (Cyp 1A1) enzyme in H4IIE rat hepatoma cells, statistical variation of the Cyp 1A1 response was significantly lower (C.V. = 5 %) when using the developed mixture generator compared to that using the conventional gradient generator (C.V. = 12 %).	Methylcholanthrene	100-103	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	221-228
25174530-5	2014	The knockout of beta-catenin also impairs the zonal pattern of AhR target gene induction by 3MC.	Methylcholanthrene	92-95	catenin (cadherin associated protein), beta 1	Mus musculus	16-28
25174530-5	2014	The knockout of beta-catenin also impairs the zonal pattern of AhR target gene induction by 3MC.	Methylcholanthrene	92-95	aryl-hydrocarbon receptor	Mus musculus	63-66
25384044-0	2014	Increased CD112 expression in methylcholanthrene-induced tumors in CD155-deficient mice.	Methylcholanthrene	30-48	poliovirus receptor	Mus musculus	67-72
25261897-3	2014	The Au@AgPt nanorattles are loaded onto the MC by physical adsorption.	Methylcholanthrene	44-46	angiopoietin 1	Homo sapiens	7-11
25085111-1	2014	LM escape immune surveillance, in part, as a result of the expansion of CD11b+MC, which alter the intrahepatic microenvironment to promote tumor tolerance.	Methylcholanthrene	78-80	integrin alpha M	Mus musculus	72-77
25085111-8	2014	We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity.	Methylcholanthrene	28-30	CD80 antigen	Mus musculus	47-51
25085111-8	2014	We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity.	Methylcholanthrene	28-30	integrin alpha M	Mus musculus	89-94
25085111-8	2014	We implicated hepatic CD11b+MC as mediators of CD80 down-modulation on HBC ex vivo via a CD11b-dependent mechanism that required cell-to-cell contact and STAT3 activity.	Methylcholanthrene	28-30	signal transducer and activator of transcription 3	Mus musculus	154-159
25085111-9	2014	Therefore, CD11b+MC may compromise the ability of HBC to promote T cell activation in the setting of LM as a result of diminished expression of CD80.	Methylcholanthrene	17-19	CD80 antigen	Mus musculus	144-148
25261897-8	2014	The large specific surface area of MC and MC@Au@AgPt were characterized by the BET method.	Methylcholanthrene	42-44	angiopoietin 1	Homo sapiens	48-52
25261897-8	2014	The large specific surface area of MC and MC@Au@AgPt were characterized by the BET method.	Methylcholanthrene	42-44	delta/notch like EGF repeat containing	Homo sapiens	79-82
24814190-10	2014	Vasa in spermatogonia concentrates in small areas of the cytoplasm and is surrounded by mitochondria, which is reminiscent of MC.	Methylcholanthrene	126-128	probable ATP-dependent RNA helicase DDX4	Oryzias latipes	0-4
25258363-5	2014	Both displayed high affinity for the sequence when C or 5 mC was present and much reduced affinity when 5 hmC or 5 fC was present, indicating that they differentiate primarily oxidized C from unoxidized C, rather than methylated C from unmethylated C. 5 caC affected the two proteins differently, abolishing binding by Egr1 but not by WT1.	Methylcholanthrene	58-60	early growth response 1	Homo sapiens	319-323
25258363-5	2014	Both displayed high affinity for the sequence when C or 5 mC was present and much reduced affinity when 5 hmC or 5 fC was present, indicating that they differentiate primarily oxidized C from unoxidized C, rather than methylated C from unmethylated C. 5 caC affected the two proteins differently, abolishing binding by Egr1 but not by WT1.	Methylcholanthrene	58-60	WT1 transcription factor	Homo sapiens	335-338
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	83-103	aryl hydrocarbon receptor	Homo sapiens	48-73
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	83-103	aryl hydrocarbon receptor	Homo sapiens	75-78
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	83-103	H3 histone pseudogene 16	Homo sapiens	240-243
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	83-103	dynactin subunit 6	Homo sapiens	244-247
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	83-103	ras homolog family member A	Homo sapiens	266-270
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	105-108	aryl hydrocarbon receptor	Homo sapiens	48-73
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	105-108	aryl hydrocarbon receptor	Homo sapiens	75-78
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	105-108	H3 histone pseudogene 16	Homo sapiens	240-243
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	105-108	dynactin subunit 6	Homo sapiens	244-247
24535918-1	2014	We previously identified that activation of the aryl hydrocarbon receptor (AhR) by 3-methylcholanthrene (3MC) exerts antiproliferative and antimigratory effects on human umbilical vein endothelial cells (HUVECs) through the upregulation of p21/p27 transcription and RhoA activation.	Methylcholanthrene	105-108	ras homolog family member A	Homo sapiens	266-270
24535918-2	2014	In this study, we investigated the mechanisms of 3MC-mediated downregulation of cytosolic p21/ p27, and the effects of 3MC on RhoA activation and cell migration, in mouse cerebral vascular endothelial cells (MCVECs).	Methylcholanthrene	49-52	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	90-93
24535918-2	2014	In this study, we investigated the mechanisms of 3MC-mediated downregulation of cytosolic p21/ p27, and the effects of 3MC on RhoA activation and cell migration, in mouse cerebral vascular endothelial cells (MCVECs).	Methylcholanthrene	49-52	cyclin-dependent kinase inhibitor 1B	Mus musculus	95-98
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	H3 histone pseudogene 16	Homo sapiens	62-65
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	dynactin subunit 6	Homo sapiens	66-69
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	aryl hydrocarbon receptor	Homo sapiens	78-81
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	ras homolog family member A	Homo sapiens	82-86
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	phosphatase and tensin homolog	Homo sapiens	87-91
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	AKT serine/threonine kinase 1	Homo sapiens	106-109
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	H3 histone pseudogene 16	Homo sapiens	148-151
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	dynactin subunit 6	Homo sapiens	152-155
24535918-3	2014	Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN-mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback.	Methylcholanthrene	27-30	ras homolog family member A	Homo sapiens	175-179
24535918-4	2014	Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells.	Methylcholanthrene	140-143	H3 histone pseudogene 16	Homo sapiens	18-21
24535918-4	2014	Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells.	Methylcholanthrene	140-143	dynactin subunit 6	Homo sapiens	22-25
24535918-4	2014	Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells.	Methylcholanthrene	140-143	H3 histone pseudogene 16	Homo sapiens	50-53
24535918-4	2014	Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC-treated cells.	Methylcholanthrene	140-143	dynactin subunit 6	Homo sapiens	54-57
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	AKT serine/threonine kinase 1	Homo sapiens	36-39
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	ras homolog family member A	Homo sapiens	64-68
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	ras homolog family member A	Homo sapiens	80-84
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	phosphatase and tensin homolog	Homo sapiens	85-89
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	ras homolog family member A	Homo sapiens	80-84
24535918-6	2014	Treatment with YS-49 activated PI3K/Akt, a downstream target of RhoA, to reduce RhoA/PTEN activation in the 3MC-treated cells, whereas treatment with wortmannin, a PI3K inhibitor, activated RhoA/PTEN.	Methylcholanthrene	108-111	phosphatase and tensin homolog	Homo sapiens	195-199
25349783-3	2014	It has been proposed that after binding of ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3methylcholanthrene (3-MC), or beta-naphthoflavone (beta-NF), the AhR dissociates from HSP90 and translocates to the nucleus.	Methylcholanthrene	103-122	aryl hydrocarbon receptor	Homo sapiens	169-172
25349783-3	2014	It has been proposed that after binding of ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3methylcholanthrene (3-MC), or beta-naphthoflavone (beta-NF), the AhR dissociates from HSP90 and translocates to the nucleus.	Methylcholanthrene	103-122	heat shock protein 90 alpha family class A member 1	Homo sapiens	190-195
25349783-3	2014	It has been proposed that after binding of ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3methylcholanthrene (3-MC), or beta-naphthoflavone (beta-NF), the AhR dissociates from HSP90 and translocates to the nucleus.	Methylcholanthrene	124-128	aryl hydrocarbon receptor	Homo sapiens	169-172
25349783-3	2014	It has been proposed that after binding of ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3methylcholanthrene (3-MC), or beta-naphthoflavone (beta-NF), the AhR dissociates from HSP90 and translocates to the nucleus.	Methylcholanthrene	124-128	heat shock protein 90 alpha family class A member 1	Homo sapiens	190-195
25232488-7	2014	Additionally, GATA3 silencing via short hairpin RNA (shRNA) promoted cell proliferation of SVHUC with exposure to a chemical carcinogen 3-methylcholanthrene.	Methylcholanthrene	136-156	GATA binding protein 3	Mus musculus	14-19
25232488-8	2014	In vitro transformation assay with 3-methylcholanthrene then showed a significantly higher number of colonies in SVHUC-AR/GATA3-shRNA, compared with control SVHUC, and R1881 further induced colony formation.	Methylcholanthrene	35-55	androgen receptor	Mus musculus	113-121
25232488-8	2014	In vitro transformation assay with 3-methylcholanthrene then showed a significantly higher number of colonies in SVHUC-AR/GATA3-shRNA, compared with control SVHUC, and R1881 further induced colony formation.	Methylcholanthrene	35-55	GATA binding protein 3	Mus musculus	122-127
25189612-5	2014	Western blot was also employed to investigate the renal injury molecule-1 (Kim-1) expression in HEK-293 cells exposed to MC.	Methylcholanthrene	121-123	hepatitis A virus cellular receptor 1	Homo sapiens	75-80
24938130-8	2014	Furthermore, 3-methylcholanthrene, an AhR agonist, induces low bone mass with increased bone resorption in control mice, but not in AhR(DeltaOc/DeltaOc) mice.	Methylcholanthrene	13-33	aryl-hydrocarbon receptor	Mus musculus	38-41
25314276-7	2014	We now demonstrate that in SC-MC co-cultures, siRNA mediated knockdown of NRP2 in SCs decreased the formation of SC clusters while these SCs maintained their capacity to align in bands of Bungner-like columnar arrays.	Methylcholanthrene	30-32	neuropilin 2	Homo sapiens	74-78
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	18-38	nuclear respiratory factor 1	Mus musculus	61-65
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	78-84
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	18-38	nuclear respiratory factor 1	Mus musculus	127-131
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	40-44	nuclear respiratory factor 1	Mus musculus	61-65
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	40-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	78-84
25092871-3	2014	Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression.	Methylcholanthrene	40-44	nuclear respiratory factor 1	Mus musculus	127-131
25011081-6	2014	In terms of kinetic parameters for acetate oxidizing bacteria, estimation by MC-NLLS and DEA were, respectively, km 1.12 and 3.25 +- 0.56 kg COD kg COD(-1)d(-1), KS 0.20 and 0.29 +- 0.018 kg COD m(-3) and Yac-st 0.14 and 0.10 +- 0.016 kg COD kg COD(-1).	Methylcholanthrene	77-79	retinitis pigmentosa GTPase regulator	Homo sapiens	148-154
25011081-6	2014	In terms of kinetic parameters for acetate oxidizing bacteria, estimation by MC-NLLS and DEA were, respectively, km 1.12 and 3.25 +- 0.56 kg COD kg COD(-1)d(-1), KS 0.20 and 0.29 +- 0.018 kg COD m(-3) and Yac-st 0.14 and 0.10 +- 0.016 kg COD kg COD(-1).	Methylcholanthrene	77-79	retinitis pigmentosa GTPase regulator	Homo sapiens	245-251
24969701-8	2014	CYP1As inhibition by alpha-naphthoflavone or anti-CYP1As antibodies significantly reduced omega-1 4 HETE formation in the lungs and liver, whereas CYP1As induction by 3-methylcholanthrene resulted in a significant increase in omega-1 4 HETEs formation in the heart, lungs, kidney, and livers by 370, 646, 532, and 848%, respectively.	Methylcholanthrene	167-187	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-4
25124514-7	2014	A low dose of 3MC activated the aryl hydrocarbon receptor, which negatively regulated lipid synthesis in the livers.	Methylcholanthrene	14-17	aryl-hydrocarbon receptor	Mus musculus	32-57
24996270-6	2014	Correspondingly, mRNA expression of candidates for SCFA(-)/HCO3(-) exchangers, namely downregulated in adenoma (DRA), putative anion transporter 1 (PAT1), and anion exchanger 2 (AE2) were increased in the MC group.	Methylcholanthrene	205-207	HLA class II histocompatibility antigen, DR alpha chain	Capra hircus	112-115
24996270-7	2014	Further, upregulation in monocarboxylate transporter 1 (MCT1) and monocarboxylate transporter 4 (MCT4) mRNA abundances was observed in the MC group.	Methylcholanthrene	56-58	monocarboxylate transporter 1	Capra hircus	25-54
25924357-3	2014	The promising PROX performance over the IrFe/MC can be attributed to the intrinsic surface properties of MC and its specific interaction with metal species.	Methylcholanthrene	45-47	pyruvate dehydrogenase complex component X	Homo sapiens	14-18
25189612-8	2014	MC (1:1) at 41.25 and 82.50 microg/mL could elevate the Kim-1 expression in HEK-293 cells.	Methylcholanthrene	0-2	hepatitis A virus cellular receptor 1	Homo sapiens	56-61
24967965-9	2014	We next observed PINK1 accumulation in the mitochondrial membrane and parkin translocation into the mitochondria from the cytosol in the rotenone-treated RPE-MC cells, which indicates that increased mitophagy accompanies MC in ARPE-19 cells.	Methylcholanthrene	158-160	PTEN induced kinase 1	Homo sapiens	17-22
24727239-7	2014	It was shown that miR-21, 221, 222, and 429 expression levels decreased in the liver of DDT-, BP-, and MC-treated rats, whereas increases were observed in CYP1A1 and CYP2B1 mRNA expression levels and protein content, and EROD and PROD activities.	Methylcholanthrene	103-105	microRNA 21	Rattus norvegicus	18-24
24472833-8	2014	Finally, we found that in vivo inhibition of either PDGF-BB or Shh signaling reduces NG2(+) MC recruitment into neovessels and subsequently reduces neovessel life span.	Methylcholanthrene	92-94	sonic hedgehog	Mus musculus	63-66
24591650-6	2014	F318L and F318A mutations resulted in the conversion of AhR agonists beta-naphthoflavone and 3-methylcholanthrene, respectively, into partial agonists/antagonists.	Methylcholanthrene	93-113	aryl-hydrocarbon receptor	Mus musculus	56-59
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Methylcholanthrene	111-131	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	31-37
24146099-8	2014	However, in MCT, myocardial HSP70 expression increased by 42.7% versus con and MC (p = 0.016), HSF-1 by 12% versus con and MC (p &lt; 0.05), and total nuclei count increased by 37% versus MC (p &lt; 0.05).	Methylcholanthrene	12-14	LOW QUALITY PROTEIN: heat shock 70 kDa protein 1-like	Oryctolagus cuniculus	28-33
24146099-8	2014	However, in MCT, myocardial HSP70 expression increased by 42.7% versus con and MC (p = 0.016), HSF-1 by 12% versus con and MC (p &lt; 0.05), and total nuclei count increased by 37% versus MC (p &lt; 0.05).	Methylcholanthrene	79-81	LOW QUALITY PROTEIN: heat shock 70 kDa protein 1-like	Oryctolagus cuniculus	28-33
24146099-8	2014	However, in MCT, myocardial HSP70 expression increased by 42.7% versus con and MC (p = 0.016), HSF-1 by 12% versus con and MC (p &lt; 0.05), and total nuclei count increased by 37% versus MC (p &lt; 0.05).	Methylcholanthrene	79-81	LOW QUALITY PROTEIN: heat shock 70 kDa protein 1-like	Oryctolagus cuniculus	28-33
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Methylcholanthrene	111-131	peptidylprolyl isomerase G	Homo sapiens	31-34
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Methylcholanthrene	133-137	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	31-37
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Methylcholanthrene	133-137	peptidylprolyl isomerase G	Homo sapiens	31-34
24663500-8	2014	Similarly, the known CYP inducers- 3-MC, CPA and ethanol have also shown significantly high docking scores with all the three studied CYP regulators.	Methylcholanthrene	35-39	peptidylprolyl isomerase G	Homo sapiens	21-24
24663500-8	2014	Similarly, the known CYP inducers- 3-MC, CPA and ethanol have also shown significantly high docking scores with all the three studied CYP regulators.	Methylcholanthrene	35-39	peptidylprolyl isomerase G	Homo sapiens	134-137
24658119-3	2014	AhR/RhoA activation mediated by 3MC was essential for the upregulation of retinoblastoma 2 (pRb2) and histone deacetylase 1 (HDAC1), whereas their nuclear translocation was primarily modulated by RhoA activation.	Methylcholanthrene	32-35	ras homolog family member A	Homo sapiens	4-8
24658119-3	2014	AhR/RhoA activation mediated by 3MC was essential for the upregulation of retinoblastoma 2 (pRb2) and histone deacetylase 1 (HDAC1), whereas their nuclear translocation was primarily modulated by RhoA activation.	Methylcholanthrene	32-35	proline rich protein BstNI subfamily 2	Homo sapiens	92-96
24658119-0	2014	3-Methylcholanthrene, an AhR agonist, caused cell-cycle arrest by histone deacetylation through a RhoA-dependent recruitment of HDAC1 and pRb2 to E2F1 complex.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	25-28
24658119-3	2014	AhR/RhoA activation mediated by 3MC was essential for the upregulation of retinoblastoma 2 (pRb2) and histone deacetylase 1 (HDAC1), whereas their nuclear translocation was primarily modulated by RhoA activation.	Methylcholanthrene	32-35	histone deacetylase 1	Homo sapiens	102-123
24658119-0	2014	3-Methylcholanthrene, an AhR agonist, caused cell-cycle arrest by histone deacetylation through a RhoA-dependent recruitment of HDAC1 and pRb2 to E2F1 complex.	Methylcholanthrene	0-20	ras homolog family member A	Homo sapiens	98-102
24658119-3	2014	AhR/RhoA activation mediated by 3MC was essential for the upregulation of retinoblastoma 2 (pRb2) and histone deacetylase 1 (HDAC1), whereas their nuclear translocation was primarily modulated by RhoA activation.	Methylcholanthrene	32-35	histone deacetylase 1	Homo sapiens	125-130
24658119-0	2014	3-Methylcholanthrene, an AhR agonist, caused cell-cycle arrest by histone deacetylation through a RhoA-dependent recruitment of HDAC1 and pRb2 to E2F1 complex.	Methylcholanthrene	0-20	histone deacetylase 1	Homo sapiens	128-133
24658119-6	2014	Co-immunoprecipitation and electrophoretic mobility shift assay (EMSA) results showed that simvastatin prevented the 3MC-increased binding activities of E2F1 proteins in their promoter regions.	Methylcholanthrene	117-120	E2F transcription factor 1	Homo sapiens	153-157
24658119-0	2014	3-Methylcholanthrene, an AhR agonist, caused cell-cycle arrest by histone deacetylation through a RhoA-dependent recruitment of HDAC1 and pRb2 to E2F1 complex.	Methylcholanthrene	0-20	proline rich protein BstNI subfamily 2	Homo sapiens	138-142
24658119-7	2014	Additionally, RhoA inhibitors (statins) reversed the effect of 3MC in inhibiting DNA synthesis by decreasing the nuclear translocation of pRb2/HDAC1, leading to a recovery of the levels of cell-cycle regulatory proteins.	Methylcholanthrene	63-66	ras homolog family member A	Homo sapiens	14-18
24658119-0	2014	3-Methylcholanthrene, an AhR agonist, caused cell-cycle arrest by histone deacetylation through a RhoA-dependent recruitment of HDAC1 and pRb2 to E2F1 complex.	Methylcholanthrene	0-20	E2F transcription factor 1	Homo sapiens	146-150
24658119-7	2014	Additionally, RhoA inhibitors (statins) reversed the effect of 3MC in inhibiting DNA synthesis by decreasing the nuclear translocation of pRb2/HDAC1, leading to a recovery of the levels of cell-cycle regulatory proteins.	Methylcholanthrene	63-66	proline rich protein BstNI subfamily 2	Homo sapiens	138-142
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	67-87	H3 histone pseudogene 16	Homo sapiens	175-178
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	67-87	interferon alpha inducible protein 27	Homo sapiens	183-186
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	67-87	cyclin dependent kinase 2	Homo sapiens	254-258
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	89-92	H3 histone pseudogene 16	Homo sapiens	175-178
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	89-92	interferon alpha inducible protein 27	Homo sapiens	183-186
24658119-1	2014	We previously showed that treating vascular endothelial cells with 3-methylcholanthrene (3MC) caused cell-cycle arrest in the Go/G1 phase; this resulted from the induction of p21 and p27 and a decreased level and activity of the cyclin-dependent kinase, Cdk2.	Methylcholanthrene	89-92	cyclin dependent kinase 2	Homo sapiens	254-258
24658119-3	2014	AhR/RhoA activation mediated by 3MC was essential for the upregulation of retinoblastoma 2 (pRb2) and histone deacetylase 1 (HDAC1), whereas their nuclear translocation was primarily modulated by RhoA activation.	Methylcholanthrene	32-35	aryl hydrocarbon receptor	Homo sapiens	0-3
24658119-7	2014	Additionally, RhoA inhibitors (statins) reversed the effect of 3MC in inhibiting DNA synthesis by decreasing the nuclear translocation of pRb2/HDAC1, leading to a recovery of the levels of cell-cycle regulatory proteins.	Methylcholanthrene	63-66	histone deacetylase 1	Homo sapiens	143-148
24658119-8	2014	In summary, 3MC decreased cell proliferation by the epigenetic modification of histone through an AhR/RhoA-dependent mechanism that can be rescued by statins.	Methylcholanthrene	12-15	aryl hydrocarbon receptor	Homo sapiens	98-101
24658119-8	2014	In summary, 3MC decreased cell proliferation by the epigenetic modification of histone through an AhR/RhoA-dependent mechanism that can be rescued by statins.	Methylcholanthrene	12-15	ras homolog family member A	Homo sapiens	102-106
24486526-5	2014	D2 suppresses the 3-methylcholanthrene-induced, dioxin response element (DRE)-driven luciferase activity in Hep3B cells and exogenous Arnt reverses this D2 suppression.	Methylcholanthrene	18-38	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	134-138
24566440-6	2014	LOOH (p &lt; 0.01), IL-6 (p &lt; 0.05) and hsCRP (p &lt; 0.05) responses to trials were lower in the MC group versus PLA.	Methylcholanthrene	101-103	interleukin 6	Homo sapiens	20-24
24681596-2	2014	Previous reports have demonstrated that 3-methylcholanthrene (3MC) is capable of altering the expression of aryl hydrocarbon receptor (AHR)-regulated genes and antioxidant genes in liver, but little is known about the expression patterns in other tissues.	Methylcholanthrene	40-60	aryl-hydrocarbon receptor	Mus musculus	108-133
24681596-2	2014	Previous reports have demonstrated that 3-methylcholanthrene (3MC) is capable of altering the expression of aryl hydrocarbon receptor (AHR)-regulated genes and antioxidant genes in liver, but little is known about the expression patterns in other tissues.	Methylcholanthrene	40-60	aryl-hydrocarbon receptor	Mus musculus	135-138
24681596-2	2014	Previous reports have demonstrated that 3-methylcholanthrene (3MC) is capable of altering the expression of aryl hydrocarbon receptor (AHR)-regulated genes and antioxidant genes in liver, but little is known about the expression patterns in other tissues.	Methylcholanthrene	62-65	aryl-hydrocarbon receptor	Mus musculus	108-133
24681596-2	2014	Previous reports have demonstrated that 3-methylcholanthrene (3MC) is capable of altering the expression of aryl hydrocarbon receptor (AHR)-regulated genes and antioxidant genes in liver, but little is known about the expression patterns in other tissues.	Methylcholanthrene	62-65	aryl-hydrocarbon receptor	Mus musculus	135-138
24681596-3	2014	To investigate whether similar effects could occur in the extrahepatic tissues, adult male ICR mice were received an intraperitoneal injection of 100 mg/kg 3MC and then analyzed after 6 and 24 h. We observed that the constitutive expression of AHR- and antioxidant-related genes was in a tissue-specific manner.	Methylcholanthrene	156-159	aryl-hydrocarbon receptor	Mus musculus	244-247
24681596-4	2014	Moreover, acute 3MC exposure significantly increased the mRNA levels of Cyp1a1 and Cyp1b1 in all the lung, kidney and heart.	Methylcholanthrene	16-19	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	72-78
24681596-4	2014	Moreover, acute 3MC exposure significantly increased the mRNA levels of Cyp1a1 and Cyp1b1 in all the lung, kidney and heart.	Methylcholanthrene	16-19	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	83-89
24681596-5	2014	As to antioxidant genes, 3MC induced the transcription of glutathione reductase (Gr) in the lung and kidney at 24 h and the transcription of glutathione peroxidase 1 (Gpx1) in the lung and kidney at 6 and 24 h. Glutathione-S-transferase A1 (Gsta1) was significantly reduced in the kidney at 24 h, while no effect was observed in the lung and heart.	Methylcholanthrene	25-28	glutathione reductase	Mus musculus	58-79
24681596-5	2014	As to antioxidant genes, 3MC induced the transcription of glutathione reductase (Gr) in the lung and kidney at 24 h and the transcription of glutathione peroxidase 1 (Gpx1) in the lung and kidney at 6 and 24 h. Glutathione-S-transferase A1 (Gsta1) was significantly reduced in the kidney at 24 h, while no effect was observed in the lung and heart.	Methylcholanthrene	25-28	glutathione peroxidase 1	Mus musculus	141-165
24681596-5	2014	As to antioxidant genes, 3MC induced the transcription of glutathione reductase (Gr) in the lung and kidney at 24 h and the transcription of glutathione peroxidase 1 (Gpx1) in the lung and kidney at 6 and 24 h. Glutathione-S-transferase A1 (Gsta1) was significantly reduced in the kidney at 24 h, while no effect was observed in the lung and heart.	Methylcholanthrene	25-28	glutathione peroxidase 1	Mus musculus	167-171
24681596-5	2014	As to antioxidant genes, 3MC induced the transcription of glutathione reductase (Gr) in the lung and kidney at 24 h and the transcription of glutathione peroxidase 1 (Gpx1) in the lung and kidney at 6 and 24 h. Glutathione-S-transferase A1 (Gsta1) was significantly reduced in the kidney at 24 h, while no effect was observed in the lung and heart.	Methylcholanthrene	25-28	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	211-239
24681596-5	2014	As to antioxidant genes, 3MC induced the transcription of glutathione reductase (Gr) in the lung and kidney at 24 h and the transcription of glutathione peroxidase 1 (Gpx1) in the lung and kidney at 6 and 24 h. Glutathione-S-transferase A1 (Gsta1) was significantly reduced in the kidney at 24 h, while no effect was observed in the lung and heart.	Methylcholanthrene	25-28	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	241-246
24681596-6	2014	The mRNA levels of NAD(P)H: quinone oxidoreductase 1 (Nqo1) were induced by 3MC in all the lung, kidney and heart.	Methylcholanthrene	76-79	NAD(P)H dehydrogenase, quinone 1	Mus musculus	19-52
24681596-6	2014	The mRNA levels of NAD(P)H: quinone oxidoreductase 1 (Nqo1) were induced by 3MC in all the lung, kidney and heart.	Methylcholanthrene	76-79	NAD(P)H dehydrogenase, quinone 1	Mus musculus	54-58
24606747-9	2014	Compared with the NC group, the expressions of INF-gamma, IL-12 and CP of serum increased in the MC group (P&lt;0.05 or P&lt;0.01).	Methylcholanthrene	97-99	interleukin 12B	Rattus norvegicus	58-63
24606747-10	2014	The expressions of IL-4 and IL-10 in the MC group were lower than those in the NC group (P&lt;0.01).	Methylcholanthrene	41-43	interleukin 4	Rattus norvegicus	19-23
24606747-10	2014	The expressions of IL-4 and IL-10 in the MC group were lower than those in the NC group (P&lt;0.01).	Methylcholanthrene	41-43	interleukin 10	Rattus norvegicus	28-33
24606747-11	2014	Compared with the NC group, the expressions of INF-gamma and CP of colon tissue significantly increased (P&lt;0.01 or P&lt;0.05), and the expression of IL-4 decreased in the MC group (P&lt;0.05).	Methylcholanthrene	174-176	interleukin 4	Rattus norvegicus	152-156
24575771-14	2014	Pharmacological inhibition of EZH2 using either DZNep or MC inhibitors phenocopied the genetic knockdown of EZH2 preventing cell proliferation and restoring myogenic differentiation both in vitro and in vivo.	Methylcholanthrene	57-59	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	30-34
23907410-11	2014	In 12 patients with MC, FLT3-ITD and NPM1 mutations were found, and these patients showed signs of hematological relapse.	Methylcholanthrene	20-22	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
23907410-12	2014	Our combined analysis of NPM1/FLT3-ITD mutations and hematopoietic chimerism improved the characterization of patients with MC after HSCT.	Methylcholanthrene	124-126	nucleophosmin 1	Homo sapiens	25-29
23907410-12	2014	Our combined analysis of NPM1/FLT3-ITD mutations and hematopoietic chimerism improved the characterization of patients with MC after HSCT.	Methylcholanthrene	124-126	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
25102695-6	2014	RESULTS: Compared with the NC group, paw swelling, AI, IFN-gamma, and Th1/Th2 were increased, and pulmonary function parameters, IL-4, FoxP3 were decreased significantly in the MC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	177-179	interferon gamma	Rattus norvegicus	55-64
24322980-3	2014	Experimental metastasis of MC-38GFP and Lewis lung (3LL) carcinoma cells was attenuated in Fuc-TVII(-/-) mice, which express minimal amount of selectin ligands.	Methylcholanthrene	27-29	fucosyltransferase 7	Mus musculus	91-99
25102695-6	2014	RESULTS: Compared with the NC group, paw swelling, AI, IFN-gamma, and Th1/Th2 were increased, and pulmonary function parameters, IL-4, FoxP3 were decreased significantly in the MC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	177-179	interleukin 4	Rattus norvegicus	129-133
25102695-6	2014	RESULTS: Compared with the NC group, paw swelling, AI, IFN-gamma, and Th1/Th2 were increased, and pulmonary function parameters, IL-4, FoxP3 were decreased significantly in the MC group (P &lt; 0.05 or P &lt; 0.01).	Methylcholanthrene	177-179	forkhead box P3	Rattus norvegicus	135-140
25203349-5	2014	High levels circulation of IP-10 have been found in HCV+MC, especially in patients with clinically active vasculitis.	Methylcholanthrene	56-58	C-X-C motif chemokine ligand 10	Homo sapiens	27-32
23692809-9	2014	CONCLUSIONS: Collectively, it is speculated that PPAR-gamma agonistic activity, anti-inflammatory, and antioxidative potential is critical for antinociceptive effect of MC in neuropathic pain.	Methylcholanthrene	169-171	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	49-59
24734226-5	2014	In this study, we evaluated the efficacy of delivering an MC-liposome vector containing a 3.2 kb androgen receptor (AR; HCC metastasis suppressor) cDNA into Hepatitis B Virus- (HBV-) induced HCC mouse livers.	Methylcholanthrene	58-60	androgen receptor	Mus musculus	97-114
24817304-11	2014	However, 3-MC dose-dependently inhibited (p &lt; 0.05) EC cells proliferation via AhR-mediated pathway.	Methylcholanthrene	9-13	aryl hydrocarbon receptor	Homo sapiens	82-85
25366958-4	2014	Patients with HCV chronic infection, or with MC+HCV, in presence of autoimmune thyroiditis, show higher serum levels of T-helper (Th)1 (C-X-C motif) ligand 10 (CXCL10) chemokine than patients without thyroiditis.	Methylcholanthrene	45-47	C-X-C motif chemokine ligand 10	Homo sapiens	160-166
24090375-12	2014	Finally, Western blot analysis confirmed significantly higher levels of HIF-1-alpha protein by MC-shPHD2, compared with PL-shPHD2 and PBS.	Methylcholanthrene	95-97	hypoxia inducible factor 1, alpha subunit	Mus musculus	72-83
24362577-4	2013	The CYP1A1 and 1A2, and CYP3A4 mRNA expression levels increased significantly in the PXB-mouse livers with 20 mg/kg of 3-MC (Cmax, 12.2 ng/mL), and 10 mg/kg rifampicin (Cmax, 6.9 microg/mL), respectively.	Methylcholanthrene	119-123	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	4-18
25374602-4	2014	Patients with HCV chronic infection, or with MC + HCV, in presence of autoimmune thyroiditis, show higher serum levels of T-helper (Th)1 (C-X-C motif) ligand 10 (CXCL10) chemokine, but normal levels of Th2 (C-C motif) ligand 2 chemokine, than patients without thyroiditis.	Methylcholanthrene	45-47	C-X-C motif chemokine ligand 10	Homo sapiens	162-168
24052572-3	2014	We and others have shown recently that neoplastic MC in ASM and MCL express antiapoptotic Mcl-1, Bcl-2, and Bcl-xL.	Methylcholanthrene	50-52	C-type lectin domain family 4 member D	Homo sapiens	64-67
24052572-3	2014	We and others have shown recently that neoplastic MC in ASM and MCL express antiapoptotic Mcl-1, Bcl-2, and Bcl-xL.	Methylcholanthrene	50-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	90-95
24052572-3	2014	We and others have shown recently that neoplastic MC in ASM and MCL express antiapoptotic Mcl-1, Bcl-2, and Bcl-xL.	Methylcholanthrene	50-52	BCL2 apoptosis regulator	Homo sapiens	97-102
24052572-3	2014	We and others have shown recently that neoplastic MC in ASM and MCL express antiapoptotic Mcl-1, Bcl-2, and Bcl-xL.	Methylcholanthrene	50-52	BCL2 like 1	Homo sapiens	108-114
24136190-4	2014	Guinea pig hepatic cytosolic AhR activated in vitro by equipotent concentrations of TCDD, 3-methylcholanthrene, beta-naphthoflavone, indirubin, L-kynurenine, or YH439 was incubated with a pool of DNA oligonucleotides containing a 15-base pair variable region consisting of all possible nucleotides.	Methylcholanthrene	90-110	aryl hydrocarbon receptor	Cavia porcellus	29-32
24115492-6	2014	Speedup of up to 72 x compared with SC and 2.6 x compared with MC was also observed for the PDE solve.	Methylcholanthrene	63-65	aldehyde dehydrogenase 7 family member A1	Homo sapiens	92-95
24787921-8	2014	More specifically, we suggest that MC imbalance marks many chronic conditions and because of their involvement with Abeta pathology, could reflect that Abeta may be a vital manifestation and marker of underlying MC imbalance.	Methylcholanthrene	35-37	amyloid beta precursor protein	Homo sapiens	116-121
24787921-8	2014	More specifically, we suggest that MC imbalance marks many chronic conditions and because of their involvement with Abeta pathology, could reflect that Abeta may be a vital manifestation and marker of underlying MC imbalance.	Methylcholanthrene	35-37	amyloid beta precursor protein	Homo sapiens	152-157
24787921-8	2014	More specifically, we suggest that MC imbalance marks many chronic conditions and because of their involvement with Abeta pathology, could reflect that Abeta may be a vital manifestation and marker of underlying MC imbalance.	Methylcholanthrene	212-214	amyloid beta precursor protein	Homo sapiens	116-121
24787921-8	2014	More specifically, we suggest that MC imbalance marks many chronic conditions and because of their involvement with Abeta pathology, could reflect that Abeta may be a vital manifestation and marker of underlying MC imbalance.	Methylcholanthrene	212-214	amyloid beta precursor protein	Homo sapiens	152-157
24787921-9	2014	Thus, careful targeting of MC imbalance may provide an alternative or complementary interventional approach to current Abeta treatment strategies.	Methylcholanthrene	27-29	amyloid beta precursor protein	Homo sapiens	119-124
24362577-5	2013	The CYP1A1 mRNA expression level increased significantly in PXB-cells with 250 ng/mL of 3-MC, indicating lower sensitivity than in vivo.	Methylcholanthrene	88-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	4-10
24362577-6	2013	The CYP1A2 and CYP3A4 mRNA expression levels increased significantly with 50 ng/mL of 3-MC, and 5 mug/mL of rifampicin, respectively, which indicated that the sensitivities were similar between in vivo and in vitro studies.	Methylcholanthrene	86-90	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	4-10
24258258-7	2013	OAS was significantly worse for MC patients but not for MF patients compared to patients with UF tumors (MF p = 0.321; MC p = 0.001).	Methylcholanthrene	32-34	SPARC related modular calcium binding 1	Homo sapiens	0-3
24403255-1	2013	Interleukin 4 (IL-4) was shown to be tumor-promoting in full carcinogenesis studies using 3-methylcholanthrene (MCA).	Methylcholanthrene	90-110	interleukin 4	Mus musculus	0-13
24403255-1	2013	Interleukin 4 (IL-4) was shown to be tumor-promoting in full carcinogenesis studies using 3-methylcholanthrene (MCA).	Methylcholanthrene	90-110	interleukin 4	Mus musculus	15-19
24403255-1	2013	Interleukin 4 (IL-4) was shown to be tumor-promoting in full carcinogenesis studies using 3-methylcholanthrene (MCA).	Methylcholanthrene	112-115	interleukin 4	Mus musculus	0-13
24403255-1	2013	Interleukin 4 (IL-4) was shown to be tumor-promoting in full carcinogenesis studies using 3-methylcholanthrene (MCA).	Methylcholanthrene	112-115	interleukin 4	Mus musculus	15-19
24258258-7	2013	OAS was significantly worse for MC patients but not for MF patients compared to patients with UF tumors (MF p = 0.321; MC p = 0.001).	Methylcholanthrene	119-121	SPARC related modular calcium binding 1	Homo sapiens	0-3
23994707-2	2013	We have reported for the first time the chemotherapeutic potential of MC in human promyelocytic leukemia HL-60 cells by means of apoptosis and disruption of the PI3K/AKT/mTOR signaling cascade.	Methylcholanthrene	70-72	AKT serine/threonine kinase 1	Homo sapiens	166-169
23994707-2	2013	We have reported for the first time the chemotherapeutic potential of MC in human promyelocytic leukemia HL-60 cells by means of apoptosis and disruption of the PI3K/AKT/mTOR signaling cascade.	Methylcholanthrene	70-72	mechanistic target of rapamycin kinase	Homo sapiens	170-174
24282531-7	2013	RESULTS: The mean serum concentrations of TFF3 in patients with CKD, metastatic and secondary carcinoma (MC) and acute gastroenteritis (AG) (200.9 ng/ml, 95.7 ng/ml and 71.7 ng/ml, respectively) were significantly higher than those in patients with other common clinical diseases.	Methylcholanthrene	105-107	trefoil factor 3	Homo sapiens	42-46
23994707-5	2013	Both MC and thymol induce apoptosis in HL-60 cells, which is evident by Hoechst staining, cell cycle analysis and immuno-expression of Bcl-xL, caspase-3,-8,-9 and PARP-1 cleavage.	Methylcholanthrene	5-7	BCL2 like 1	Homo sapiens	135-141
23994707-5	2013	Both MC and thymol induce apoptosis in HL-60 cells, which is evident by Hoechst staining, cell cycle analysis and immuno-expression of Bcl-xL, caspase-3,-8,-9 and PARP-1 cleavage.	Methylcholanthrene	5-7	caspase 3	Homo sapiens	143-158
23994707-5	2013	Both MC and thymol induce apoptosis in HL-60 cells, which is evident by Hoechst staining, cell cycle analysis and immuno-expression of Bcl-xL, caspase-3,-8,-9 and PARP-1 cleavage.	Methylcholanthrene	5-7	poly(ADP-ribose) polymerase 1	Homo sapiens	163-169
23994707-7	2013	Interestingly, both MC and thymol inhibit the downstream and upstream signaling of PI3K/AKT/mTOR pathway.	Methylcholanthrene	20-22	AKT serine/threonine kinase 1	Homo sapiens	88-91
23994707-7	2013	Interestingly, both MC and thymol inhibit the downstream and upstream signaling of PI3K/AKT/mTOR pathway.	Methylcholanthrene	20-22	mechanistic target of rapamycin kinase	Homo sapiens	92-96
24312318-7	2013	Based on fluorescence probe-coupled laser scanning imaging microscopy, NARP significantly enhanced mitochondrial reactive oxygen species (mROS) formation and mitochondrial Ca(2+) (mCa(2+)) accumulation in response to H/RO, which augmented the depletion of cardiolipin, resulting in the retardation of mitochondrial movement.	Methylcholanthrene	180-183	neuronal pentraxin 2	Homo sapiens	71-75
22842906-0	2013	DAT by perceived MC interaction on human prefrontal activity and connectivity during emotion processing.	Methylcholanthrene	17-19	solute carrier family 6 member 3	Homo sapiens	0-3
22842906-6	2013	RESULTS: An interaction between facial expression, DAT genotype and MC was found in left IFG, such that low MC and homozygosity for the 10-repeat allele are associated with greater activity during processing of fearful faces.	Methylcholanthrene	68-70	solute carrier family 6 member 3	Homo sapiens	51-54
22842906-6	2013	RESULTS: An interaction between facial expression, DAT genotype and MC was found in left IFG, such that low MC and homozygosity for the 10-repeat allele are associated with greater activity during processing of fearful faces.	Methylcholanthrene	108-110	solute carrier family 6 member 3	Homo sapiens	51-54
24091107-3	2013	We found that dexamethasone dose- and time-dependently suppresses CYP1A1 transactivation in gene reporter assays, CYP1A1 mRNA induction, and upregulation of 7-ethoxyresorufin-O-deethylase (EROD) activity by 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in JEG-3 cells.	Methylcholanthrene	207-227	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	66-72
24091107-3	2013	We found that dexamethasone dose- and time-dependently suppresses CYP1A1 transactivation in gene reporter assays, CYP1A1 mRNA induction, and upregulation of 7-ethoxyresorufin-O-deethylase (EROD) activity by 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in JEG-3 cells.	Methylcholanthrene	229-231	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	66-72
24091107-4	2013	Co-transfection of JEG-3 cells with glucocorticoid receptor (GR) expression construct and treatment with dexamethasone abolished the effect of MC on CYP1A1 promoter construct in transient transfection gene reporter assays.	Methylcholanthrene	143-145	nuclear receptor subfamily 3 group C member 1	Homo sapiens	36-59
24091107-4	2013	Co-transfection of JEG-3 cells with glucocorticoid receptor (GR) expression construct and treatment with dexamethasone abolished the effect of MC on CYP1A1 promoter construct in transient transfection gene reporter assays.	Methylcholanthrene	143-145	nuclear receptor subfamily 3 group C member 1	Homo sapiens	61-63
24091107-4	2013	Co-transfection of JEG-3 cells with glucocorticoid receptor (GR) expression construct and treatment with dexamethasone abolished the effect of MC on CYP1A1 promoter construct in transient transfection gene reporter assays.	Methylcholanthrene	143-145	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	149-155
24091107-5	2013	RU486, a GR antagonist, suppressed the effect of dexamethasone on MC-induced transactivation of AHR responsive reporter constructs.	Methylcholanthrene	66-68	nuclear receptor subfamily 3 group C member 1	Homo sapiens	9-11
24091107-5	2013	RU486, a GR antagonist, suppressed the effect of dexamethasone on MC-induced transactivation of AHR responsive reporter constructs.	Methylcholanthrene	66-68	aryl hydrocarbon receptor	Homo sapiens	96-99
23994556-4	2013	Cotreatment with 3-methylcholanthrene and dexamethasone, agonists of AHR and GR respectively, synergistically increased MT2A mRNA levels in HepG2 cells.	Methylcholanthrene	17-37	aryl hydrocarbon receptor	Homo sapiens	69-72
23994556-4	2013	Cotreatment with 3-methylcholanthrene and dexamethasone, agonists of AHR and GR respectively, synergistically increased MT2A mRNA levels in HepG2 cells.	Methylcholanthrene	17-37	nuclear receptor subfamily 3 group C member 1	Homo sapiens	77-79
23994556-4	2013	Cotreatment with 3-methylcholanthrene and dexamethasone, agonists of AHR and GR respectively, synergistically increased MT2A mRNA levels in HepG2 cells.	Methylcholanthrene	17-37	metallothionein 2A	Homo sapiens	120-124
23904439-7	2013	Culturing of MCs in the presence of S1P enhanced their degranulation responses, and when the S1P-treated MCs were used to reconstitute MC-deficient (Kit(W-sh)) mice, they caused enhanced anaphylaxis.	Methylcholanthrene	13-15	sphingosine-1-phosphate receptor 1	Mus musculus	36-39
23273579-8	2013	While treatment with MC increased the expression of MC inducible cytochrome P450 (CYP) 1A1, 1A2, 1B1, 2A2 &amp; 3A1 and their associated transcription factors in PBL, an increase in the expression of CYP2B1, 2B2, 2C11 &amp; 3A1 and their transcription factor was observed in PBL after PB treatment.	Methylcholanthrene	21-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	200-206
23904439-9	2013	Our findings argue that dysregulation in the metabolism of S1P is a contributing factor in modulating MC responsiveness and the allergic response.	Methylcholanthrene	102-104	sphingosine-1-phosphate receptor 1	Mus musculus	59-62
23983257-5	2013	Anti-CD73 mAb also significantly enhanced the activity of anti-PD-1 mAb against 3-methylcholanthrene (MCA)-induced fibrosarcomas.	Methylcholanthrene	80-100	5' nucleotidase, ecto	Mus musculus	5-9
24649274-10	2013	For the MC of presence of effusion, SMRP and carcinoembryonic antigen (CEA) levels, the AUC for the differentiation between MM and lung cancer (0.92; 95% CI: 0.88-0.97) and the differentiation between MM and individuals with asbestos exposure (0.93; 95% CI: 0.87-1.0) was significantly higher compared to that for SMRP alone (P=0.0001 and 0.0058, respectively).	Methylcholanthrene	8-10	mesothelin	Homo sapiens	36-40
24649274-10	2013	For the MC of presence of effusion, SMRP and carcinoembryonic antigen (CEA) levels, the AUC for the differentiation between MM and lung cancer (0.92; 95% CI: 0.88-0.97) and the differentiation between MM and individuals with asbestos exposure (0.93; 95% CI: 0.87-1.0) was significantly higher compared to that for SMRP alone (P=0.0001 and 0.0058, respectively).	Methylcholanthrene	8-10	CEA cell adhesion molecule 3	Homo sapiens	45-69
24649274-10	2013	For the MC of presence of effusion, SMRP and carcinoembryonic antigen (CEA) levels, the AUC for the differentiation between MM and lung cancer (0.92; 95% CI: 0.88-0.97) and the differentiation between MM and individuals with asbestos exposure (0.93; 95% CI: 0.87-1.0) was significantly higher compared to that for SMRP alone (P=0.0001 and 0.0058, respectively).	Methylcholanthrene	8-10	CEA cell adhesion molecule 3	Homo sapiens	71-74
24649274-10	2013	For the MC of presence of effusion, SMRP and carcinoembryonic antigen (CEA) levels, the AUC for the differentiation between MM and lung cancer (0.92; 95% CI: 0.88-0.97) and the differentiation between MM and individuals with asbestos exposure (0.93; 95% CI: 0.87-1.0) was significantly higher compared to that for SMRP alone (P=0.0001 and 0.0058, respectively).	Methylcholanthrene	8-10	mesothelin	Homo sapiens	314-318
23982178-6	2013	In addition, Ahr is an attractive molecule because tobacco smoke is a well-known environmental risk factor for RA development and Ahr agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, 3-methyl cholanthrene, and benzo[a]pyrene, are major toxic components in cigarettes.	Methylcholanthrene	189-210	aryl hydrocarbon receptor	Homo sapiens	13-16
24049096-1	2013	BACKGROUND: Mosaic IDH1 mutations are described as the cause of metaphyseal chondromatosis with increased urinary excretion of D-2-hydroxyglutarate (MC-HGA), and mutations in IDH2 as the cause of D-2-hydroxyglutaric aciduria (D-2HGA) type II.	Methylcholanthrene	149-151	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	19-23
24049096-5	2013	METHODS: We performed amplicon deep sequencing using the 454 GS Junior platform, next to Sanger sequencing, to identify and confirm mosaicism of IDH1 or IDH2 mutations in MC-HGA or D-2HGA, respectively.	Methylcholanthrene	171-173	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	145-149
24049096-5	2013	METHODS: We performed amplicon deep sequencing using the 454 GS Junior platform, next to Sanger sequencing, to identify and confirm mosaicism of IDH1 or IDH2 mutations in MC-HGA or D-2HGA, respectively.	Methylcholanthrene	171-173	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	153-157
23983257-5	2013	Anti-CD73 mAb also significantly enhanced the activity of anti-PD-1 mAb against 3-methylcholanthrene (MCA)-induced fibrosarcomas.	Methylcholanthrene	102-105	5' nucleotidase, ecto	Mus musculus	5-9
23831537-5	2013	The treatment of PRP obtained from healthy donors with polyphenolic-polysaccharide conjugates from M. chamomilla (L.) (MC) resulted in a dose-dependent, decrease of platelet aggregation induced by multiple agonists (ADP, collagen and arachidonic acid).	Methylcholanthrene	119-121	prion protein	Homo sapiens	17-20
23846873-0	2013	Downregulation of mouse hepatic CYP3A protein by 3-methylcholanthrene does not require cytochrome P450-dependent metabolism.	Methylcholanthrene	49-69	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	32-37
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	101-121	aryl-hydrocarbon receptor	Mus musculus	4-29
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	101-121	aryl-hydrocarbon receptor	Mus musculus	31-34
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	101-121	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	91-97
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	123-125	aryl-hydrocarbon receptor	Mus musculus	4-29
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	123-125	aryl-hydrocarbon receptor	Mus musculus	31-34
23846873-1	2013	The aryl hydrocarbon receptor (AHR)-dependent induction of cytochromes P450 (P450) such as CYP1A1 by 3-methylcholanthrene (MC) and related polycyclic aromatic hydrocarbons is well characterized.	Methylcholanthrene	123-125	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	91-97
23958683-3	2013	Knockout of Stat1 enhanced the development of sarcomas induced by the chemical carcinogen 3-methylcholanthrene (MCA).	Methylcholanthrene	90-110	signal transducer and activator of transcription 1	Mus musculus	12-17
23958683-3	2013	Knockout of Stat1 enhanced the development of sarcomas induced by the chemical carcinogen 3-methylcholanthrene (MCA).	Methylcholanthrene	112-115	signal transducer and activator of transcription 1	Mus musculus	12-17
23846873-2	2013	We reported previously that MC treatment triggers a pronounced downregulation, particularly at the protein level, of mouse hepatic Cyp3a11, a counterpart of the key human drug-metabolizing enzyme CYP3A4.	Methylcholanthrene	28-30	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	131-138
23846873-2	2013	We reported previously that MC treatment triggers a pronounced downregulation, particularly at the protein level, of mouse hepatic Cyp3a11, a counterpart of the key human drug-metabolizing enzyme CYP3A4.	Methylcholanthrene	28-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	196-202
23846873-5	2013	MC treatment caused suppression of CYP3A11 mRNA, CYP3A protein immunoreactivity, and CYP3A catalytic activity in WT mice, and the MC effects at the mRNA and protein levels were maintained in LCN mice.	Methylcholanthrene	0-2	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	35-42
23846873-5	2013	MC treatment caused suppression of CYP3A11 mRNA, CYP3A protein immunoreactivity, and CYP3A catalytic activity in WT mice, and the MC effects at the mRNA and protein levels were maintained in LCN mice.	Methylcholanthrene	0-2	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	35-40
23846873-5	2013	MC treatment caused suppression of CYP3A11 mRNA, CYP3A protein immunoreactivity, and CYP3A catalytic activity in WT mice, and the MC effects at the mRNA and protein levels were maintained in LCN mice.	Methylcholanthrene	0-2	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	49-54
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	54-56	flavin containing monooxygenase 3	Mus musculus	0-33
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	54-56	flavin containing monooxygenase 3	Mus musculus	35-39
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	54-56	aryl-hydrocarbon receptor	Mus musculus	98-101
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	54-56	flavin containing monooxygenase 3	Mus musculus	221-225
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	269-271	flavin containing monooxygenase 3	Mus musculus	0-33
23846873-6	2013	Flavin-containing monooxygenase-3 (Fmo3) induction by MC was suggested previously to occur via an AHR-dependent mechanism requiring conversion of the parent compound to DNA-damaging reactive metabolites; however, hepatic FMO3 mRNA levels were dramatically increased by MC in both WT and LCN mice.	Methylcholanthrene	269-271	flavin containing monooxygenase 3	Mus musculus	35-39
23846873-8	2013	These results indicate that MC downregulates mouse hepatic CYP3A protein via a pretranslational mechanism that does not require hepatic microsomal P450-dependent activity.	Methylcholanthrene	28-30	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	59-64
23831537-6	2013	In this study we also observed that the MC reduced platelet aggregation in PRP obtained from patients with cardiovascular disorders.	Methylcholanthrene	40-42	prion protein	Homo sapiens	75-78
24022930-6	2013	Compared to MC group,the expression of E, AI, TGF-beta1 and Smad3 were reduced, while FEF50, FEF75, MMF, PEF, Treg, Foxp3 and Smad7 were elevated in XFC group (P &lt;0.05 or P &lt;0.01).	Methylcholanthrene	12-14	SMAD family member 3	Rattus norvegicus	60-65
23873764-6	2013	For both MC-IN and MC-OUT patients, an AFP slope &gt; 15 ng/mL/month and mRECIST progression were unique independent risk factors for HCC recurrence and patient death.	Methylcholanthrene	9-11	alpha fetoprotein	Homo sapiens	39-42
24104122-1	2013	In this study, we produce InGaN/GaN microcolumn LED (MC-LED) arrays having nonpolar metal sidewall contacts using a top-down method, where the metal contacts only with the sidewall of the columnar LEDs with an open top for transparency.	Methylcholanthrene	53-55	gigaxonin	Homo sapiens	28-31
23846855-0	2013	3-methylcholanthrene induces neurotoxicity in developing neurons derived from human CD34+Thy1+ stem cells by activation of aryl hydrocarbon receptor.	Methylcholanthrene	0-20	CD34 molecule	Homo sapiens	84-88
23846855-0	2013	3-methylcholanthrene induces neurotoxicity in developing neurons derived from human CD34+Thy1+ stem cells by activation of aryl hydrocarbon receptor.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	123-148
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	aryl hydrocarbon receptor	Homo sapiens	137-162
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	aryl hydrocarbon receptor	Homo sapiens	164-167
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	173-219
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	221-225
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	cAMP responsive element binding protein 1	Homo sapiens	267-304
23846855-2	2013	Three-dimensional (3D) molecular docking demonstrates the strong hydrogen bonding and hydrophobic interactions of MC with amino acids of aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) within 4 A and subsequent inhibition of cAMP response element-binding protein (CREB), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.	Methylcholanthrene	114-116	cAMP responsive element binding protein 1	Homo sapiens	306-310
23792966-9	2013	Together, these insights into the function of MASP-3 reveal how a mutation in this enzyme causes it to be inactive and thus contribute to the 3MC syndrome.	Methylcholanthrene	142-145	MBL associated serine protease 1	Homo sapiens	46-52
23640815-11	2013	Interestingly, there was an inverse relationship between MC and GC layer c-fos expression, with little c-fos expression in the GC layer in ventral sections where MC expression was strong, and the opposite in dorsal hippocampus.	Methylcholanthrene	57-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
23688867-10	2013	Moreover, carcinogen 3-MC induced skin cancer development was attenuated in the lesion of PDCD5 transgenic mice by enhancing apoptosis.	Methylcholanthrene	21-25	programmed cell death 5	Mus musculus	90-95
23688867-11	2013	Pro-apoptotic protein Bax expression was up-regulated in the 3-MC treated skin of transgenic mice.	Methylcholanthrene	61-65	BCL2-associated X protein	Mus musculus	22-25
23328087-1	2013	TET1 is a member of the recently identified family of epigenetic regulators, TET1-3 which catalyze the enzymatic conversion of the methyl mark on cytosine (methylcytosine, mC) to the hydroxymethyl mark (hmC).	Methylcholanthrene	172-174	tet methylcytosine dioxygenase 1	Homo sapiens	0-4
23328087-1	2013	TET1 is a member of the recently identified family of epigenetic regulators, TET1-3 which catalyze the enzymatic conversion of the methyl mark on cytosine (methylcytosine, mC) to the hydroxymethyl mark (hmC).	Methylcholanthrene	172-174	tet methylcytosine dioxygenase 1	Homo sapiens	77-81
23846855-4	2013	In concurrence with in silico data, MC exposure significantly up regulates the expression and activity of AHR, CYP1A1 and glutathione S-transferase P1-1 (GSTP1-1) and down regulates the expression of CREB, AMPA and NMDA receptors in hUCBSC-derived neuronal cells at various maturity (0, 2, 4, 8 days of differentiation).	Methylcholanthrene	36-38	aryl hydrocarbon receptor	Homo sapiens	106-109
23846855-4	2013	In concurrence with in silico data, MC exposure significantly up regulates the expression and activity of AHR, CYP1A1 and glutathione S-transferase P1-1 (GSTP1-1) and down regulates the expression of CREB, AMPA and NMDA receptors in hUCBSC-derived neuronal cells at various maturity (0, 2, 4, 8 days of differentiation).	Methylcholanthrene	36-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	111-117
23846855-4	2013	In concurrence with in silico data, MC exposure significantly up regulates the expression and activity of AHR, CYP1A1 and glutathione S-transferase P1-1 (GSTP1-1) and down regulates the expression of CREB, AMPA and NMDA receptors in hUCBSC-derived neuronal cells at various maturity (0, 2, 4, 8 days of differentiation).	Methylcholanthrene	36-38	glutathione S-transferase pi 1	Homo sapiens	154-161
23846855-4	2013	In concurrence with in silico data, MC exposure significantly up regulates the expression and activity of AHR, CYP1A1 and glutathione S-transferase P1-1 (GSTP1-1) and down regulates the expression of CREB, AMPA and NMDA receptors in hUCBSC-derived neuronal cells at various maturity (0, 2, 4, 8 days of differentiation).	Methylcholanthrene	36-38	cAMP responsive element binding protein 1	Homo sapiens	200-204
23846855-5	2013	MC-mediated significant down regulation in the expression of stage-specific neuronal markers (Nestin, neural cell adhesion molecule-NCAM, synaptophysin-SYP, CREB, AMPA and N-methyl-D-aspartate receptor subunit 2A-NR2A) was also noticed in cells all through the differentiation.	Methylcholanthrene	0-2	neural cell adhesion molecule 1	Homo sapiens	102-136
23846855-5	2013	MC-mediated significant down regulation in the expression of stage-specific neuronal markers (Nestin, neural cell adhesion molecule-NCAM, synaptophysin-SYP, CREB, AMPA and N-methyl-D-aspartate receptor subunit 2A-NR2A) was also noticed in cells all through the differentiation.	Methylcholanthrene	0-2	synaptophysin	Homo sapiens	138-151
23846855-5	2013	MC-mediated significant down regulation in the expression of stage-specific neuronal markers (Nestin, neural cell adhesion molecule-NCAM, synaptophysin-SYP, CREB, AMPA and N-methyl-D-aspartate receptor subunit 2A-NR2A) was also noticed in cells all through the differentiation.	Methylcholanthrene	0-2	synaptophysin	Homo sapiens	152-155
23846855-5	2013	MC-mediated significant down regulation in the expression of stage-specific neuronal markers (Nestin, neural cell adhesion molecule-NCAM, synaptophysin-SYP, CREB, AMPA and N-methyl-D-aspartate receptor subunit 2A-NR2A) was also noticed in cells all through the differentiation.	Methylcholanthrene	0-2	cAMP responsive element binding protein 1	Homo sapiens	157-161
23837668-4	2013	To overcome this bottleneck, here we report the development of a poly(beta-amino ester) (PBAE)-based, biodegradable nanoparticulate platform for efficient delivery of MC DNA driven by a Ubc promoter in vitro and in vivo.	Methylcholanthrene	167-169	ubiquitin C	Homo sapiens	186-189
23857971-7	2013	Second, we found that the overall accuracy of the MC was remarkable: 98% to 77% for AITL and 98% to 93% for ALK-negative ALCL in test and validation sets of patient cases, respectively.	Methylcholanthrene	50-52	ALK receptor tyrosine kinase	Homo sapiens	108-111
23559389-3	2013	CXCL11 was significantly higher in MC + HCV than in controls (264 +- 279 vs 70 +- 16 pg/mL, respectively; P = 0.0002; univariate analysis of variance (ANOVA)), in particular in 23 MC + HCV with active vasculitis vs those without (293 +- 221 vs 168 +- 57 pg/mL, respectively; P &lt; 0.001; ANOVA).	Methylcholanthrene	35-37	C-X-C motif chemokine ligand 11	Homo sapiens	0-6
23559389-3	2013	CXCL11 was significantly higher in MC + HCV than in controls (264 +- 279 vs 70 +- 16 pg/mL, respectively; P = 0.0002; univariate analysis of variance (ANOVA)), in particular in 23 MC + HCV with active vasculitis vs those without (293 +- 221 vs 168 +- 57 pg/mL, respectively; P &lt; 0.001; ANOVA).	Methylcholanthrene	35-39	C-X-C motif chemokine ligand 11	Homo sapiens	0-6
23559389-4	2013	Significantly high IL-1beta, IL-6, TNF-alpha, CXCL10, and CCL2 in MC + HCV vs healthy controls were confirmed.	Methylcholanthrene	66-68	interleukin 1 beta	Homo sapiens	19-27
23559389-4	2013	Significantly high IL-1beta, IL-6, TNF-alpha, CXCL10, and CCL2 in MC + HCV vs healthy controls were confirmed.	Methylcholanthrene	66-68	C-X-C motif chemokine ligand 10	Homo sapiens	46-52
23559389-4	2013	Significantly high IL-1beta, IL-6, TNF-alpha, CXCL10, and CCL2 in MC + HCV vs healthy controls were confirmed.	Methylcholanthrene	66-68	C-C motif chemokine ligand 2	Homo sapiens	58-62
23559389-6	2013	This study demonstrates in MC + HCV high serum levels of (a) T-helper 1 chemokines, CXCL11 and CXCL10 (related to each other) and (b) proinflammatory cytokines IL-6 and CCL2 (related to each other).	Methylcholanthrene	27-31	C-X-C motif chemokine ligand 11	Homo sapiens	84-90
23559389-6	2013	This study demonstrates in MC + HCV high serum levels of (a) T-helper 1 chemokines, CXCL11 and CXCL10 (related to each other) and (b) proinflammatory cytokines IL-6 and CCL2 (related to each other).	Methylcholanthrene	27-31	C-X-C motif chemokine ligand 10	Homo sapiens	95-101
23559389-6	2013	This study demonstrates in MC + HCV high serum levels of (a) T-helper 1 chemokines, CXCL11 and CXCL10 (related to each other) and (b) proinflammatory cytokines IL-6 and CCL2 (related to each other).	Methylcholanthrene	27-31	interleukin 6	Homo sapiens	160-164
23559389-6	2013	This study demonstrates in MC + HCV high serum levels of (a) T-helper 1 chemokines, CXCL11 and CXCL10 (related to each other) and (b) proinflammatory cytokines IL-6 and CCL2 (related to each other).	Methylcholanthrene	27-31	C-C motif chemokine ligand 2	Homo sapiens	169-173
23758843-6	2013	The percentage of methylated cytosines (%mC) in LINE-1, Alu, and inducible nitric oxide synthase gene (iNOS) were quantified using pyrosequencing.	Methylcholanthrene	41-43	nitric oxide synthase 2	Homo sapiens	103-107
23521747-0	2013	A MC motif in silkworm Argonaute 1 is indispensible for translation repression.	Methylcholanthrene	2-4	argonaute 1	Bombyx mori	23-34
23538035-4	2013	The accepted pathway for MC detoxication is GSH conjugation: here the MC-RR conjugation with GSH catalyzed by 5 recombinant human GSTs and human liver cytosol (HLC) has been characterized and appeared to be more efficient than MC-LR conjugation.	Methylcholanthrene	25-27	hematopoietic prostaglandin D synthase	Homo sapiens	130-134
23350962-4	2013	To identify genes that regulate the NKG2D ligand H60a, we performed a microarray analysis of 3"-methylcholanthrene-induced sarcoma cell lines expressing high versus low H60a levels.	Methylcholanthrene	93-114	killer cell lectin like receptor K1	Homo sapiens	36-41
23521747-9	2013	Substitutions of two conserved phenylalanines (F522 and F557) by valines in the MC motif strongly impaired the function of BmAgo1 in translation repression and its localization in P-bodies, suggesting that these two amino acid residues in the MC motif of BmAgo1 are prerequisites for mRNA translation repression in B. mori.	Methylcholanthrene	80-82	argonaute 1	Bombyx mori	123-129
23521747-9	2013	Substitutions of two conserved phenylalanines (F522 and F557) by valines in the MC motif strongly impaired the function of BmAgo1 in translation repression and its localization in P-bodies, suggesting that these two amino acid residues in the MC motif of BmAgo1 are prerequisites for mRNA translation repression in B. mori.	Methylcholanthrene	80-82	argonaute 1	Bombyx mori	255-261
23521747-9	2013	Substitutions of two conserved phenylalanines (F522 and F557) by valines in the MC motif strongly impaired the function of BmAgo1 in translation repression and its localization in P-bodies, suggesting that these two amino acid residues in the MC motif of BmAgo1 are prerequisites for mRNA translation repression in B. mori.	Methylcholanthrene	243-245	argonaute 1	Bombyx mori	123-129
23521747-9	2013	Substitutions of two conserved phenylalanines (F522 and F557) by valines in the MC motif strongly impaired the function of BmAgo1 in translation repression and its localization in P-bodies, suggesting that these two amino acid residues in the MC motif of BmAgo1 are prerequisites for mRNA translation repression in B. mori.	Methylcholanthrene	243-245	argonaute 1	Bombyx mori	255-261
23423838-4	2013	Stable knockdown of ASAH1 in PC-3/Mc cells caused an accumulation of ceramides, inhibition of clonogenic potential, increased requirement for growth factors, and inhibition of tumorigenesis and lung metastases.	Methylcholanthrene	34-36	N-acylsphingosine amidohydrolase 1	Homo sapiens	20-25
23190297-9	2013	The oxidase activity affording 5-OH-BP-3 was enhanced in liver microsomes of dexamethasone-, phenobarbital- and 3-methylcholanthrene-treated rats.	Methylcholanthrene	112-132	Blood pressure QTL 3	Rattus norvegicus	36-40
23603339-4	2013	In primary human hepatocytes, DHEA diminished the increase in CYP1A activities (7-ethoxyresorufin O-dealkylation and phenacetin O-dealkylation) and in CYP1A2 mRNA level induced by 3-methylcholanthrene, but did not alter the amount of CYP1A1 and CYP1B1 mRNA.	Methylcholanthrene	180-200	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	151-157
23603339-4	2013	In primary human hepatocytes, DHEA diminished the increase in CYP1A activities (7-ethoxyresorufin O-dealkylation and phenacetin O-dealkylation) and in CYP1A2 mRNA level induced by 3-methylcholanthrene, but did not alter the amount of CYP1A1 and CYP1B1 mRNA.	Methylcholanthrene	180-200	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	234-240
23603339-4	2013	In primary human hepatocytes, DHEA diminished the increase in CYP1A activities (7-ethoxyresorufin O-dealkylation and phenacetin O-dealkylation) and in CYP1A2 mRNA level induced by 3-methylcholanthrene, but did not alter the amount of CYP1A1 and CYP1B1 mRNA.	Methylcholanthrene	180-200	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	245-251
23700472-8	2013	In addition, Tg(cyp1a:gfp) medaka fry also responded to two other AhR agonists, 3-methylcholanthrene and benzo[a]pyrene, for GFP induction, but no significant GFP induction was observed towards several other chemicals tested, indicating the specificity of this transgenic line.	Methylcholanthrene	80-100	cytochrome P450 1A1	Oryzias latipes	16-21
23700472-8	2013	In addition, Tg(cyp1a:gfp) medaka fry also responded to two other AhR agonists, 3-methylcholanthrene and benzo[a]pyrene, for GFP induction, but no significant GFP induction was observed towards several other chemicals tested, indicating the specificity of this transgenic line.	Methylcholanthrene	80-100	aryl hydrocarbon receptor 1b	Oryzias latipes	66-69
23333597-3	2013	Inhibition of AURKA and TPX2 using siRNA mimicked enforced GLIPR1 expression in the induction of apoptosis and MC.	Methylcholanthrene	111-113	aurora kinase A	Homo sapiens	14-19
23333597-3	2013	Inhibition of AURKA and TPX2 using siRNA mimicked enforced GLIPR1 expression in the induction of apoptosis and MC.	Methylcholanthrene	111-113	TPX2 microtubule nucleation factor	Homo sapiens	24-28
23333597-3	2013	Inhibition of AURKA and TPX2 using siRNA mimicked enforced GLIPR1 expression in the induction of apoptosis and MC.	Methylcholanthrene	111-113	GLI pathogenesis related 1	Homo sapiens	59-65
23333597-4	2013	Recombinant GLIPR1-DeltaTM protein inhibited AURKA and TPX2 expression, induced apoptosis and MC, and suppressed orthotopic xenograft tumor growth.	Methylcholanthrene	94-96	GLI pathogenesis related 1	Homo sapiens	12-18
23588955-2	2013	This is the first systematic review/pooled analysis to synthesize all available data evaluating the efficacy and safety of intrathecal (IT) administration of trastuzumab for the treatment of MC in HER2-positive breast cancer patients.	Methylcholanthrene	191-193	erb-b2 receptor tyrosine kinase 2	Homo sapiens	197-201
23588955-16	2013	However, clinical trials are urgently needed to establish the definite role of IT trastuzumab in HER2-positive metastatic breast cancer patients with MC.	Methylcholanthrene	150-152	erb-b2 receptor tyrosine kinase 2	Homo sapiens	97-101
23539447-5	2013	We found that FSP1+ /S100A4+ fibroblasts accumulated around the carcinogen where they produced collagens, encapsulating MCA and protecting epithelial cells from DNA damage.	Methylcholanthrene	120-123	S100 calcium binding protein A4	Mus musculus	14-18
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	23-43	interleukin 9	Mus musculus	60-63
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	23-43	interleukin 9	Mus musculus	64-68
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	23-43	interleukin 9	Mus musculus	122-125
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	23-43	interleukin 9	Mus musculus	126-130
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	23-43	aryl-hydrocarbon receptor	Mus musculus	186-189
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	45-48	interleukin 9	Mus musculus	60-63
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	45-48	interleukin 9	Mus musculus	64-68
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	45-48	interleukin 9	Mus musculus	122-125
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	45-48	interleukin 9	Mus musculus	126-130
23478803-3	2013	Treatment of mice with 3-methylcholanthrene (3MC) increased p40(phox) gene expression in the liver, but this induction of p40(phox) gene expression was diminished by the deletion of the AhR gene in the liver.	Methylcholanthrene	45-48	aryl-hydrocarbon receptor	Mus musculus	186-189
23478803-4	2013	Consistent with the in vivo results, the expression of the p40(phox) gene was increased in 3MC-treated Hepa1c1c7 cells in an AhR-dependent manner.	Methylcholanthrene	91-94	interleukin 9	Mus musculus	59-68
23478803-4	2013	Consistent with the in vivo results, the expression of the p40(phox) gene was increased in 3MC-treated Hepa1c1c7 cells in an AhR-dependent manner.	Methylcholanthrene	91-94	aryl-hydrocarbon receptor	Mus musculus	125-128
23585279-2	2013	Recently, AID has been proposed to also mediate epigenetic reprogramming by demethylating methylated cytidines (mC) possibly through deamination.	Methylcholanthrene	112-114	activation-induced cytidine deaminase	Danio rerio	10-13
23585279-4	2013	We and others have previously shown that mC is a poor substrate for human AID.	Methylcholanthrene	41-43	activation induced cytidine deaminase	Homo sapiens	74-77
23585279-5	2013	Here, we examined the ability of bony fish AID to deaminate mC.	Methylcholanthrene	60-62	activation-induced cytidine deaminase	Danio rerio	43-46
23585279-6	2013	We report that zebrafish AID was unique among all orthologs in that it efficiently deaminates mC.	Methylcholanthrene	94-96	activation-induced cytidine deaminase	Danio rerio	25-28
23585279-7	2013	Analysis of domain-swapped and mutant AID revealed that mC specificity is independent of the overall high-catalytic efficiency of zebrafish AID.	Methylcholanthrene	56-58	activation-induced cytidine deaminase	Danio rerio	38-41
23585279-8	2013	Structural modeling with or without bound DNA suggests that efficient deamination of mC by zebrafish AID is likely not due to a larger catalytic pocket allowing for better fit of mC, but rather because of subtle differences in the flexibility of its structure.	Methylcholanthrene	85-87	activation-induced cytidine deaminase	Danio rerio	101-104
23585279-8	2013	Structural modeling with or without bound DNA suggests that efficient deamination of mC by zebrafish AID is likely not due to a larger catalytic pocket allowing for better fit of mC, but rather because of subtle differences in the flexibility of its structure.	Methylcholanthrene	179-181	activation-induced cytidine deaminase	Danio rerio	101-104
23637889-4	2013	Macrophage-conditioned (MC) medium (25% with adipocyte maintenance media) markedly inhibited protein expression of the nuclear factor-kappaB (NFkappaB) subunit inhibitor kappaBalpha (IkappaBalpha) (71%, P&lt;0.001) and increased NFkappaB p65 (1.5-fold, P = 0.026) compared with controls.	Methylcholanthrene	24-26	NFKB inhibitor alpha	Homo sapiens	119-196
23193992-7	2013	Application of 3-methylcholanthrene, the AHR agonist, enhances BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and ARNT-YFP (AAPA cells), while suppressing BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and HSP90-YFP (AAPH cells).	Methylcholanthrene	15-35	aryl hydrocarbon receptor	Homo sapiens	41-44
23193992-7	2013	Application of 3-methylcholanthrene, the AHR agonist, enhances BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and ARNT-YFP (AAPA cells), while suppressing BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and HSP90-YFP (AAPH cells).	Methylcholanthrene	15-35	aryl hydrocarbon receptor	Homo sapiens	99-102
23193992-7	2013	Application of 3-methylcholanthrene, the AHR agonist, enhances BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and ARNT-YFP (AAPA cells), while suppressing BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and HSP90-YFP (AAPH cells).	Methylcholanthrene	15-35	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	128-132
23193992-7	2013	Application of 3-methylcholanthrene, the AHR agonist, enhances BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and ARNT-YFP (AAPA cells), while suppressing BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and HSP90-YFP (AAPH cells).	Methylcholanthrene	15-35	aryl hydrocarbon receptor	Homo sapiens	99-102
23193992-7	2013	Application of 3-methylcholanthrene, the AHR agonist, enhances BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and ARNT-YFP (AAPA cells), while suppressing BRET signals in cells co-expressing AHR-RL, AIP-His, P23-His and HSP90-YFP (AAPH cells).	Methylcholanthrene	15-35	heat shock protein 90 alpha family class A member 1	Homo sapiens	234-239
23905389-12	2013	(2) Compared with the NC group, the mRNA and protein expression levels of MMP-9 in the myocardial tissue of the MC group were obviously up-regulated, while the mRNA and protein expression levels of TIMP-1 were obviously down-regulated (P &lt;0.	Methylcholanthrene	112-114	matrix metallopeptidase 9	Rattus norvegicus	74-79
23905389-14	2013	The mRNA and protein expression levels of MMP-9 decreased, and the mRNA and protein expression levels of TIMP-1 obviously increased in the XFC group, showing statistical difference when compared with the MC group (P &lt; 0.	Methylcholanthrene	204-206	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	105-111
23357051-2	2013	Activating mutations in KIT have thus been linked to clonal MC proliferation associated with systemic mastocytosis.	Methylcholanthrene	60-62	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	24-27
23357051-3	2013	SCF also modulates MC function by inducing MC chemotaxis and by potentiating antigen (Ag)/IgE-mediated MC degranulation.	Methylcholanthrene	19-21	kit ligand	Mus musculus	0-3
23357051-3	2013	SCF also modulates MC function by inducing MC chemotaxis and by potentiating antigen (Ag)/IgE-mediated MC degranulation.	Methylcholanthrene	43-45	kit ligand	Mus musculus	0-3
23357051-3	2013	SCF also modulates MC function by inducing MC chemotaxis and by potentiating antigen (Ag)/IgE-mediated MC degranulation.	Methylcholanthrene	43-45	kit ligand	Mus musculus	0-3
23357051-5	2013	Studies to determine how native and mutated KIT may modulate MC chemotaxis and activation have, however, been limited due to the lack of availability of a suitable functional MC line lacking native KIT which would allow transduction of KIT constructs.	Methylcholanthrene	61-63	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-47
23357051-6	2013	Here we describe a novel mouse MC line which allows the study of normal and mutated KIT constructs.	Methylcholanthrene	31-33	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-87
23357051-11	2013	This cell line thus presents a novel system to delineate how MC function is modulated by native and mutated KIT and for the identification of novel inhibitors of these processes.	Methylcholanthrene	61-63	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	108-111
23637889-4	2013	Macrophage-conditioned (MC) medium (25% with adipocyte maintenance media) markedly inhibited protein expression of the nuclear factor-kappaB (NFkappaB) subunit inhibitor kappaBalpha (IkappaBalpha) (71%, P&lt;0.001) and increased NFkappaB p65 (1.5-fold, P = 0.026) compared with controls.	Methylcholanthrene	24-26	nuclear factor kappa B subunit 1	Homo sapiens	142-150
23637889-4	2013	Macrophage-conditioned (MC) medium (25% with adipocyte maintenance media) markedly inhibited protein expression of the nuclear factor-kappaB (NFkappaB) subunit inhibitor kappaBalpha (IkappaBalpha) (71%, P&lt;0.001) and increased NFkappaB p65 (1.5-fold, P = 0.026) compared with controls.	Methylcholanthrene	24-26	RELA proto-oncogene, NF-kB subunit	Homo sapiens	238-241
23593313-5	2013	Over-expression of human PTB1 stimulated the HRV2 IRES-mediated translation, resulting in increased growth of PV1(RIPO) in murine cells and human neuronal SK-N-MC cells.	Methylcholanthrene	160-162	polypyrimidine tract binding protein 1	Homo sapiens	25-29
23461631-8	2013	Hence, spiropyran SAMs on gold can undergo reversible photochemical switching from the SP to the MC form with both UV and NIR and the reverse reaction induced by irradiation with visible light or heating.	Methylcholanthrene	97-99	NOC2 like nucleolar associated transcriptional repressor	Homo sapiens	122-125
23268359-8	2013	Moreover, 3-methylcholanthrene induced Cyp1a1 while fenofibrate induced Cyp2j9 and Cyp4f13 mRNA levels in HL-1 cells.	Methylcholanthrene	10-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	39-45
22934830-3	2013	2. qRT-PCR studies demonstrated significant constitutive mRNA expression of CYP2A-isoenzymes in PBL isolated from male and female rats which further increases significantly after pretreatment with nicotine or 3-methylcholanthrene (MC) indicating responsiveness of CYP2A-isoenzymes in PBL.	Methylcholanthrene	209-229	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
22934830-3	2013	2. qRT-PCR studies demonstrated significant constitutive mRNA expression of CYP2A-isoenzymes in PBL isolated from male and female rats which further increases significantly after pretreatment with nicotine or 3-methylcholanthrene (MC) indicating responsiveness of CYP2A-isoenzymes in PBL.	Methylcholanthrene	209-229	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	264-269
22934830-3	2013	2. qRT-PCR studies demonstrated significant constitutive mRNA expression of CYP2A-isoenzymes in PBL isolated from male and female rats which further increases significantly after pretreatment with nicotine or 3-methylcholanthrene (MC) indicating responsiveness of CYP2A-isoenzymes in PBL.	Methylcholanthrene	231-233	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
22934830-3	2013	2. qRT-PCR studies demonstrated significant constitutive mRNA expression of CYP2A-isoenzymes in PBL isolated from male and female rats which further increases significantly after pretreatment with nicotine or 3-methylcholanthrene (MC) indicating responsiveness of CYP2A-isoenzymes in PBL.	Methylcholanthrene	231-233	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	264-269
23333391-4	2013	To mimic MC, a mutated Atoh1 protein was stably expressed in undifferentiated colon cancer cells.	Methylcholanthrene	9-11	atonal bHLH transcription factor 1	Homo sapiens	23-28
23333391-8	2013	In conclusion, the Atoh1 protein regulates malignant potential rather than the differentiation phenotype of MC, suggesting the mechanism by which MC and SRCC are more malignant than non-mucinous adenocarcinoma.	Methylcholanthrene	146-148	atonal bHLH transcription factor 1	Homo sapiens	19-24
23417359-8	2013	When adjusted for other covariates, including age, estrogen receptor, HER2/neu expressions, and RCB score, a high MC was associated with a significantly higher risk of developing distant metastases (hazard ratio 11.21, 95 % CI [2.19, 57.37]; p = 0.004).	Methylcholanthrene	114-116	estrogen receptor 1	Homo sapiens	51-68
23315936-6	2013	MC neurons are still born in the ceh-19 mutants but display various morphological defects.	Methylcholanthrene	0-2	Homeobox protein ceh-19	Caenorhabditis elegans	33-39
23417359-8	2013	When adjusted for other covariates, including age, estrogen receptor, HER2/neu expressions, and RCB score, a high MC was associated with a significantly higher risk of developing distant metastases (hazard ratio 11.21, 95 % CI [2.19, 57.37]; p = 0.004).	Methylcholanthrene	114-116	erb-b2 receptor tyrosine kinase 2	Homo sapiens	70-74
23417359-8	2013	When adjusted for other covariates, including age, estrogen receptor, HER2/neu expressions, and RCB score, a high MC was associated with a significantly higher risk of developing distant metastases (hazard ratio 11.21, 95 % CI [2.19, 57.37]; p = 0.004).	Methylcholanthrene	114-116	erb-b2 receptor tyrosine kinase 2	Homo sapiens	75-78
23241877-2	2013	Our recent studies in methylcholanthrene-induced fibrosarcomas have indicated the appearance and rapid growth of tumor variants deficient in producing the T cell chemoattractant chemokine CXCL9/Mig, an important component of antitumor immunity.	Methylcholanthrene	22-40	C-X-C motif chemokine ligand 9	Homo sapiens	188-193
23169610-0	2013	The role of cytochrome P450-dependent metabolism in the regulation of mouse hepatic growth hormone signaling components and target genes by 3-methylcholanthrene.	Methylcholanthrene	140-160	growth hormone	Mus musculus	84-98
23169610-1	2013	3-Methylcholanthrene (MC) is a readily metabolized aryl hydrocarbon receptor (AHR) agonist.	Methylcholanthrene	0-20	aryl-hydrocarbon receptor	Mus musculus	51-76
23169610-1	2013	3-Methylcholanthrene (MC) is a readily metabolized aryl hydrocarbon receptor (AHR) agonist.	Methylcholanthrene	0-20	aryl-hydrocarbon receptor	Mus musculus	78-81
23169610-1	2013	3-Methylcholanthrene (MC) is a readily metabolized aryl hydrocarbon receptor (AHR) agonist.	Methylcholanthrene	22-24	aryl-hydrocarbon receptor	Mus musculus	51-76
23169610-1	2013	3-Methylcholanthrene (MC) is a readily metabolized aryl hydrocarbon receptor (AHR) agonist.	Methylcholanthrene	22-24	aryl-hydrocarbon receptor	Mus musculus	78-81
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	growth hormone	Mus musculus	40-54
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	growth hormone	Mus musculus	56-58
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	96-115
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	117-123
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	growth hormone	Mus musculus	171-173
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	signal transducer and activator of transcription 5B	Mus musculus	178-229
23169610-2	2013	MC disrupts expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	signal transducer and activator of transcription 5B	Mus musculus	231-237
23169610-4	2013	MC caused mild induction of Por and a hepatic inflammatory marker in wild-type mice, whereas MC caused strong induction of AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 in wild-type and LCN mice.	Methylcholanthrene	0-2	cytochrome p450 oxidoreductase	Mus musculus	28-31
23169610-4	2013	MC caused mild induction of Por and a hepatic inflammatory marker in wild-type mice, whereas MC caused strong induction of AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 in wild-type and LCN mice.	Methylcholanthrene	93-95	aryl-hydrocarbon receptor	Mus musculus	123-126
23169610-4	2013	MC caused mild induction of Por and a hepatic inflammatory marker in wild-type mice, whereas MC caused strong induction of AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 in wild-type and LCN mice.	Methylcholanthrene	93-95	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	141-147
23169610-4	2013	MC caused mild induction of Por and a hepatic inflammatory marker in wild-type mice, whereas MC caused strong induction of AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 in wild-type and LCN mice.	Methylcholanthrene	93-95	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	149-155
23169610-4	2013	MC caused mild induction of Por and a hepatic inflammatory marker in wild-type mice, whereas MC caused strong induction of AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 in wild-type and LCN mice.	Methylcholanthrene	93-95	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	161-167
23169610-5	2013	Two mouse hepatic STAT5b target genes, Cyp2d9 and major urinary protein 2 (Mup2), were suppressed by MC in wild-type mice, and the CYP2D9 mRNA response was maintained in LCN mice.	Methylcholanthrene	101-103	signal transducer and activator of transcription 5B	Mus musculus	18-24
23169610-5	2013	Two mouse hepatic STAT5b target genes, Cyp2d9 and major urinary protein 2 (Mup2), were suppressed by MC in wild-type mice, and the CYP2D9 mRNA response was maintained in LCN mice.	Methylcholanthrene	101-103	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	39-45
23169610-5	2013	Two mouse hepatic STAT5b target genes, Cyp2d9 and major urinary protein 2 (Mup2), were suppressed by MC in wild-type mice, and the CYP2D9 mRNA response was maintained in LCN mice.	Methylcholanthrene	101-103	major urinary protein 2	Mus musculus	50-73
23169610-5	2013	Two mouse hepatic STAT5b target genes, Cyp2d9 and major urinary protein 2 (Mup2), were suppressed by MC in wild-type mice, and the CYP2D9 mRNA response was maintained in LCN mice.	Methylcholanthrene	101-103	major urinary protein 2	Mus musculus	75-79
23169610-6	2013	In wild-type mice only, MC decreased hepatic GH receptor (GHR) mRNA but increased GHR protein levels.	Methylcholanthrene	24-26	growth hormone receptor	Mus musculus	45-56
23169610-6	2013	In wild-type mice only, MC decreased hepatic GH receptor (GHR) mRNA but increased GHR protein levels.	Methylcholanthrene	24-26	growth hormone receptor	Mus musculus	58-61
23169610-6	2013	In wild-type mice only, MC decreased hepatic GH receptor (GHR) mRNA but increased GHR protein levels.	Methylcholanthrene	24-26	growth hormone receptor	Mus musculus	82-85
23169610-7	2013	There was an apparent impairment of STAT5 phosphorylation by MC in wild-type and LCN mice, but large interanimal variation prevented achievement of statistical significance.	Methylcholanthrene	61-63	signal transducer and activator of transcription 5A	Mus musculus	36-41
23169610-9	2013	These results indicate that the effects of MC on hepatic GH signaling components and target genes are complex, involving aspects that are both dependent and independent of hepatic microsomal P450-mediated activity.	Methylcholanthrene	43-45	growth hormone	Mus musculus	57-59
23241877-2	2013	Our recent studies in methylcholanthrene-induced fibrosarcomas have indicated the appearance and rapid growth of tumor variants deficient in producing the T cell chemoattractant chemokine CXCL9/Mig, an important component of antitumor immunity.	Methylcholanthrene	22-40	C-X-C motif chemokine ligand 9	Homo sapiens	194-197
23023762-3	2013	Combined use of SNP-A with MC improved the detection rate in comparison with MC alone: acute myeloid leukemia (AML) with normal karyotype (NK), 32% versus 0%; core binding factor (CBF)-AML 40% versus 29%; myelodysplastic syndrome (MDS), 54% versus 39%; chronic myeloid leukemia (CML), 24% versus 3%; and acute lymphoblastic leukemia (ALL), 88% versus 63%.	Methylcholanthrene	27-29	CCAAT enhancer binding protein zeta	Homo sapiens	159-178
24158104-9	2013	Furthermore, cultured human MC showed increased ACE2 mRNA and protein after treatment with IL-1beta, a pro-inflammatory cytokine in IgAN.	Methylcholanthrene	28-30	angiotensin converting enzyme 2	Homo sapiens	48-52
24158104-9	2013	Furthermore, cultured human MC showed increased ACE2 mRNA and protein after treatment with IL-1beta, a pro-inflammatory cytokine in IgAN.	Methylcholanthrene	28-30	interleukin 1 beta	Homo sapiens	91-99
24158104-9	2013	Furthermore, cultured human MC showed increased ACE2 mRNA and protein after treatment with IL-1beta, a pro-inflammatory cytokine in IgAN.	Methylcholanthrene	28-30	IGAN1	Homo sapiens	132-136
24080824-9	2013	TGF-beta1 protein levels in the DM group were significantly increased versus control animals and normalized in the DM+MC group.	Methylcholanthrene	118-120	transforming growth factor, beta 1	Rattus norvegicus	0-9
24080824-10	2013	An increase in ED1(+)/arginase I(+) macrophages and IL-10 renal expression was observed in the DM+MC group versus DM group.	Methylcholanthrene	98-100	interleukin 10	Rattus norvegicus	52-57
24080824-11	2013	CONCLUSIONS: Bone marrow-derived MC therapy was able to prevent glomerular alterations and TGF-beta1 protein overexpression and modulated glomerular arginase I(+) macrophage infiltration in rats subjected to early diabetic nephropathy.	Methylcholanthrene	33-35	transforming growth factor, beta 1	Rattus norvegicus	91-100
24109615-10	2013	Through this study, we show an effective method to simulate light diffusion on tissue with characteristics for radial beam LED based on MC simulation.	Methylcholanthrene	136-138	small integral membrane protein 10 like 2A	Homo sapiens	123-126
23023762-3	2013	Combined use of SNP-A with MC improved the detection rate in comparison with MC alone: acute myeloid leukemia (AML) with normal karyotype (NK), 32% versus 0%; core binding factor (CBF)-AML 40% versus 29%; myelodysplastic syndrome (MDS), 54% versus 39%; chronic myeloid leukemia (CML), 24% versus 3%; and acute lymphoblastic leukemia (ALL), 88% versus 63%.	Methylcholanthrene	27-29	CCAAT enhancer binding protein zeta	Homo sapiens	180-183
23527708-4	2013	MC+HCV-p showed significantly higher mean CXCL9 and CXCL11 levels than controls (P less than 0.001, for both), in particular, in 32 patients with active vasculitis (P less than 0.001).	Methylcholanthrene	0-2	C-X-C motif chemokine ligand 9	Homo sapiens	42-47
23527708-4	2013	MC+HCV-p showed significantly higher mean CXCL9 and CXCL11 levels than controls (P less than 0.001, for both), in particular, in 32 patients with active vasculitis (P less than 0.001).	Methylcholanthrene	0-2	C-X-C motif chemokine ligand 11	Homo sapiens	52-58
23527708-7	2013	Our study demonstrates in MC+HCV-p vs controls: (i) high serum CXCL9, and CXCL11, significantly associated with the presence of active vasculitis; (ii) a strong relationship between circulating CXCL9 and CXCL11.	Methylcholanthrene	26-28	C-X-C motif chemokine ligand 9	Homo sapiens	63-68
23527708-7	2013	Our study demonstrates in MC+HCV-p vs controls: (i) high serum CXCL9, and CXCL11, significantly associated with the presence of active vasculitis; (ii) a strong relationship between circulating CXCL9 and CXCL11.	Methylcholanthrene	26-28	C-X-C motif chemokine ligand 11	Homo sapiens	74-80
23527708-7	2013	Our study demonstrates in MC+HCV-p vs controls: (i) high serum CXCL9, and CXCL11, significantly associated with the presence of active vasculitis; (ii) a strong relationship between circulating CXCL9 and CXCL11.	Methylcholanthrene	26-28	C-X-C motif chemokine ligand 9	Homo sapiens	194-199
23527708-7	2013	Our study demonstrates in MC+HCV-p vs controls: (i) high serum CXCL9, and CXCL11, significantly associated with the presence of active vasculitis; (ii) a strong relationship between circulating CXCL9 and CXCL11.	Methylcholanthrene	26-28	C-X-C motif chemokine ligand 11	Homo sapiens	204-210
22899400-14	2013	Further research is required to delineate the molecular and clinical features of the ~34% of MC cases with neither HER2 amplification nor KRAS mutations.	Methylcholanthrene	93-95	erb-b2 receptor tyrosine kinase 2	Homo sapiens	115-119
23330018-13	2013	The present case showed that MC can express KIT and PDGFRA.	Methylcholanthrene	29-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
23330018-13	2013	The present case showed that MC can express KIT and PDGFRA.	Methylcholanthrene	29-31	platelet derived growth factor receptor alpha	Homo sapiens	52-58
23041154-8	2012	These events attenuated caspase-3 activity and bax/Bcl-2 ratio leading to higher viability of the H(2)O(2)-treated SK-N-MC cells.	Methylcholanthrene	120-122	caspase 3	Homo sapiens	24-33
23043076-5	2012	In Wsh+MC, ovalbumin challenge induced a relocation of mast cells from the perivascular space and central airways to the parenchyma.	Methylcholanthrene	7-9	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	11-20
23043076-9	2012	A mast cell-dependent increase in IgE and IL-33 together with impairment of the IL-23/IL-17 axis was evoked in Wsh and Wsh+MC mice by allergen challenge.	Methylcholanthrene	123-125	interleukin 33	Mus musculus	42-47
23043076-9	2012	A mast cell-dependent increase in IgE and IL-33 together with impairment of the IL-23/IL-17 axis was evoked in Wsh and Wsh+MC mice by allergen challenge.	Methylcholanthrene	123-125	interleukin 23, alpha subunit p19	Mus musculus	80-85
23043076-9	2012	A mast cell-dependent increase in IgE and IL-33 together with impairment of the IL-23/IL-17 axis was evoked in Wsh and Wsh+MC mice by allergen challenge.	Methylcholanthrene	123-125	interleukin 17A	Mus musculus	86-91
23041154-8	2012	These events attenuated caspase-3 activity and bax/Bcl-2 ratio leading to higher viability of the H(2)O(2)-treated SK-N-MC cells.	Methylcholanthrene	120-122	BCL2 associated X, apoptosis regulator	Homo sapiens	47-50
23041154-8	2012	These events attenuated caspase-3 activity and bax/Bcl-2 ratio leading to higher viability of the H(2)O(2)-treated SK-N-MC cells.	Methylcholanthrene	120-122	BCL2 apoptosis regulator	Homo sapiens	51-56
23131371-9	2012	The EEG data showed that the MC and the PMR groups were associated with an increase of posterior theta (3.5-7.5 Hz) and a decrease of midfrontal beta-2 band (20-29.5 Hz) activity during the end phase of relaxation treatment.	Methylcholanthrene	29-31	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	145-151
23095743-10	2012	ARTN also enhanced mammosphere formation and the ALDH1+ population in estrogen receptor-positive mammary carcinoma (ER+MC) cells.	Methylcholanthrene	119-121	artemin	Homo sapiens	0-4
23026235-2	2012	AhR is ligand activated transcription factor with high affinities for aromatic planar compounds such as beta-naphthoflavone (BNF), 3-methylcholanthrene (3-MC), benzo[a]pyrene (BaP) or dioxin (TCDD).	Methylcholanthrene	131-151	aryl hydrocarbon receptor	Rattus norvegicus	0-3
22859831-3	2012	We find that the effect of PGE(2) on FcepsilonRI-dependent MC degranulation varies from activating to suppressing, depending on the relative ratio of EP(2) to EP(3) expression on these cells with suppression evident only in cells having increased EP(2) to EP(3) expression.	Methylcholanthrene	59-61	Fc epsilon receptor Ia	Homo sapiens	37-48
22859831-4	2012	Consistent with a role for EP(2) in suppressing MC responses in vitro, we found that a selective EP(2) agonist, Butaprost, inhibited MC-mediated FcepsilonRI-induced immediate hypersensitivity in a model of PCA.	Methylcholanthrene	48-50	Fc epsilon receptor Ia	Homo sapiens	145-156
22859831-4	2012	Consistent with a role for EP(2) in suppressing MC responses in vitro, we found that a selective EP(2) agonist, Butaprost, inhibited MC-mediated FcepsilonRI-induced immediate hypersensitivity in a model of PCA.	Methylcholanthrene	133-135	Fc epsilon receptor Ia	Homo sapiens	145-156
22859831-8	2012	Collectively, the findings demonstrate that EP(2) suppresses the Fyn-mediated signals that are central to FcepsilonRI-dependent MC degranulation, suggesting that engagement of the EP(2) on MCs may be beneficial in dampening allergic responses.	Methylcholanthrene	128-130	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	65-68
22859831-8	2012	Collectively, the findings demonstrate that EP(2) suppresses the Fyn-mediated signals that are central to FcepsilonRI-dependent MC degranulation, suggesting that engagement of the EP(2) on MCs may be beneficial in dampening allergic responses.	Methylcholanthrene	128-130	Fc epsilon receptor Ia	Homo sapiens	106-117
22986739-4	2012	The suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sarcomas in mice deficient for NLRP3 was NK cell and IFN-gamma-dependent.	Methylcholanthrene	69-87	NLR family, pyrin domain containing 3	Mus musculus	133-138
22986739-4	2012	The suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sarcomas in mice deficient for NLRP3 was NK cell and IFN-gamma-dependent.	Methylcholanthrene	69-87	interferon gamma	Mus musculus	155-164
22986739-4	2012	The suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sarcomas in mice deficient for NLRP3 was NK cell and IFN-gamma-dependent.	Methylcholanthrene	89-92	NLR family, pyrin domain containing 3	Mus musculus	133-138
22986739-4	2012	The suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sarcomas in mice deficient for NLRP3 was NK cell and IFN-gamma-dependent.	Methylcholanthrene	89-92	interferon gamma	Mus musculus	155-164
23026235-2	2012	AhR is ligand activated transcription factor with high affinities for aromatic planar compounds such as beta-naphthoflavone (BNF), 3-methylcholanthrene (3-MC), benzo[a]pyrene (BaP) or dioxin (TCDD).	Methylcholanthrene	153-157	aryl hydrocarbon receptor	Rattus norvegicus	0-3
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	aryl-hydrocarbon receptor	Mus musculus	22-25
22766105-8	2012	CONCLUSIONS: We demonstrated markedly high serum levels of CXCL9 in MC+HCV (vs. HCV+ patients or healthy controls), significantly associated with the presence of active vasculitis.	Methylcholanthrene	68-70	C-X-C motif chemokine ligand 9	Homo sapiens	59-64
22766105-9	2012	A strong relation among high levels of circulating IFN-gamma, TNF-alpha and serum CXCL9 has been shown in MC+HCV.	Methylcholanthrene	106-108	interferon gamma	Homo sapiens	51-60
22766105-9	2012	A strong relation among high levels of circulating IFN-gamma, TNF-alpha and serum CXCL9 has been shown in MC+HCV.	Methylcholanthrene	106-108	tumor necrosis factor	Homo sapiens	62-71
22766105-9	2012	A strong relation among high levels of circulating IFN-gamma, TNF-alpha and serum CXCL9 has been shown in MC+HCV.	Methylcholanthrene	106-108	C-X-C motif chemokine ligand 9	Homo sapiens	82-87
22886749-8	2012	This study suggests that the combined use of SNP-A with MC in the CBF AML can provide important prognostic value, especially in the inv(16)/t(16;16) subgroup or in the patients without the D816 C-KIT mutation.	Methylcholanthrene	56-58	CCAAT enhancer binding protein zeta	Homo sapiens	66-69
23039894-9	2012	Finally, we estimated BAFF levels after complete depletion of B cells with rituximab in patients with chronic HCV with MC (n = 3).	Methylcholanthrene	119-121	TNF superfamily member 13b	Homo sapiens	22-26
23039894-10	2012	Serum levels of BAFF were increased in chronic HCV with MC, but not in chronic HBV infection, suggesting an association between BAFF and cryoglobulinaemia.	Methylcholanthrene	56-58	TNF superfamily member 13b	Homo sapiens	16-20
22634562-0	2012	The aryl hydrocarbon receptor ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene regulate distinct genetic networks.	Methylcholanthrene	78-98	aryl hydrocarbon receptor	Homo sapiens	4-29
22634562-2	2012	3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	72-97
22634562-2	2012	3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	99-102
22634562-2	2012	3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling.	Methylcholanthrene	22-26	aryl hydrocarbon receptor	Homo sapiens	72-97
22634562-2	2012	3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling.	Methylcholanthrene	22-26	aryl hydrocarbon receptor	Homo sapiens	99-102
22634562-6	2012	Like DES, 3-MC induced a number of ER-regulated genes and lead to recruitment of ERalpha to the promoters of such genes.	Methylcholanthrene	10-14	estrogen receptor 1	Homo sapiens	81-88
22634562-7	2012	Interestingly, in contrast to DES, the estrogenic effects exerted by 3-MC were exclusively observed in ERalpha, but not in ERbeta-expressing cells, suggesting ER isoform selectivity of 3-MC-derived metabolites.	Methylcholanthrene	69-73	estrogen receptor 1	Homo sapiens	103-110
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	growth hormone	Mus musculus	98-112
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	growth hormone	Mus musculus	114-116
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	154-173
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	175-181
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	growth hormone	Mus musculus	229-231
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	signal transducer and activator of transcription 5B	Mus musculus	236-287
22978700-2	2012	A readily metabolized AHR agonist, 3-methylcholanthrene, disrupts the expression of mouse hepatic growth hormone (GH) signaling components and suppresses cytochrome P450 2D9 (Cyp2d9), a male-specific gene controlled by pulsatile GH via signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	35-55	signal transducer and activator of transcription 5B	Mus musculus	289-295
22765310-2	2012	METHOD: Human native Vim was citrullinated with rabbit PAD in vitro and detected using a Western blot assay with anti-modified citrulline antibody (anti-MC Ab).	Methylcholanthrene	153-155	vimentin	Homo sapiens	21-24
22765310-7	2012	RESULTS: Our Western blot assay with anti-MC Ab indicated that the amount of cVim increased significantly after Vim had been incubated with rabbit PAD in vitro.	Methylcholanthrene	42-44	vimentin	Oryctolagus cuniculus	78-81
22609128-5	2012	This paper describes the initial experimental studies performed to enable the extension of the MC model based loss correction method to gases other than carbon dioxide in P-10.	Methylcholanthrene	95-97	S100 calcium binding protein A10	Homo sapiens	171-175
22422555-10	2012	Co-culture of MC with MSC at 75:25 demonstrated highest levels of collagen type I and glycosaminoglycans (GAG) production, as well as the lowest levels of hypertrophic genes, such as COL10A1 and MMP13.	Methylcholanthrene	14-16	collagen type X alpha 1 chain	Homo sapiens	183-190
22422555-10	2012	Co-culture of MC with MSC at 75:25 demonstrated highest levels of collagen type I and glycosaminoglycans (GAG) production, as well as the lowest levels of hypertrophic genes, such as COL10A1 and MMP13.	Methylcholanthrene	14-16	matrix metallopeptidase 13	Homo sapiens	195-200
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	notch receptor 1	Rattus norvegicus	357-363
22475410-7	2012	Polymorphisms in the CL-11 gene (COLEC11) leading to deficiencies have recently been identified as causative for 3MC syndrome.	Methylcholanthrene	113-116	collectin subfamily member 11	Homo sapiens	21-26
22475410-7	2012	Polymorphisms in the CL-11 gene (COLEC11) leading to deficiencies have recently been identified as causative for 3MC syndrome.	Methylcholanthrene	113-116	collectin subfamily member 11	Homo sapiens	33-40
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	notch receptor 1	Rattus norvegicus	222-227
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	notch receptor 3	Rattus norvegicus	246-252
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	jagged canonical Notch ligand 1	Rattus norvegicus	365-373
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	notch receptor 4	Rattus norvegicus	257-263
23297568-7	2012	RESULTS: In the MC group, E and the AI were increased and pulmonary function significantly decreased; the structure of alveolar type-III cells was damaged; ratios ofTreg in peripheral blood were reduced; and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Deltal in lung tissue were significantly increased whereas expression of Notch1, Jagged 1 and Jagged2 were significantly decreased.	Methylcholanthrene	16-18	jagged canonical Notch ligand 2	Rattus norvegicus	378-385
22438059-13	2012	The most highly expressed SP4 isoform is likely to contribute to MC aggregation and longevity in mastocytosis, and augment the pathophysiology of allergic diseases.	Methylcholanthrene	65-67	Sp4 transcription factor	Homo sapiens	26-29
22802418-5	2012	However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells.	Methylcholanthrene	60-62	Nef	Human immunodeficiency virus 1	9-12
22802418-5	2012	However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells.	Methylcholanthrene	60-62	lymphocyte cytosolic protein 2	Homo sapiens	161-167
22802418-5	2012	However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells.	Methylcholanthrene	60-62	Nef	Human immunodeficiency virus 1	193-196
22802418-9	2012	These modulations in MC formation and composition depended on Nef"s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery.	Methylcholanthrene	21-23	S100 calcium binding protein B	Homo sapiens	62-65
22802418-9	2012	These modulations in MC formation and composition depended on Nef"s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery.	Methylcholanthrene	21-23	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	156-159
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	243-245	GRAS family transcription factor	Arabidopsis thaliana	39-42
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	243-245	GRAS family transcription factor	Arabidopsis thaliana	78-82
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	243-245	GRAS family transcription factor	Arabidopsis thaliana	210-213
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	243-245	GRAS family transcription factor	Arabidopsis thaliana	210-213
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	290-292	GRAS family transcription factor	Arabidopsis thaliana	39-42
22826238-7	2012	Here we show that the abundance of the SHR protein changes dynamically as the root develops, and that the pattern of cell division within the endodermis is sensitive to the dose of this protein: high levels of SHR prevent the formation of the MC, whereas intermediate levels of SHR promote MC formation.	Methylcholanthrene	290-292	GRAS family transcription factor	Arabidopsis thaliana	78-82
22573320-4	2012	Furthermore, expression of the MC domains of Sup35, which retains the C-terminal domain of Sup35, but lacks the N-terminal prion domain, almost completely rescued HttQP103 toxicity, but was less effective in rescuing HttQ103 toxicity.	Methylcholanthrene	31-33	translation termination factor GTPase eRF3	Saccharomyces cerevisiae S288C	45-50
22669972-6	2012	In this study, we observed that deficiency of either Fas or FasL resulted in significantly increased incidence of 3-methylcholanthrene-induced spontaneous sarcoma development in mice.	Methylcholanthrene	114-134	Fas ligand (TNF superfamily, member 6)	Mus musculus	60-64
22503605-2	2012	We report a boy whose ictal MEG focus was localized to the same sublobar region before and after head turning when MC was applied, but which was erroneously localized to a different area without MC.	Methylcholanthrene	115-117	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	28-31
22503605-2	2012	We report a boy whose ictal MEG focus was localized to the same sublobar region before and after head turning when MC was applied, but which was erroneously localized to a different area without MC.	Methylcholanthrene	195-197	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	28-31
21492502-4	2012	At stages II-III, a second pathway transports Vg1 and VegT mRNAs to the area where the MC content merges with the vegetal cortex.	Methylcholanthrene	87-89	growth differentiation factor 1 S homeolog	Xenopus laevis	46-49
21492502-4	2012	At stages II-III, a second pathway transports Vg1 and VegT mRNAs to the area where the MC content merges with the vegetal cortex.	Methylcholanthrene	87-89	vegt protein S homeolog	Xenopus laevis	54-58
21492502-10	2012	XNOA 36 protein immunolocalization, using an antibody employed for the library immunoscreening that depicted XNOA 36 expression colonies, labels the migrating MC, the cytoplasm of stage I oocytes and in particular the vegetal cortex facing the MC.	Methylcholanthrene	159-161	zinc finger protein 330 S homeolog	Xenopus laevis	0-7
21492502-10	2012	XNOA 36 protein immunolocalization, using an antibody employed for the library immunoscreening that depicted XNOA 36 expression colonies, labels the migrating MC, the cytoplasm of stage I oocytes and in particular the vegetal cortex facing the MC.	Methylcholanthrene	159-161	zinc finger protein 330 S homeolog	Xenopus laevis	109-116
21492502-10	2012	XNOA 36 protein immunolocalization, using an antibody employed for the library immunoscreening that depicted XNOA 36 expression colonies, labels the migrating MC, the cytoplasm of stage I oocytes and in particular the vegetal cortex facing the MC.	Methylcholanthrene	244-246	zinc finger protein 330 S homeolog	Xenopus laevis	0-7
22573320-4	2012	Furthermore, expression of the MC domains of Sup35, which retains the C-terminal domain of Sup35, but lacks the N-terminal prion domain, almost completely rescued HttQP103 toxicity, but was less effective in rescuing HttQ103 toxicity.	Methylcholanthrene	31-33	translation termination factor GTPase eRF3	Saccharomyces cerevisiae S288C	91-96
22034857-7	2012	The average fold increase in cell numbers on VN-coated MC per serial passage was 8.5+-1.0, which was similar to LN-coated MC (8.5+-0.9).	Methylcholanthrene	55-57	vitronectin	Homo sapiens	45-47
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	128-148	protein tyrosine kinase 2	Homo sapiens	37-58
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	128-148	protein tyrosine kinase 2	Homo sapiens	60-63
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	128-148	ras homolog family member A	Homo sapiens	65-69
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	128-148	aryl hydrocarbon receptor	Homo sapiens	88-113
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	128-148	aryl hydrocarbon receptor	Homo sapiens	115-118
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	150-153	protein tyrosine kinase 2	Homo sapiens	37-58
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	150-153	protein tyrosine kinase 2	Homo sapiens	60-63
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	150-153	ras homolog family member A	Homo sapiens	65-69
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	150-153	aryl hydrocarbon receptor	Homo sapiens	88-113
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	150-153	aryl hydrocarbon receptor	Homo sapiens	115-118
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	199-202	protein tyrosine kinase 2	Homo sapiens	37-58
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	199-202	protein tyrosine kinase 2	Homo sapiens	60-63
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	199-202	ras homolog family member A	Homo sapiens	65-69
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	199-202	aryl hydrocarbon receptor	Homo sapiens	88-113
22720799-1	2012	We have demonstrated previously that focal adhesion kinase (FAK)/RhoA alteration by the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigratory effects of 3MC in human umbilical vascular endothelial cells.	Methylcholanthrene	199-202	aryl hydrocarbon receptor	Homo sapiens	115-118
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	aryl-hydrocarbon receptor	Mus musculus	37-40
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	ras homolog family member A	Mus musculus	41-45
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	catenin (cadherin associated protein), beta 1	Mus musculus	98-110
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	protein kinase C, delta	Mus musculus	119-127
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	catenin (cadherin associated protein), beta 1	Mus musculus	147-159
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	aryl-hydrocarbon receptor	Mus musculus	198-201
22720799-4	2012	PTEN phosphorylation by 3MC-mediated AhR/RhoA activation increased the proteasomal degradation of beta-catenin through PKCdelta/pGSK3beta-mediated beta-catenin phosphorylation; the crucial roles of AhR/RhoA in this process were verified by using gain- or loss-of-function experiments.	Methylcholanthrene	24-27	ras homolog family member A	Mus musculus	202-206
22720799-8	2012	The results indicate that the binding activities of beta-catenin decreased in mouse cerebrovascular endothelial cells treated with 3MC.	Methylcholanthrene	131-134	catenin (cadherin associated protein), beta 1	Mus musculus	52-64
22720799-9	2012	In addition, simvastatin and pravastatin treatment reversed 3MC-mediated alterations in mouse cerebrovascular endothelial cells by RhoA inactivation, and the in vitro findings were substantiated by an in vivo blood-brain barrier assay.	Methylcholanthrene	60-63	ras homolog family member A	Mus musculus	131-135
22720799-10	2012	Thus, endothelial barrier dysfunction due to 3MC occurs through AhR/RhoA-mediated beta-catenin down-regulation, which is reversed by simvastatin treatment in vivo.	Methylcholanthrene	45-48	aryl-hydrocarbon receptor	Mus musculus	64-67
22720799-10	2012	Thus, endothelial barrier dysfunction due to 3MC occurs through AhR/RhoA-mediated beta-catenin down-regulation, which is reversed by simvastatin treatment in vivo.	Methylcholanthrene	45-48	ras homolog family member A	Mus musculus	68-72
22720799-10	2012	Thus, endothelial barrier dysfunction due to 3MC occurs through AhR/RhoA-mediated beta-catenin down-regulation, which is reversed by simvastatin treatment in vivo.	Methylcholanthrene	45-48	catenin (cadherin associated protein), beta 1	Mus musculus	82-94
22505044-5	2012	3MC exposure was also found to induce developing follicle atresia and aberrant primordial follicle activation via the stimulation of PI3K/Akt and mammalian target of rapamycin (mTOR) signaling pathways.	Methylcholanthrene	0-3	AKT serine/threonine kinase 1	Homo sapiens	138-141
22505044-5	2012	3MC exposure was also found to induce developing follicle atresia and aberrant primordial follicle activation via the stimulation of PI3K/Akt and mammalian target of rapamycin (mTOR) signaling pathways.	Methylcholanthrene	0-3	mechanistic target of rapamycin kinase	Homo sapiens	146-175
22505044-5	2012	3MC exposure was also found to induce developing follicle atresia and aberrant primordial follicle activation via the stimulation of PI3K/Akt and mammalian target of rapamycin (mTOR) signaling pathways.	Methylcholanthrene	0-3	mechanistic target of rapamycin kinase	Homo sapiens	177-181
22505044-6	2012	Inhibition of PI3K/Akt signaling resulted in the severe depletion of the primordial follicle pool, with further analysis identifying increased Akt1-stimulated Bad phosphoinhibition in 3MC-treated primordial follicles.	Methylcholanthrene	184-187	AKT serine/threonine kinase 1	Homo sapiens	19-22
22505044-6	2012	Inhibition of PI3K/Akt signaling resulted in the severe depletion of the primordial follicle pool, with further analysis identifying increased Akt1-stimulated Bad phosphoinhibition in 3MC-treated primordial follicles.	Methylcholanthrene	184-187	AKT serine/threonine kinase 1	Homo sapiens	143-147
22856136-2	2012	Treatment of rats with benzo(a)pyren (BP) or 3-methylcholantrene (MC) significantly up-regulated CYP1A1, CYP1B1 gene expression in liver, uterus and ovary, whereas alfa-naphthoflavone (alpha-NF) did not have any effect.	Methylcholanthrene	66-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	97-103
22856136-2	2012	Treatment of rats with benzo(a)pyren (BP) or 3-methylcholantrene (MC) significantly up-regulated CYP1A1, CYP1B1 gene expression in liver, uterus and ovary, whereas alfa-naphthoflavone (alpha-NF) did not have any effect.	Methylcholanthrene	66-68	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	105-111
22396496-5	2012	CD73 deficiency suppressed the development of 3-methylcholanthrene (MCA)-induced fibrosarcomas through a mechanism relying upon IFN-gamma, natural killer (NK) cells, and CD8(+) T cells.	Methylcholanthrene	46-66	interferon gamma	Mus musculus	128-137
22396496-5	2012	CD73 deficiency suppressed the development of 3-methylcholanthrene (MCA)-induced fibrosarcomas through a mechanism relying upon IFN-gamma, natural killer (NK) cells, and CD8(+) T cells.	Methylcholanthrene	68-71	interferon gamma	Mus musculus	128-137
22411109-6	2012	RESULTS: Higher S100B levels were found in patients who sustained a TBI than in those in the MC and TC groups (DTBI &amp; MTBI &gt;TC &amp; MC).	Methylcholanthrene	93-95	S100 calcium binding protein B	Homo sapiens	16-21
22262798-11	2012	Thus, MC progenitors that develop in SCF + IL-4 can be induced to express NOS2 after receiving appropriate signals, such as IFN-gamma, and subsequently produce NO.	Methylcholanthrene	6-8	kit ligand	Mus musculus	37-40
22262798-11	2012	Thus, MC progenitors that develop in SCF + IL-4 can be induced to express NOS2 after receiving appropriate signals, such as IFN-gamma, and subsequently produce NO.	Methylcholanthrene	6-8	interleukin 4	Mus musculus	43-47
22262798-11	2012	Thus, MC progenitors that develop in SCF + IL-4 can be induced to express NOS2 after receiving appropriate signals, such as IFN-gamma, and subsequently produce NO.	Methylcholanthrene	6-8	nitric oxide synthase 2, inducible	Mus musculus	74-78
22262798-11	2012	Thus, MC progenitors that develop in SCF + IL-4 can be induced to express NOS2 after receiving appropriate signals, such as IFN-gamma, and subsequently produce NO.	Methylcholanthrene	6-8	interferon gamma	Mus musculus	124-133
22588935-8	2012	The expression of SIRT1 was significantly lower and UCP2 significantly higher in MC group than in the control group (P&lt;0.05).	Methylcholanthrene	81-83	sirtuin 1	Rattus norvegicus	18-23
22588935-8	2012	The expression of SIRT1 was significantly lower and UCP2 significantly higher in MC group than in the control group (P&lt;0.05).	Methylcholanthrene	81-83	uncoupling protein 2	Rattus norvegicus	52-56
23587228-13	2012	CONCLUSIONS: MC induced drop in VEGF, and was effective, minimally toxic regimen for the treatment of metastatic breast cancer patients.	Methylcholanthrene	13-15	vascular endothelial growth factor A	Homo sapiens	32-36
22411109-6	2012	RESULTS: Higher S100B levels were found in patients who sustained a TBI than in those in the MC and TC groups (DTBI &amp; MTBI &gt;TC &amp; MC).	Methylcholanthrene	140-142	S100 calcium binding protein B	Homo sapiens	16-21
20449626-7	2012	Nevertheless, the TSP-1 level driven by MC did not correlate to clinical benefit.	Methylcholanthrene	40-42	thrombospondin 1	Homo sapiens	18-23
22264940-8	2012	Changes in circular dichroism spectra of BSA in presence of MC 540 depict secondary structural changes of the protein.	Methylcholanthrene	60-62	albumin	Homo sapiens	41-44
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	162-164	secretoglobin family 1A member 1	Homo sapiens	23-27
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	162-164	secretoglobin family 1A member 1	Homo sapiens	197-201
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	285-287	secretoglobin family 1A member 1	Homo sapiens	23-27
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	285-287	secretoglobin family 1A member 1	Homo sapiens	197-201
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	285-287	secretoglobin family 1A member 1	Homo sapiens	23-27
22309677-8	2012	RESULTS: The levels of CC16 correlated with nNO levels (r2 = 0.37; p = 0.02) in allergic subjects.The levels of both biomarkers showed inverse relationships with MC occurrence, as higher levels of CC16 (p = 0.03) and nNO (p = 0.05) were found in allergic subjects with no demonstrable MC compared to the levels in subjects with demonstrable MC.	Methylcholanthrene	285-287	secretoglobin family 1A member 1	Homo sapiens	197-201
22309677-11	2012	CONCLUSIONS: The correlation between nasal CC16 and nNO levels in patients with allergic rhinitis, along with an inverse relationship between their levels and the occurrences of MC in allergic inflammation, may indicate that both biomarkers have anti-inflammatory effects by suppression of cell recruitment.	Methylcholanthrene	178-180	secretoglobin family 1A member 1	Homo sapiens	43-47
22323705-8	2012	For activating pumping, the SER-7 serotonin receptor in the MC motor neurons in the feeding organ activated cholinergic transmission from MC to the pharyngeal muscles by activating the Gsalpha signaling pathway.	Methylcholanthrene	60-62	G_PROTEIN_RECEP_F1_2 domain-containing protein	Caenorhabditis elegans	28-33
22158523-3	2012	Compared with pcDNA-hES, MC-mediated endostatin gene transfer in vitro resulted in seven-fold greater endostatin expression levels in transfected cells and inhibited the growth of Human umbilical vein endothelial cells (HUVEC) more efficiently.	Methylcholanthrene	25-27	collagen type XVIII alpha 1 chain	Homo sapiens	37-47
22158523-3	2012	Compared with pcDNA-hES, MC-mediated endostatin gene transfer in vitro resulted in seven-fold greater endostatin expression levels in transfected cells and inhibited the growth of Human umbilical vein endothelial cells (HUVEC) more efficiently.	Methylcholanthrene	25-27	collagen type XVIII alpha 1 chain	Homo sapiens	102-112
22158523-4	2012	HUVEC cell migration and tube-formation assays suggested that MC-mediated endostatin gene has significant anti-migration and anti-tube-formation capacity than that in pcDNA-hES.	Methylcholanthrene	62-64	collagen type XVIII alpha 1 chain	Homo sapiens	74-84
22158523-4	2012	HUVEC cell migration and tube-formation assays suggested that MC-mediated endostatin gene has significant anti-migration and anti-tube-formation capacity than that in pcDNA-hES.	Methylcholanthrene	62-64	ribosome binding protein 1	Homo sapiens	173-176
22158523-7	2012	MC-mediated intratumoral endostatin expression in vivo was 2.2-17.9 times higher than pcDNA-hES in xenografted mice and lasted for 20 days.	Methylcholanthrene	0-2	collagen, type XVIII, alpha 1	Mus musculus	25-35
22024363-5	2012	Unexpectedly, COL-MC-cultured MSCs underwent spontaneous osteogenesis without exogenous addition of biochemical factors, as evidenced by increased osteogenic genes expression, ALP activity, calcium deposition, and collagen I secretion.	Methylcholanthrene	18-20	ATHS	Homo sapiens	176-179
22673034-5	2012	The levels of CYP1A1, CYP1A2, and UGT1A1 mRNA expression were increased by omeprazole and 3-methylcholanthrene.	Methylcholanthrene	90-110	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	14-20
22673034-5	2012	The levels of CYP1A1, CYP1A2, and UGT1A1 mRNA expression were increased by omeprazole and 3-methylcholanthrene.	Methylcholanthrene	90-110	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	22-28
22673034-5	2012	The levels of CYP1A1, CYP1A2, and UGT1A1 mRNA expression were increased by omeprazole and 3-methylcholanthrene.	Methylcholanthrene	90-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
22442690-4	2012	When exposed to cord blood plasma, mononuclear cells (MCs) produced significantly lower TLR4-mediated IL-12p70 and higher IL-10 compared to MC exposed to adult plasma.	Methylcholanthrene	54-56	toll like receptor 4	Homo sapiens	88-92
21437905-5	2012	Similarly to freshly isolated cells, cultured hepatocytes also retain the ability to respond to 3-methylcholanthrene (3MC) and phenobarbital (PB), two known CYP inducers.	Methylcholanthrene	96-116	peptidylprolyl isomerase G	Homo sapiens	157-160
21437905-5	2012	Similarly to freshly isolated cells, cultured hepatocytes also retain the ability to respond to 3-methylcholanthrene (3MC) and phenobarbital (PB), two known CYP inducers.	Methylcholanthrene	118-121	peptidylprolyl isomerase G	Homo sapiens	157-160
23028684-5	2012	We hypothesize that selection at FADS variants, which increase LC-PUFA synthesis from plant-based MC-PUFAs, played an important role in allowing African populations obligatorily tethered to marine sources for LC-PUFAs in isolated geographic regions, to rapidly expand throughout the African continent 60-80 kya.	Methylcholanthrene	98-100	stearoyl-CoA desaturase	Homo sapiens	33-37
23028684-5	2012	We hypothesize that selection at FADS variants, which increase LC-PUFA synthesis from plant-based MC-PUFAs, played an important role in allowing African populations obligatorily tethered to marine sources for LC-PUFAs in isolated geographic regions, to rapidly expand throughout the African continent 60-80 kya.	Methylcholanthrene	98-100	pumilio RNA binding family member 3	Homo sapiens	66-70
22496599-5	2012	The presence of PPARgamma on MC was assayed in a Western Blot analysis.	Methylcholanthrene	29-31	peroxisome proliferator activated receptor gamma	Homo sapiens	16-25
22442690-4	2012	When exposed to cord blood plasma, mononuclear cells (MCs) produced significantly lower TLR4-mediated IL-12p70 and higher IL-10 compared to MC exposed to adult plasma.	Methylcholanthrene	54-56	interleukin 10	Homo sapiens	122-127
22025298-0	2011	Whole-exome sequencing detects somatic mutations of IDH1 in metaphyseal chondromatosis with D-2-hydroxyglutaric aciduria (MC-HGA).	Methylcholanthrene	122-124	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	52-56
21798286-4	2011	However, HuMCs from the remaining donors and the LAD2 human MC line responded to PGE(2) and sulprostone with marked enhancement of antigen-mediated degranulation and IL-8 production in a similar manner to that observed in mouse BMMCs.	Methylcholanthrene	11-13	C-X-C motif chemokine ligand 8	Homo sapiens	166-170
22101270-9	2011	Anisomycin, a JNK activator, impaired Foretinib-induced MC and inhibition or knockdown of JNK phenotyped its effect on MC.	Methylcholanthrene	119-121	mitogen-activated protein kinase 8	Homo sapiens	90-93
22101270-12	2011	Collectively, our data show that the multikinase inhibitor Foretinib induces MC in CML cells and other cell lines via JNK-dependent inhibition of Plk1 expression and triggered apoptosis by a caspase 2-mediated mechanism.	Methylcholanthrene	77-79	mitogen-activated protein kinase 8	Homo sapiens	118-121
22101270-12	2011	Collectively, our data show that the multikinase inhibitor Foretinib induces MC in CML cells and other cell lines via JNK-dependent inhibition of Plk1 expression and triggered apoptosis by a caspase 2-mediated mechanism.	Methylcholanthrene	77-79	polo like kinase 1	Homo sapiens	146-150
21952774-3	2011	The efficiency of immobilized AChE was monitored by biochemical assay, which was carried out by mixing enzyme-immobilized MC microspheres with model substrate acetylcholine (ACh), and subsequent quantitative determination of substrate ACh and product choline using graphene oxide-based MALDI-TOF-MS with no background inference.	Methylcholanthrene	122-124	acetylcholinesterase (Cartwright blood group)	Homo sapiens	30-34
21903590-5	2011	We demonstrated that the MC-let-7a-1~let-7d cluster was encoded by a single polycistronic transcript driven by a 10-kb upstream promoter, with two MYC-binding sites.	Methylcholanthrene	25-27	microRNA let-7a-1	Homo sapiens	28-36
21903590-5	2011	We demonstrated that the MC-let-7a-1~let-7d cluster was encoded by a single polycistronic transcript driven by a 10-kb upstream promoter, with two MYC-binding sites.	Methylcholanthrene	25-27	microRNA let-7d	Homo sapiens	37-43
21903590-5	2011	We demonstrated that the MC-let-7a-1~let-7d cluster was encoded by a single polycistronic transcript driven by a 10-kb upstream promoter, with two MYC-binding sites.	Methylcholanthrene	25-27	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	147-150
22042869-8	2011	Loss of Mc reduces Swi2 and Swi5 to levels comparable to those in P cells and disrupts RPC spreading across the mat2/3 region.	Methylcholanthrene	8-10	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Homo sapiens	19-23
22042869-8	2011	Loss of Mc reduces Swi2 and Swi5 to levels comparable to those in P cells and disrupts RPC spreading across the mat2/3 region.	Methylcholanthrene	8-10	SWI5 homologous recombination repair protein	Homo sapiens	28-32
22042869-8	2011	Loss of Mc reduces Swi2 and Swi5 to levels comparable to those in P cells and disrupts RPC spreading across the mat2/3 region.	Methylcholanthrene	8-10	methionine adenosyltransferase 2A	Homo sapiens	112-116
22042869-10	2011	We demonstrate that Mc localization at LTRs and at swi2 requires Abp1, a homolog of transposon-derived CENP-B protein and that loss of Abp1 impairs Swi2 protein expression and the donor choice mechanism.	Methylcholanthrene	20-22	amine oxidase copper containing 1	Homo sapiens	65-69
22042869-10	2011	We demonstrate that Mc localization at LTRs and at swi2 requires Abp1, a homolog of transposon-derived CENP-B protein and that loss of Abp1 impairs Swi2 protein expression and the donor choice mechanism.	Methylcholanthrene	20-22	centromere protein B	Homo sapiens	103-109
22025298-6	2011	Thus, somatic mutations in IDH1 may explain all features of MC-HGA, including sporadic occurrence, metaphyseal disorganization, and chondromatosis, urinary excretion of D-2-hydroxy-glutaric acid, and reduced cerebral myelinization.	Methylcholanthrene	60-62	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	27-31
21250977-13	2011	CONCLUSIONS AND IMPLICATIONS: Capsaicin alone weakly induced CYP1A1 expression, and 3-MC-induced CYP1A1 levels were suppressed by capsaicin.	Methylcholanthrene	84-88	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	97-103
21250977-14	2011	Activation of C/EBPbeta and inhibition of 3-MC-induced AhR transactivation by capsaicin contributed to the suppression of CYP1A1 expression.	Methylcholanthrene	42-46	aryl-hydrocarbon receptor	Mus musculus	55-58
21250977-9	2011	Additionally, capsaicin significantly inhibited 3-MC-induced CYP1A1 mRNA and protein level and xenobiotic response element-luciferase activity.	Methylcholanthrene	48-52	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	61-67
21250977-10	2011	Capsaicin also inhibited 3-MC-induced AhR transactivation and nuclear localization of AhRs.	Methylcholanthrene	25-29	aryl-hydrocarbon receptor	Mus musculus	38-41
21250977-14	2011	Activation of C/EBPbeta and inhibition of 3-MC-induced AhR transactivation by capsaicin contributed to the suppression of CYP1A1 expression.	Methylcholanthrene	42-46	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	122-128
21982597-8	2011	Thus, MC-derived IL-2 contributes to the maintenance of suppression in chronic allergic skin inflammation.	Methylcholanthrene	6-8	interleukin 2	Mus musculus	17-21
21250977-12	2011	Capsaicin-induced C/EBPbeta activation inhibited induction of CYP1A1 mRNA and protein by 3-MC.	Methylcholanthrene	89-93	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	18-27
21250977-12	2011	Capsaicin-induced C/EBPbeta activation inhibited induction of CYP1A1 mRNA and protein by 3-MC.	Methylcholanthrene	89-93	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	62-68
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	94-96	matrix metallopeptidase 1	Homo sapiens	174-178
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	130-132	GLI family zinc finger 2	Homo sapiens	64-69
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	130-132	matrix metallopeptidase 1	Homo sapiens	174-178
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	130-132	matrix metallopeptidase 3	Homo sapiens	200-204
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	130-132	matrix metallopeptidase 1	Homo sapiens	252-256
21935932-6	2011	Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner.	Methylcholanthrene	130-132	matrix metallopeptidase 3	Homo sapiens	278-282
21935932-10	2011	Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1beta on MMP1 and MMP3 production.	Methylcholanthrene	67-69	mitogen-activated protein kinase 14	Homo sapiens	14-17
21935932-10	2011	Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1beta on MMP1 and MMP3 production.	Methylcholanthrene	67-69	mitogen-activated protein kinase 1	Homo sapiens	19-22
21935932-10	2011	Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1beta on MMP1 and MMP3 production.	Methylcholanthrene	67-69	mitogen-activated protein kinase 8	Homo sapiens	27-30
21935932-10	2011	Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1beta on MMP1 and MMP3 production.	Methylcholanthrene	67-69	matrix metallopeptidase 1	Homo sapiens	85-89
21935932-10	2011	Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1beta on MMP1 and MMP3 production.	Methylcholanthrene	67-69	matrix metallopeptidase 3	Homo sapiens	94-98
21848673-7	2011	Unlike NM II-B, which is detected only after tumor formation, II-A is detectable as early as day 7 after a second dose of 3MC.	Methylcholanthrene	122-125	ATPase, class II, type 9A	Mus musculus	62-66
21681764-6	2011	Higher polyphenol oxidase (PPO) activity and total phenolic content were found in MC, dry CR (DCR) and asymptomatic tissue of wet CR (asympWCR) fruits than in healthy fruits, as well as significantly higher catalase and peroxidase activities in DCR and symptomatic tissue of WCR (sympWCR) fruits respectively, while asympWCR fruits showed a marked increase in malondialdehyde content, membrane permeability and superoxide production and a significant decrease in superoxide dismutase activity.	Methylcholanthrene	82-84	polyphenol oxidase, chloroplastic	Malus domestica	7-25
21681764-6	2011	Higher polyphenol oxidase (PPO) activity and total phenolic content were found in MC, dry CR (DCR) and asymptomatic tissue of wet CR (asympWCR) fruits than in healthy fruits, as well as significantly higher catalase and peroxidase activities in DCR and symptomatic tissue of WCR (sympWCR) fruits respectively, while asympWCR fruits showed a marked increase in malondialdehyde content, membrane permeability and superoxide production and a significant decrease in superoxide dismutase activity.	Methylcholanthrene	82-84	polyphenol oxidase, chloroplastic	Malus domestica	27-30
21681764-7	2011	CONCLUSION: The findings suggest that PPO and phenolic compounds may play a key role in the defence system of apple fruits against MC and CR.	Methylcholanthrene	131-133	polyphenol oxidase, chloroplastic	Malus domestica	38-41
20196164-8	2011	The expression levels of Bcl-2, Bax, p53, and GRP 78 in MC-RR-treated groups were altered significantly compared to the control, but no obvious alteration was found in CHOP expression.	Methylcholanthrene	56-58	B cell leukemia/lymphoma 2	Mus musculus	25-30
21140449-7	2011	The positive rate of sGP73 in angioma, FNH, ICC, and MC was 0, 50, 63.3, 53.3%, respectively; AFP/GP73 was 0.796 with the sensitivity of 81.4% and specificity of 70.0% when differentiating MC from AFP-negative HCC.	Methylcholanthrene	53-55	golgi membrane protein 1	Homo sapiens	22-26
20196164-8	2011	The expression levels of Bcl-2, Bax, p53, and GRP 78 in MC-RR-treated groups were altered significantly compared to the control, but no obvious alteration was found in CHOP expression.	Methylcholanthrene	56-58	BCL2-associated X protein	Mus musculus	32-35
20196164-8	2011	The expression levels of Bcl-2, Bax, p53, and GRP 78 in MC-RR-treated groups were altered significantly compared to the control, but no obvious alteration was found in CHOP expression.	Methylcholanthrene	56-58	transformation related protein 53, pseudogene	Mus musculus	37-40
20196164-8	2011	The expression levels of Bcl-2, Bax, p53, and GRP 78 in MC-RR-treated groups were altered significantly compared to the control, but no obvious alteration was found in CHOP expression.	Methylcholanthrene	56-58	heat shock protein 5	Mus musculus	46-52
21666223-4	2011	In this article, we show that only CYP1A1 messenger RNA (mRNA), but not CYP1A2, CYP1B1, UGT1A1, BCRP, AHR, ARNT, and AHRR mRNAs, is significantly induced in human term placental trophoblast cultures after exposure to prototype AHR ligands/activators 2,3,7,8-tetrachlorodibenzo-p-dioxin, 3-methylcholanthrene, omeprazole, and beta-naphthoflavone.	Methylcholanthrene	287-307	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	35-41
21676547-4	2011	Following immunization and infection, chickens fed the VAC- or MC-supplemented diets showed increased body weights, greater profilin antibody levels, and/or greater lymphocyte proliferation compared with non-supplemented controls.	Methylcholanthrene	63-65	ETH_00010645	Eimeria tenella	124-132
21676547-5	2011	Prior to Eimeria infection, immunized chickens on the MC-supplemented diet showed reduced IFN-gamma and IL-6 levels, but increased expression of TNFSF15, compared with non-supplemented controls.	Methylcholanthrene	54-56	interferon gamma	Gallus gallus	90-99
21676547-5	2011	Prior to Eimeria infection, immunized chickens on the MC-supplemented diet showed reduced IFN-gamma and IL-6 levels, but increased expression of TNFSF15, compared with non-supplemented controls.	Methylcholanthrene	54-56	interleukin 6	Gallus gallus	104-108
21676547-5	2011	Prior to Eimeria infection, immunized chickens on the MC-supplemented diet showed reduced IFN-gamma and IL-6 levels, but increased expression of TNFSF15, compared with non-supplemented controls.	Methylcholanthrene	54-56	tumor necrosis factor superfamily member 15	Gallus gallus	145-152
21676547-6	2011	Post-infection levels of IFN-gamma and IL-6 were increased, while IL-17F transcripts were decreased, with MC-supplementation.	Methylcholanthrene	106-108	interleukin 17F	Gallus gallus	66-72
21676547-8	2011	Finally, immunized chickens fed the MC-supplemented diet exhibited increased MHC class II(+), CD4(+), CD8(+), TCR1+, or TCR2(+) T cells compared with nonsupplemented controls.	Methylcholanthrene	36-38	CD8a molecule	Gallus gallus	102-105
21832258-5	2011	In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity.	Methylcholanthrene	251-271	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
21878502-3	2011	We demonstrate here a crucial role of the gammaH2AX-ATM-p53 pathway in the regulation of the apoptotic outcome of MC resulting from cells entering mitosis with damaged DNA.	Methylcholanthrene	114-116	tumor protein p53	Homo sapiens	56-59
21724697-4	2011	RESULTS: MC+HCV patients showed significantly higher mean CXCL11 serum levels than controls (254 +- 295, 68 +- 16 pg/ml, respectively; p = 0.0002; ANOVA).	Methylcholanthrene	9-11	C-X-C motif chemokine ligand 11	Homo sapiens	58-64
21724697-6	2011	IFN-gamma levels were significantly higher in MC+HCV than in controls [6.1 (range 0.8-114.5), 1.4 (range 0.7-2.4) pg/ml, respectively; p &lt; 0.05; Mann-Whitney U test].	Methylcholanthrene	46-49	interferon gamma	Homo sapiens	0-9
21724697-10	2011	A strong relationship between circulating IFN-gamma and CXCL11 was shown, strongly supporting the role of a T helper 1 immune response in the pathogenesis of MC+HCV.	Methylcholanthrene	158-161	interferon gamma	Homo sapiens	42-51
21724697-10	2011	A strong relationship between circulating IFN-gamma and CXCL11 was shown, strongly supporting the role of a T helper 1 immune response in the pathogenesis of MC+HCV.	Methylcholanthrene	158-161	C-X-C motif chemokine ligand 11	Homo sapiens	56-62
21199647-8	2011	The AGRP ligand however, produced a significant increase in food intake in the wild type as well as the MC(3) and MC(4) knockout mice and it had a prolonged affect for several days.	Methylcholanthrene	104-106	agouti related neuropeptide	Mus musculus	4-8
21635889-5	2011	Compared with the NC group, the MC group had significantly decreased activity of super-oxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) and significantly elevated malondialdehyde (MDA) and calcium ion content (p &lt; 0.001).	Methylcholanthrene	32-34	catalase	Rattus norvegicus	134-154
21635889-5	2011	Compared with the NC group, the MC group had significantly decreased activity of super-oxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) and significantly elevated malondialdehyde (MDA) and calcium ion content (p &lt; 0.001).	Methylcholanthrene	32-34	catalase	Rattus norvegicus	156-159
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	negative elongation factor complex member C/D	Homo sapiens	28-31
21622132-3	2011	The results showed that CA125 and CEA in CSF were optimal diagnostic indices distinguishing between MC patients and cancer patients without leptomeningeal disease.	Methylcholanthrene	100-102	mucin 16, cell surface associated	Homo sapiens	24-29
21622132-3	2011	The results showed that CA125 and CEA in CSF were optimal diagnostic indices distinguishing between MC patients and cancer patients without leptomeningeal disease.	Methylcholanthrene	100-102	CEA cell adhesion molecule 3	Homo sapiens	34-37
21622132-3	2011	The results showed that CA125 and CEA in CSF were optimal diagnostic indices distinguishing between MC patients and cancer patients without leptomeningeal disease.	Methylcholanthrene	100-102	colony stimulating factor 2	Homo sapiens	41-44
21622132-5	2011	In addition, CEA in CSF was the optimal diagnostic index distinguishing MC patients from meningitis patients.	Methylcholanthrene	72-74	CEA cell adhesion molecule 3	Homo sapiens	13-16
21622132-5	2011	In addition, CEA in CSF was the optimal diagnostic index distinguishing MC patients from meningitis patients.	Methylcholanthrene	72-74	colony stimulating factor 2	Homo sapiens	20-23
21725930-8	2011	CONCLUSIONS: Replacement of glucose with NAG in the dialysis fluid can slow down aging of MC.	Methylcholanthrene	90-92	N-acetyl-alpha-glucosaminidase	Homo sapiens	41-44
21645857-4	2011	To understand how this uncapped RNA is bound tightly by eIF4E, we employ SHAPE probing, phylogenetic comparisons with new PTEs discovered in panico- and carmoviruses, footprinting of the eIF4E binding site, and 3D RNA modeling using NAST, MC-Fold, and MC-Sym to predict a compact, 3D structure of the RNA.	Methylcholanthrene	239-241	eukaryotic translation initiation factor 4E	Homo sapiens	56-61
21645857-4	2011	To understand how this uncapped RNA is bound tightly by eIF4E, we employ SHAPE probing, phylogenetic comparisons with new PTEs discovered in panico- and carmoviruses, footprinting of the eIF4E binding site, and 3D RNA modeling using NAST, MC-Fold, and MC-Sym to predict a compact, 3D structure of the RNA.	Methylcholanthrene	252-254	eukaryotic translation initiation factor 4E	Homo sapiens	56-61
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	negative elongation factor complex member C/D	Homo sapiens	130-133
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	interleukin 15	Homo sapiens	157-162
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	interleukin 12B	Homo sapiens	164-173
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	Epstein-Barr virus induced 3	Homo sapiens	179-183
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	negative elongation factor complex member C/D	Homo sapiens	130-133
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	C-X-C motif chemokine ligand 16	Homo sapiens	267-273
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	C-C motif chemokine ligand 13	Homo sapiens	275-280
21183242-8	2011	Conversely, MC induced more Th1-promoting transcriptional changes than LPS or TNF-alpha, including increased transcript levels of Th1-type cytokines such as IL-15, IL-12beta, and EBI3 (IL-27beta) and MHC class I molecules, Th1-promoting changes in the transcripts of CXCL16, CCL13, and CCL18, and reduced transcript levels of MHC class II molecules.	Methylcholanthrene	12-14	C-C motif chemokine ligand 18	Homo sapiens	286-291
21484085-7	2011	In the dissemination model, MC-26 cell line-derived hepatic metastases grew significantly faster in CD39 over-expressing transgenics, when compared to CD39 deficient mice.	Methylcholanthrene	28-30	ectonucleoside triphosphate diphosphohydrolase 1	Mus musculus	100-104
21460390-1	2011	AIMS: To audit the cellular expression of the innate antibacterial enzyme lysozyme in colonic biopsies from a cohort of patients having microscopic colitis (MC-collagenous colitis (CC) or lymphocytic colitis (LC)).	Methylcholanthrene	157-159	lysozyme	Homo sapiens	74-82
21613483-3	2011	First, we showed by electrophysiology that 2-AG produced by diacylglycerol lipase alpha (DGLalpha) mediated both depolarization-induced suppression of excitation and its enhancement by group I metabotropic glutamate receptor activation at MC-GC synapses, as they were abolished in DGLalpha-knock-out mice.	Methylcholanthrene	239-241	diacylglycerol lipase, alpha	Mus musculus	60-87
21613483-3	2011	First, we showed by electrophysiology that 2-AG produced by diacylglycerol lipase alpha (DGLalpha) mediated both depolarization-induced suppression of excitation and its enhancement by group I metabotropic glutamate receptor activation at MC-GC synapses, as they were abolished in DGLalpha-knock-out mice.	Methylcholanthrene	239-241	diacylglycerol lipase, alpha	Mus musculus	89-97
21613483-4	2011	Immunohistochemistry revealed that DGLalpha was enriched in the neck portion of GC spines forming synapses with MC terminals, whereas cannabinoid CB(1) receptors accumulated in the terminal portion of MC axons.	Methylcholanthrene	112-114	diacylglycerol lipase, alpha	Mus musculus	35-43
21613483-5	2011	On the other hand, the major 2-AG-degrading enzyme, monoacylglycerol lipase (MGL), was absent at MC-GC synapses but was expressed in astrocytes and some inhibitory terminals.	Methylcholanthrene	97-99	monoglyceride lipase	Mus musculus	52-75
21613483-5	2011	On the other hand, the major 2-AG-degrading enzyme, monoacylglycerol lipase (MGL), was absent at MC-GC synapses but was expressed in astrocytes and some inhibitory terminals.	Methylcholanthrene	97-99	monoglyceride lipase	Mus musculus	77-80
21490601-2	2011	Recently, TET1 was found to hydroxylate the methyl group of mC, converting it to 5-hydroxymethyl cytosine (hmC).	Methylcholanthrene	60-62	tet methylcytosine dioxygenase 1	Homo sapiens	10-14
21573215-10	2011	NPC xenograft models in nude mice were used to investigate the targeted antitumor efficacy of mc-oriP-IFNgamma.	Methylcholanthrene	94-96	interferon gamma	Mus musculus	102-110
21440431-1	2011	The present paper presents the novel use of MC microparticles (MCMPs) as a novel fluorescent sensing platform for thrombin detection.	Methylcholanthrene	44-46	coagulation factor II, thrombin	Homo sapiens	114-122
21573215-16	2011	CONCLUSIONS/SIGNIFICANCE: This study demonstrates the feasibility of mc-oriP-IFNgamma as a safe and highly effective targeted gene therapeutic system for the treatment of EBV positive NPC.	Methylcholanthrene	69-71	interferon gamma	Homo sapiens	77-85
21163286-0	2011	Aberrant methylation accounts for cell adhesion-related gene silencing during 3-methylcholanthrene and diethylnitrosamine induced multistep rat lung carcinogenesis associated with overexpression of DNA methyltransferases 1 and 3a.	Methylcholanthrene	78-98	DNA methyltransferase 1	Rattus norvegicus	198-229
20697367-8	2011	In contrast, 8 of 18 patients showed MC involving CD33 PB with a median of one month (0.5-2) before relapse.	Methylcholanthrene	37-39	CD33 molecule	Homo sapiens	50-54
21623587-4	2011	Biocompatibility was assessed by LDH-release into the supernatant and HSP-72 expression in MC lysates.	Methylcholanthrene	91-93	heat shock protein family A (Hsp70) member 1A	Homo sapiens	70-76
21623587-5	2011	RESULTS: Short-term exposure of MC to pure PDF (Modality A) resulted in concordant LDH release and upregulation of HSP-72, regardless of heat or filter sterilization.	Methylcholanthrene	32-34	heat shock protein family A (Hsp70) member 1A	Homo sapiens	115-121
21623587-6	2011	In contrast, both test systems that exposed MC to heat-sterilized PDF during the recovery period (Modalities B and C) resulted in severe cellular lethality but low HSP-72 expression.	Methylcholanthrene	44-46	heat shock protein family A (Hsp70) member 1A	Homo sapiens	164-170
21128935-3	2011	MATERIALS AND METHODS: We studied the effects of MC on expressions and activities of protein kinase C (PKC) in peripheral nerve of streptozotocin-induced diabetic rats.	Methylcholanthrene	49-51	protein kinase C, alpha	Rattus norvegicus	103-106
21128935-10	2011	The decreased PKC activity in diabetic nerve was associated with reduced expression of membrane PKCalpha and increased membrane expression of PKCbetaII, and MC treatment corrected these changes.	Methylcholanthrene	157-159	protein kinase C, alpha	Rattus norvegicus	14-17
21128935-13	2011	CONCLUSIONS: This study suggested that correction of impaired neural signalling of PKC and oxidative stress-induced damage may be a major attribute to the beneficial effects of MC on diabetic nerve.	Methylcholanthrene	177-179	protein kinase C, alpha	Rattus norvegicus	83-86
20946947-4	2011	3-MC (25 muM) strongly induced CYP1A transcription.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily A	Salmo salar	31-36
20719865-5	2011	RESULTS: Significant associations were found between the MC measures and the corresponding CLCM indices and CAB performance scores that were relevant to the presence, accuracy, and completeness of content in oral narratives.	Methylcholanthrene	57-59	neural proliferation, differentiation and control 1	Homo sapiens	108-111
21053929-4	2011	Many EDCs act through multiple mechanisms as exemplified by chemicals that bind both AhR and ER, such as 3-methylcholanthrene.	Methylcholanthrene	105-125	aryl hydrocarbon receptor	Homo sapiens	85-88
21385538-2	2011	The aims of the study were to evaluate serum levels of IL-6 in MC+HCV patients and to correlate this parameter with the presence of AT and with circulating levels of TNF-alpha.	Methylcholanthrene	63-65	interleukin 6	Homo sapiens	55-59
22060274-1	2011	INTRODUCTION: ARTEMIN (ARTN) is an estrogen regulated growth factor, the expression of which promotes resistance to antiestrogen therapies and predicts poorer survival outcome of patients with estrogen receptor (ER) positive mammary carcinoma (ER+MC) treated with tamoxifen.	Methylcholanthrene	247-249	artemin	Homo sapiens	14-21
22060274-1	2011	INTRODUCTION: ARTEMIN (ARTN) is an estrogen regulated growth factor, the expression of which promotes resistance to antiestrogen therapies and predicts poorer survival outcome of patients with estrogen receptor (ER) positive mammary carcinoma (ER+MC) treated with tamoxifen.	Methylcholanthrene	247-249	artemin	Homo sapiens	23-27
21385538-4	2011	RESULTS: MC+HCV patients showed significantly (p&lt;0.01; Mann-Whitney U-test) higher IL-6 (median 8.1ng/l, range 0.7-651) serum levels than controls (median 0.6ng/l, range 0.5-41), or AT (median 2.8ng/l, range 0.5-67).	Methylcholanthrene	9-12	interleukin 6	Homo sapiens	86-90
21385538-5	2011	MC+AT showed significantly (p&lt;0.01; Mann-Whitney U-test) higher mean IL-6 (median 15.8ng/l, range 0.5-781) than controls, AT and MC+HCV.	Methylcholanthrene	0-3	interleukin 6	Homo sapiens	72-76
21385538-6	2011	Serum TNF-alpha levels were significantly higher in MC+HCV (median 9.9ng/l, range 1.5-283) or MC+AT (median 11.2ng/l, range 1.6-412) than in controls (median 1.0ng/l, range 0.6-6.4), or AT (median 1.7ng/l, range 0.6-11.8) (p&lt;0.01, for each comparison).	Methylcholanthrene	52-55	tumor necrosis factor	Homo sapiens	6-15
21385538-7	2011	CONCLUSIONS: Our study demonstrates significantly higher serum levels of IL-6 and TNF-alpha in patients with MC+HCV and MC+AT compared to healthy controls.	Methylcholanthrene	109-112	interleukin 6	Homo sapiens	73-77
21385538-7	2011	CONCLUSIONS: Our study demonstrates significantly higher serum levels of IL-6 and TNF-alpha in patients with MC+HCV and MC+AT compared to healthy controls.	Methylcholanthrene	109-112	tumor necrosis factor	Homo sapiens	82-91
21385538-8	2011	Furthermore, the study first shows a significant increase in circulating IL-6 observed in MC+AT patients with respect to MC+HCV.	Methylcholanthrene	90-93	interleukin 6	Homo sapiens	73-77
20881032-0	2011	The aryl hydrocarbon receptor pathway and the response to 3-methylcholanthrene are altered in the liver of adrenalectomized rats.	Methylcholanthrene	58-78	aryl hydrocarbon receptor	Rattus norvegicus	4-29
20881032-2	2011	Adrenalectomized (ADX) rats have decreased hepatic AHR protein and lower levels of MC-induced CYP1B1 mRNA.	Methylcholanthrene	83-85	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	94-100
20881032-5	2011	AHR mRNA was induced 4-fold 6 h after MC in SHAM rats, but no induction was observed in ADX rats.	Methylcholanthrene	38-40	aryl hydrocarbon receptor	Rattus norvegicus	0-3
20881032-1	2011	The aryl hydrocarbon receptor (AHR) is activated by 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon, and environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	52-72	aryl hydrocarbon receptor	Rattus norvegicus	4-29
20881032-6	2011	The MC-induced 7-ethoxyresorufin O-deethylation (EROD) activity in ADX rats was 35% of the activity in the MC-treated SHAM group at 6 h. At 54 h after treatment, the induction of EROD activity by MC was more pronounced in ADX rats than at 6 h. To assess the overall capacity for hepatic P450-mediated metabolism, we measured NADPH-cytochrome P450 oxidoreductase (POR) activity.	Methylcholanthrene	4-6	cytochrome p450 oxidoreductase	Rattus norvegicus	363-366
20881032-1	2011	The aryl hydrocarbon receptor (AHR) is activated by 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon, and environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	52-72	aryl hydrocarbon receptor	Rattus norvegicus	31-34
20881032-8	2011	We have shown that the response to MC in ADX rats is suppressed for some, but not all, AHR-mediated responses and that reduced POR activity after ADX could contribute to a decreased capacity for P450-dependent metabolism.	Methylcholanthrene	35-37	aryl hydrocarbon receptor	Rattus norvegicus	87-90
20881032-1	2011	The aryl hydrocarbon receptor (AHR) is activated by 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon, and environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	74-76	aryl hydrocarbon receptor	Rattus norvegicus	4-29
20881032-8	2011	We have shown that the response to MC in ADX rats is suppressed for some, but not all, AHR-mediated responses and that reduced POR activity after ADX could contribute to a decreased capacity for P450-dependent metabolism.	Methylcholanthrene	35-37	cytochrome p450 oxidoreductase	Rattus norvegicus	127-130
20881032-1	2011	The aryl hydrocarbon receptor (AHR) is activated by 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon, and environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	74-76	aryl hydrocarbon receptor	Rattus norvegicus	31-34
20571097-6	2011	RESULTS: Exposure of MC to standard fluid in vitro resulted in morphological change into a non-epitheloid shape, down-regulation of E-cadherin, indicative of EMT, and in a strong induction of vascular endothelial growth factor (VEGF) expression.	Methylcholanthrene	21-23	cadherin 1	Homo sapiens	132-142
21206138-10	2011	This was not only a rare case of MC with TSH deficiency and Hashimoto"s thyroiditis; the patient also developed severe osteoporosis and possessed transient elevated levels of serum carcinoembryonic antigen (CEA).	Methylcholanthrene	33-35	CEA cell adhesion molecule 3	Homo sapiens	181-205
22353650-4	2011	Rats in the MC group received a TNF-alpha antibody (10 mg/kg) (antibody group) or were not treatment (untreated group).	Methylcholanthrene	12-14	tumor necrosis factor	Rattus norvegicus	32-41
20571097-12	2011	Accordingly, effluent MC with non-epitheloid morphology showed significantly lower levels of E-cadherin and greater levels of fibronectin, collagen I, VEGF and IL 8 when compared with MC with epitheloid phenotype.	Methylcholanthrene	22-24	vascular endothelial growth factor A	Homo sapiens	151-155
20571097-6	2011	RESULTS: Exposure of MC to standard fluid in vitro resulted in morphological change into a non-epitheloid shape, down-regulation of E-cadherin, indicative of EMT, and in a strong induction of vascular endothelial growth factor (VEGF) expression.	Methylcholanthrene	21-23	vascular endothelial growth factor A	Homo sapiens	192-226
20571097-12	2011	Accordingly, effluent MC with non-epitheloid morphology showed significantly lower levels of E-cadherin and greater levels of fibronectin, collagen I, VEGF and IL 8 when compared with MC with epitheloid phenotype.	Methylcholanthrene	22-24	C-X-C motif chemokine ligand 8	Homo sapiens	160-164
20571097-6	2011	RESULTS: Exposure of MC to standard fluid in vitro resulted in morphological change into a non-epitheloid shape, down-regulation of E-cadherin, indicative of EMT, and in a strong induction of vascular endothelial growth factor (VEGF) expression.	Methylcholanthrene	21-23	vascular endothelial growth factor A	Homo sapiens	228-232
20571097-8	2011	This could be confirmed ex vivo, as the prevalence of non-epitheloid phenotype of MC in the standard group was significantly higher with increasing PD duration and MC isolated from this group showed significantly higher levels of EMT-associated molecules including fibronectin, collagen I, VEGF, IL-8 and TGF-beta levels when compared with the low-GDP group.	Methylcholanthrene	164-166	fibronectin 1	Homo sapiens	265-276
20571097-8	2011	This could be confirmed ex vivo, as the prevalence of non-epitheloid phenotype of MC in the standard group was significantly higher with increasing PD duration and MC isolated from this group showed significantly higher levels of EMT-associated molecules including fibronectin, collagen I, VEGF, IL-8 and TGF-beta levels when compared with the low-GDP group.	Methylcholanthrene	164-166	vascular endothelial growth factor A	Homo sapiens	290-294
20571097-8	2011	This could be confirmed ex vivo, as the prevalence of non-epitheloid phenotype of MC in the standard group was significantly higher with increasing PD duration and MC isolated from this group showed significantly higher levels of EMT-associated molecules including fibronectin, collagen I, VEGF, IL-8 and TGF-beta levels when compared with the low-GDP group.	Methylcholanthrene	164-166	C-X-C motif chemokine ligand 8	Homo sapiens	296-300
20571097-8	2011	This could be confirmed ex vivo, as the prevalence of non-epitheloid phenotype of MC in the standard group was significantly higher with increasing PD duration and MC isolated from this group showed significantly higher levels of EMT-associated molecules including fibronectin, collagen I, VEGF, IL-8 and TGF-beta levels when compared with the low-GDP group.	Methylcholanthrene	164-166	transforming growth factor beta 1	Homo sapiens	305-313
20571097-12	2011	Accordingly, effluent MC with non-epitheloid morphology showed significantly lower levels of E-cadherin and greater levels of fibronectin, collagen I, VEGF and IL 8 when compared with MC with epitheloid phenotype.	Methylcholanthrene	22-24	cadherin 1	Homo sapiens	93-103
20571097-12	2011	Accordingly, effluent MC with non-epitheloid morphology showed significantly lower levels of E-cadherin and greater levels of fibronectin, collagen I, VEGF and IL 8 when compared with MC with epitheloid phenotype.	Methylcholanthrene	22-24	fibronectin 1	Homo sapiens	126-137
21647436-9	2011	The crystal structure of MC-HSP90 reveals that, in addition to the C-terminal dimerization domain, the residue W320 in the M domain plays a critical role in its oligomerization.	Methylcholanthrene	25-27	heat shock protein 90 alpha family class A member 1	Homo sapiens	28-33
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	300-320	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-49
20934494-5	2010	Real time PCR showed that MMP-2/-9 mRNA expression was up-regulated by 6.9 fold and 5.0 fold after 80-mug/L-MC treatment, respectively.	Methylcholanthrene	108-110	matrix metallopeptidase 2	Mus musculus	26-34
21786685-1	2011	Effect of carcinogenic polycyclic aromatic hydrocarbons (PAH) benzo(a)pyrene (BP) and 3-methylcholanthrene (MC) on transcription factor NF-kappaB activation was studied.	Methylcholanthrene	86-106	nuclear factor kappa B subunit 1	Homo sapiens	136-145
21786685-1	2011	Effect of carcinogenic polycyclic aromatic hydrocarbons (PAH) benzo(a)pyrene (BP) and 3-methylcholanthrene (MC) on transcription factor NF-kappaB activation was studied.	Methylcholanthrene	108-110	nuclear factor kappa B subunit 1	Homo sapiens	136-145
21786685-6	2011	NF-kappaB activation by BP and MC in hepatoma G27 cells was significantly higher in hepatima G27 cells than in HepG2 cells both in proliferating and resting cells.	Methylcholanthrene	31-33	nuclear factor kappa B subunit 1	Homo sapiens	0-9
20831858-5	2010	The intraperitoneal injection of 3-methylcholanthrene (3MC), a potent AHR ligand, into C57BL/6J mice significantly increased the levels of triglycerides and six long-chain monounsaturated fatty acids in the livers of mice, resulting in hepatic microvesicular steatosis.	Methylcholanthrene	33-53	aryl-hydrocarbon receptor	Mus musculus	70-73
20831858-5	2010	The intraperitoneal injection of 3-methylcholanthrene (3MC), a potent AHR ligand, into C57BL/6J mice significantly increased the levels of triglycerides and six long-chain monounsaturated fatty acids in the livers of mice, resulting in hepatic microvesicular steatosis.	Methylcholanthrene	55-58	aryl-hydrocarbon receptor	Mus musculus	70-73
20831858-7	2010	In an in vitro experiment using human hepatoma HepG2 cells, 3MC increased the expression level of FAT, and the downregulation of AHR by AHR siRNA led to the suppression of 3MC-induced FAT expression.	Methylcholanthrene	172-175	aryl hydrocarbon receptor	Homo sapiens	129-132
20831858-7	2010	In an in vitro experiment using human hepatoma HepG2 cells, 3MC increased the expression level of FAT, and the downregulation of AHR by AHR siRNA led to the suppression of 3MC-induced FAT expression.	Methylcholanthrene	172-175	aryl hydrocarbon receptor	Homo sapiens	136-139
20831858-8	2010	In addition, the mRNA level of peroxisome proliferator-activated receptor (PPAR) alpha, an upstream factor of FAT, was increased in the livers of 3MC-treated mice.	Methylcholanthrene	146-149	peroxisome proliferator activated receptor alpha	Mus musculus	31-86
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	300-320	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-55
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	300-320	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	56-61
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	300-320	aryl hydrocarbon receptor	Homo sapiens	215-240
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	300-320	aryl hydrocarbon receptor	Homo sapiens	242-245
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	322-325	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-49
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	322-325	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-55
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	322-325	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	56-61
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	322-325	aryl hydrocarbon receptor	Homo sapiens	215-240
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	Methylcholanthrene	322-325	aryl hydrocarbon receptor	Homo sapiens	242-245
20804740-4	2010	Importantly, a novel distal AhR-responsive element (AhRE5) located -2357/-2333bp upstream of the ABCG2 transcriptional start site has been identified and characterized as a functional unit pivotal to 3MC-mediated induction of ABCG2.	Methylcholanthrene	200-203	aryl hydrocarbon receptor	Homo sapiens	28-31
20804740-4	2010	Importantly, a novel distal AhR-responsive element (AhRE5) located -2357/-2333bp upstream of the ABCG2 transcriptional start site has been identified and characterized as a functional unit pivotal to 3MC-mediated induction of ABCG2.	Methylcholanthrene	200-203	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	97-102
20804740-4	2010	Importantly, a novel distal AhR-responsive element (AhRE5) located -2357/-2333bp upstream of the ABCG2 transcriptional start site has been identified and characterized as a functional unit pivotal to 3MC-mediated induction of ABCG2.	Methylcholanthrene	200-203	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	226-231
20804740-5	2010	Cell-based reporter assays revealed that deletion of AhRE5 and 4 dramatically attenuated 3MC-induced activation of ABCG2 reporter activity, while further deletion of the proximal AhRE3 and 2 only moderately changed the luciferase activities.	Methylcholanthrene	89-92	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	115-120
20804740-7	2010	Moreover, chromatin immunoprecipitation assays demonstrated that treatment with 3MC significantly enhanced the recruitment of AhR to the AhRE5 occupied region, and mutation of the AhRE5 site clearly dissociated AhR protein from this promoter region.	Methylcholanthrene	80-83	aryl hydrocarbon receptor	Homo sapiens	126-129
20804740-7	2010	Moreover, chromatin immunoprecipitation assays demonstrated that treatment with 3MC significantly enhanced the recruitment of AhR to the AhRE5 occupied region, and mutation of the AhRE5 site clearly dissociated AhR protein from this promoter region.	Methylcholanthrene	80-83	aryl hydrocarbon receptor	Homo sapiens	137-140
21030725-5	2010	After 16 months of exposure, the dorsal vagal complex (DVC) exhibited significant inflammation in endotoxin-treated and MC mice (COX-2 and IL-1beta P&lt;.001).	Methylcholanthrene	120-122	prostaglandin-endoperoxide synthase 2	Mus musculus	129-134
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	anaphase promoting complex subunit 2	Homo sapiens	93-99
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	anaphase promoting complex subunit 2	Homo sapiens	101-107
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	baculoviral IAP repeat containing 5	Homo sapiens	109-114
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	cyclin B1	Homo sapiens	116-125
21030725-5	2010	After 16 months of exposure, the dorsal vagal complex (DVC) exhibited significant inflammation in endotoxin-treated and MC mice (COX-2 and IL-1beta P&lt;.001).	Methylcholanthrene	120-122	interleukin 1 beta	Mus musculus	139-147
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	cyclin H	Homo sapiens	127-135
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	cell division cycle 20	Homo sapiens	137-142
20571036-6	2010	Partial RNAi silencing of TRPC1 expression in WT MCs (to the level of Fyn null MCs) mimicked the Fyn null defect in calcium influx, cortical F-actin depolymerization, and MC degranulation.	Methylcholanthrene	49-51	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	26-31
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	cyclin dependent kinase 2	Homo sapiens	144-148
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	CDC28 protein kinase regulatory subunit 1B	Homo sapiens	150-155
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	cullin 1	Homo sapiens	157-165
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	E2F transcription factor 1	Homo sapiens	167-171
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	karyopherin subunit alpha 2	Homo sapiens	173-178
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	protein kinase, membrane associated tyrosine/threonine 1	Homo sapiens	180-186
21042722-5	2010	DNA-microarray analysis revealed that MC inhibits expression of cell cycle regulatory genes (ANAPC2, ANAPC2, BIRC5, Cyclin B1, Cyclin H, CDC20, CDK2, CKS1B, Cullin 1, E2F1, KPNA2, PKMYT1 and TFDP1).	Methylcholanthrene	38-40	transcription factor Dp-1	Homo sapiens	191-196
21042722-7	2010	The potency of MC to inhibit invasiveness of breast cancer cells is linked to the suppression of secretion of the urokinase plasminogen activator (uPA) from MDA-MB-231 cells.	Methylcholanthrene	15-17	plasminogen activator, urokinase	Homo sapiens	114-145
21042722-7	2010	The potency of MC to inhibit invasiveness of breast cancer cells is linked to the suppression of secretion of the urokinase plasminogen activator (uPA) from MDA-MB-231 cells.	Methylcholanthrene	15-17	plasminogen activator, urokinase	Homo sapiens	147-150
20956342-2	2010	We have shown that in mice with impaired immunoediting, such as in IL-1alpha(-/-) and IFNgamma(-/-) mice, 3-methylcholanthrene-induced fibrosarcoma cells are immunogenic and concomitantly bear low levels of surface sialylation, whereas tumor cells derived from wild type mice are nonimmunogenic and bear higher levels of surface sialylation.	Methylcholanthrene	106-126	interleukin 1 alpha	Mus musculus	67-76
20956342-2	2010	We have shown that in mice with impaired immunoediting, such as in IL-1alpha(-/-) and IFNgamma(-/-) mice, 3-methylcholanthrene-induced fibrosarcoma cells are immunogenic and concomitantly bear low levels of surface sialylation, whereas tumor cells derived from wild type mice are nonimmunogenic and bear higher levels of surface sialylation.	Methylcholanthrene	106-126	interferon gamma	Mus musculus	86-94
21208466-2	2010	METHODS: ACE2 activity from renal homogenates was investigated by using the fluorogenic peptide substrate Mca-YVADAPK(Dnp)-OH, where Mca is (7-methoxycoumarin-4-yl)-acetyl and Dnp is 2,4-dinitrophenyl.	Methylcholanthrene	106-109	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	9-13
20571036-7	2010	Ectopic expression of Fyn or TRPC1 in Fyn null MCs restored calcium responses and cortical F-actin depolymerization and increased MC degranulation.	Methylcholanthrene	47-49	Fyn proto-oncogene	Mus musculus	22-25
20571036-7	2010	Ectopic expression of Fyn or TRPC1 in Fyn null MCs restored calcium responses and cortical F-actin depolymerization and increased MC degranulation.	Methylcholanthrene	47-49	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	29-34
20571036-7	2010	Ectopic expression of Fyn or TRPC1 in Fyn null MCs restored calcium responses and cortical F-actin depolymerization and increased MC degranulation.	Methylcholanthrene	47-49	Fyn proto-oncogene	Mus musculus	38-41
20571036-9	2010	This demonstrates that in addition to a role described previously for Orai1 in promoting MC degranulation, nonselective cation channels participate in promoting the exocytotic response.	Methylcholanthrene	89-91	ORAI calcium release-activated calcium modulator 1	Mus musculus	70-75
20732958-0	2010	Disruption of the gene for CYP1A2, which is expressed primarily in liver, leads to differential regulation of hepatic and pulmonary mouse CYP1A1 expression and augmented human CYP1A1 transcriptional activation in response to 3-methylcholanthrene in vivo.	Methylcholanthrene	225-245	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	27-33
20732958-0	2010	Disruption of the gene for CYP1A2, which is expressed primarily in liver, leads to differential regulation of hepatic and pulmonary mouse CYP1A1 expression and augmented human CYP1A1 transcriptional activation in response to 3-methylcholanthrene in vivo.	Methylcholanthrene	225-245	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	176-182
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	223-243	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	53-59
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	223-243	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	182-188
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	223-243	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	190-197
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	245-247	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	53-59
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	245-247	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	182-188
20732958-2	2010	In this study, we tested the hypothesis that hepatic CYP1A2 differentially regulates mouse hepatic and pulmonary CYP1A1 expression and suppresses transcriptional activation of human CYP1A1 (hCYP1A1) promoter in response to 3-methylcholanthrene (MC) in vivo.	Methylcholanthrene	245-247	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	190-197
20732958-3	2010	Administration of wild-type (WT) (C57BL/6J) or Cyp1a2-null mice with a single dose of MC (100 mumol/kg i.p.)	Methylcholanthrene	86-88	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	47-53
20732958-6	2010	In the lung, MC caused persistent CYP1A1 induction for up to 8 days in both genotypes, with Cyp1a2-null mice displaying a greater extent of CYP1A1 expression.	Methylcholanthrene	13-15	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	34-40
20732958-7	2010	It is noteworthy that MC caused significant augmentation of human CYP1A1 promoter activation in transgenic mice expressing the hCYP1A1 and the reporter luciferase gene on a Cyp1a2-null background, compared with transgenic mice on the WT background.	Methylcholanthrene	22-24	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	66-72
20732958-7	2010	It is noteworthy that MC caused significant augmentation of human CYP1A1 promoter activation in transgenic mice expressing the hCYP1A1 and the reporter luciferase gene on a Cyp1a2-null background, compared with transgenic mice on the WT background.	Methylcholanthrene	22-24	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	127-134
20732958-7	2010	It is noteworthy that MC caused significant augmentation of human CYP1A1 promoter activation in transgenic mice expressing the hCYP1A1 and the reporter luciferase gene on a Cyp1a2-null background, compared with transgenic mice on the WT background.	Methylcholanthrene	22-24	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	173-179
20732958-8	2010	In contrast, the mouse endogenous hepatic, but not pulmonary, persistent CYP1A1 expression was repressed by MC in the hCYP1A1-Cyp1a2-null mice.	Methylcholanthrene	108-110	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	73-79
20732958-8	2010	In contrast, the mouse endogenous hepatic, but not pulmonary, persistent CYP1A1 expression was repressed by MC in the hCYP1A1-Cyp1a2-null mice.	Methylcholanthrene	108-110	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	118-125
20732958-8	2010	In contrast, the mouse endogenous hepatic, but not pulmonary, persistent CYP1A1 expression was repressed by MC in the hCYP1A1-Cyp1a2-null mice.	Methylcholanthrene	108-110	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	126-132
20595379-1	2010	We examined the xenobiotic responsive element (XRE) responsible for induction of the mouse Cyp1a2 gene by 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) using a reporter gene assay in mouse hepatocytes in primary culture.	Methylcholanthrene	128-131	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	91-97
20601406-5	2010	We report that the methyl CpG binding domain of MeCP2 (MBD) greatly enhances C=mC CPD formation at a TCmCG site in duplex DNA and binds with equal or better affinity to the CPD-containing duplex compared with the undamaged duplex.	Methylcholanthrene	79-81	methyl-CpG binding protein 2	Homo sapiens	48-53
20929277-7	2010	Further, significantly high serum levels of CXCL10 in patients with MC + HCV compared with healthy controls were confirmed, overall in the presence of AT.	Methylcholanthrene	68-70	C-X-C motif chemokine ligand 10	Homo sapiens	44-50
20929277-9	2010	A possible therapeutic role of the anti-IL-1 receptor antagonist (Anakirna) in MC remains to be evaluated.	Methylcholanthrene	79-81	interleukin 1 receptor antagonist	Homo sapiens	40-64
20595379-0	2010	Regulatory xenobiotic responsive elements in the distal 5"-flanking region of the mouse Cyp1a2 gene required for transcriptional activation by 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	143-163	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	88-94
20595379-1	2010	We examined the xenobiotic responsive element (XRE) responsible for induction of the mouse Cyp1a2 gene by 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) using a reporter gene assay in mouse hepatocytes in primary culture.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	91-97
20348232-0	2010	3-methylcholanthrene induces differential recruitment of aryl hydrocarbon receptor to human promoters.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	57-82
20651249-0	2010	3-methylcholanthrene induces differential recruitment of aryl hydrocarbon receptor to human promoters.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	57-82
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	105-125	aryl hydrocarbon receptor	Homo sapiens	66-91
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	105-125	aryl hydrocarbon receptor	Homo sapiens	93-96
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	105-125	aryl hydrocarbon receptor	Homo sapiens	154-157
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	127-130	aryl hydrocarbon receptor	Homo sapiens	66-91
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	127-130	aryl hydrocarbon receptor	Homo sapiens	93-96
20651249-1	2010	The paper by Pansoy and coworkers investigates the effects of the aryl hydrocarbon receptor (AHR) ligand 3-methylcholanthrene (3MC) on recruitment of the AHR complex to human promoters in T47D breast cancer cells.	Methylcholanthrene	127-130	aryl hydrocarbon receptor	Homo sapiens	154-157
20651249-5	2010	A prior study with TCDD demonstrated that both 3MC and TCDD induced AHR binding to 127 common regions; however, there were significant differences in ligand (3MC vs. TCDD)-dependent AHR bound regions.	Methylcholanthrene	47-50	aryl hydrocarbon receptor	Homo sapiens	68-71
20651249-5	2010	A prior study with TCDD demonstrated that both 3MC and TCDD induced AHR binding to 127 common regions; however, there were significant differences in ligand (3MC vs. TCDD)-dependent AHR bound regions.	Methylcholanthrene	47-50	aryl hydrocarbon receptor	Homo sapiens	182-185
20651249-5	2010	A prior study with TCDD demonstrated that both 3MC and TCDD induced AHR binding to 127 common regions; however, there were significant differences in ligand (3MC vs. TCDD)-dependent AHR bound regions.	Methylcholanthrene	158-161	aryl hydrocarbon receptor	Homo sapiens	182-185
20651249-6	2010	The results illustrate the complexity of AHR signaling and also demonstrate that compared with TCDD as a reference ligand, 3MC is a selective AHR modulator.	Methylcholanthrene	123-126	aryl hydrocarbon receptor	Homo sapiens	41-44
20651249-6	2010	The results illustrate the complexity of AHR signaling and also demonstrate that compared with TCDD as a reference ligand, 3MC is a selective AHR modulator.	Methylcholanthrene	123-126	aryl hydrocarbon receptor	Homo sapiens	142-145
20621078-8	2010	Platelet VEGF-A load independently predicted MC (p=0.049) in addition to -116G/A polymorphism (p=0.035).	Methylcholanthrene	45-47	vascular endothelial growth factor A	Homo sapiens	9-15
20621078-9	2010	CONCLUSIONS: Abnormal regulation of VEGF-A due to polymorphism at position -116 might represent a genetic factor for increased VEGF-A production and MC in EH.	Methylcholanthrene	149-151	vascular endothelial growth factor A	Homo sapiens	36-42
20348232-3	2010	Here we used the techniques of chromatin immunoprecipitation and DNA microarrays (ChIP-chip) to detect AHR-bound genomic regions after 3-methylcholanthrene (3MC) treatment of T-47D human breast cancer cells.	Methylcholanthrene	135-155	aryl hydrocarbon receptor	Homo sapiens	103-106
20348232-3	2010	Here we used the techniques of chromatin immunoprecipitation and DNA microarrays (ChIP-chip) to detect AHR-bound genomic regions after 3-methylcholanthrene (3MC) treatment of T-47D human breast cancer cells.	Methylcholanthrene	157-160	aryl hydrocarbon receptor	Homo sapiens	103-106
20348232-6	2010	A comparison of identified AHR-3MC-bound regions with AHR-2,3,7,8-tetrchlorodibenzo-p-dioxin (TCDD)-bound regions from our previous study (Ahmed, S., Valen, E., Sandelin, A., and Matthews, J.	Methylcholanthrene	31-34	aryl hydrocarbon receptor	Homo sapiens	27-30
20570689-9	2010	Although FMO3 mRNA is highly induced by 3MC or TCDD in mouse liver and in Hepa-1 cells, FMO protein levels and FMO catalytic function showed only modest elevation.	Methylcholanthrene	40-43	flavin containing monooxygenase 3	Mus musculus	9-13
20570689-0	2010	Flavin-containing monooxygenase-3: induction by 3-methylcholanthrene and complex regulation by xenobiotic chemicals in hepatoma cells and mouse liver.	Methylcholanthrene	48-68	flavin containing monooxygenase 3	Mus musculus	0-33
20570689-3	2010	In mouse liver, 3-methylcholanthrene (3MC) induced FMO3 mRNA 8-fold.	Methylcholanthrene	16-36	flavin containing monooxygenase 3	Mus musculus	51-55
20348232-11	2010	Time course ChIPs for six of the regions showed that 3MC induced gene-specific changes in histone H3 acetylation and methylation and induced differential oscillatory binding of AHR, with a periodicity between 1.5 and 2 h. Re-treatment of cells with 3MC failed to alter the oscillatory binding profiles of AHR or aryl hydrocarbon receptor nuclear translocator.	Methylcholanthrene	53-56	aryl hydrocarbon receptor	Homo sapiens	177-180
20570689-3	2010	In mouse liver, 3-methylcholanthrene (3MC) induced FMO3 mRNA 8-fold.	Methylcholanthrene	38-41	flavin containing monooxygenase 3	Mus musculus	51-55
20570689-4	2010	In Hepa-1 cells, 3MC and benzo[a]pyrene (BaP) induced FMO3 mRNA &gt;30-fold.	Methylcholanthrene	17-20	flavin containing monooxygenase 3	Mus musculus	54-58
20570689-5	2010	Induction by 3MC and BaP was AHR dependent but, surprisingly, the potent AHR agonist, TCDD, did not induce FMO3 mRNA in Hepa-1 cells nor did chromatin immunoprecipitation assays detect recruitment of AHR or ARNT to Fmo3 regulatory elements after exposure to 3MC in liver or in Hepa-1 cells.	Methylcholanthrene	13-16	aryl-hydrocarbon receptor	Mus musculus	29-32
20348232-11	2010	Time course ChIPs for six of the regions showed that 3MC induced gene-specific changes in histone H3 acetylation and methylation and induced differential oscillatory binding of AHR, with a periodicity between 1.5 and 2 h. Re-treatment of cells with 3MC failed to alter the oscillatory binding profiles of AHR or aryl hydrocarbon receptor nuclear translocator.	Methylcholanthrene	53-56	aryl hydrocarbon receptor	Homo sapiens	305-308
20348232-11	2010	Time course ChIPs for six of the regions showed that 3MC induced gene-specific changes in histone H3 acetylation and methylation and induced differential oscillatory binding of AHR, with a periodicity between 1.5 and 2 h. Re-treatment of cells with 3MC failed to alter the oscillatory binding profiles of AHR or aryl hydrocarbon receptor nuclear translocator.	Methylcholanthrene	53-56	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	312-358
20348232-11	2010	Time course ChIPs for six of the regions showed that 3MC induced gene-specific changes in histone H3 acetylation and methylation and induced differential oscillatory binding of AHR, with a periodicity between 1.5 and 2 h. Re-treatment of cells with 3MC failed to alter the oscillatory binding profiles of AHR or aryl hydrocarbon receptor nuclear translocator.	Methylcholanthrene	249-252	aryl hydrocarbon receptor	Homo sapiens	177-180
20348232-12	2010	Cells became responsive to 3MC but not TCDD after 24 h of exposure to 3MC, highlighting important differences in AHR responsiveness between the two ligands.	Methylcholanthrene	27-30	aryl hydrocarbon receptor	Homo sapiens	113-116
20348232-12	2010	Cells became responsive to 3MC but not TCDD after 24 h of exposure to 3MC, highlighting important differences in AHR responsiveness between the two ligands.	Methylcholanthrene	70-73	aryl hydrocarbon receptor	Homo sapiens	113-116
20350595-7	2010	Though the basal expression of CYPs in particular was low in EpiDerm, significant induction of CYP1A1/1B1 activity was observed following treatment with 3-methylcholanthrene.	Methylcholanthrene	153-173	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	95-105
20433877-6	2010	GIP stimulated the proliferation of MC-26 cells, a mouse CRC cell line, in a concentration-dependent manner.	Methylcholanthrene	36-38	gastric inhibitory polypeptide	Mus musculus	0-3
20395535-7	2010	TCDD, 3-MC, and oltipraz significantly increased MRP4 expression at mRNA and protein levels.	Methylcholanthrene	6-10	ATP binding cassette subfamily C member 4	Homo sapiens	49-53
20692427-7	2010	These results revealed that hDAF exerted protective effects against MC complement activation.	Methylcholanthrene	68-70	CD55 molecule (Cromer blood group)	Homo sapiens	28-32
21327148-4	2010	We also discuss how Mc carrying HLA-DRB1*04 alleles is more likely to be present in the peripheral blood of RA patients compared to Mc carrying HLA-DRB1*01 alleles.	Methylcholanthrene	20-22	major histocompatibility complex, class II, DR beta 1	Homo sapiens	32-40
20525350-11	2010	The relative percentage of CD4+ T-cells was significantly greater in metastasized tumors (both MC-BMT and MC), (P &lt; 0.05) while the proportion of CD8+ T-cells was higher in MC-BMT without metastasis.	Methylcholanthrene	95-97	T-cell surface glycoprotein CD4	Canis lupus familiaris	27-30
20412032-4	2010	To assess AhR-mediated regulation, testicular CYP1B1 expression was measured following treatment of adult rats with 3-methylcholanthrene and various dosages of benzo[a]pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	116-136	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	46-52
20525350-11	2010	The relative percentage of CD4+ T-cells was significantly greater in metastasized tumors (both MC-BMT and MC), (P &lt; 0.05) while the proportion of CD8+ T-cells was higher in MC-BMT without metastasis.	Methylcholanthrene	106-108	T-cell surface glycoprotein CD4	Canis lupus familiaris	27-30
20171196-5	2010	The extent of increase and profiles of the time-dependent changes in CYP1A1 and CYP1A2 mRNA levels after TSU-16 treatment were similar to those after treatment with 3-methylcholanthrene (3MC), a well-known activator of the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	165-185	aryl hydrocarbon receptor	Homo sapiens	223-248
20478695-8	2010	In this report, we show that expression of Blimp1 is induced by treatment with AhR ligands, such as methylcolanthrene (MC) in sebocyte and keratinocyte cell lines.	Methylcholanthrene	119-121	PR domain containing 1, with ZNF domain	Mus musculus	43-49
20478695-8	2010	In this report, we show that expression of Blimp1 is induced by treatment with AhR ligands, such as methylcolanthrene (MC) in sebocyte and keratinocyte cell lines.	Methylcholanthrene	119-121	aryl-hydrocarbon receptor	Mus musculus	79-82
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	PR domain containing 1, with ZNF domain	Mus musculus	35-41
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	aryl-hydrocarbon receptor	Mus musculus	74-77
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	aryl hydrocarbon receptor nuclear translocator	Mus musculus	82-86
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	aryl-hydrocarbon receptor	Mus musculus	135-138
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	aryl hydrocarbon receptor nuclear translocator	Mus musculus	142-146
20478695-10	2010	This ligand-dependent induction of Blimp1 requires the expression of both AhR and ARNT, since transfection of siRNA specific to either AhR or ARNT significantly reduced Blimp1 mRNA in response to MC.	Methylcholanthrene	196-198	PR domain containing 1, with ZNF domain	Mus musculus	169-175
20399684-4	2010	Using siRNA in primary T cells, we show that Ub recognition by TSG101 is required for cSMAC formation, TCR MC signal termination, TCR downregulation, and segregation of TCR-MHC-peptide from PKC-theta-enriched signaling complexes.	Methylcholanthrene	107-109	tumor susceptibility 101	Homo sapiens	63-69
20171196-7	2010	Treatment of HepG2 cells and human hepatocytes with AhR-targeting siRNA suppressed the increase in both mRNA levels and CYP1A activities after treatment with TSU-16 as well as after that with omeprazole or 3MC.	Methylcholanthrene	206-209	aryl hydrocarbon receptor	Homo sapiens	52-55
20171196-9	2010	Furthermore, we demonstrated that unlabeled TSU-16 and 3MC but not omeprazole completely inhibited the specific binding of [(3)H]-3MC to mouse Hepa1c1c7 cytosol, suggesting TSU-16 as an AhR ligand.	Methylcholanthrene	55-58	aryl hydrocarbon receptor	Homo sapiens	186-189
20101216-5	2010	To test this hypothesis, we injected the carcinogen 20-methylcholanthrene in the brain of transgenic mice overexpressing the mutant forms of amyloid precursor protein (APP) and presenilin 1 (PS1), as a model of AD, and their wild-type (WT) littermates.	Methylcholanthrene	52-73	presenilin 1	Mus musculus	191-194
20051482-7	2010	In conclusion, the results of this study support the hypothesis that MC causes persistent induction of CYP1A1 in human hepatoma cells by mechanisms entailing sustained transcriptional activation of the CYP1A1 promoter via AHR-independent mechanisms.	Methylcholanthrene	69-71	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	103-109
19951702-4	2010	However, significant increase in the mRNA expression of these isoenzymes as well as AhR and ARNT in lymphocytes following pretreatment with 3-methylcholanthrene (MC) have demonstrated that responsiveness is retained in the blood lymphocytes, though the magnitude of increase is several fold lower when compared to liver.	Methylcholanthrene	140-160	aryl hydrocarbon receptor	Rattus norvegicus	84-87
19951702-4	2010	However, significant increase in the mRNA expression of these isoenzymes as well as AhR and ARNT in lymphocytes following pretreatment with 3-methylcholanthrene (MC) have demonstrated that responsiveness is retained in the blood lymphocytes, though the magnitude of increase is several fold lower when compared to liver.	Methylcholanthrene	140-160	aryl hydrocarbon receptor nuclear translocator	Rattus norvegicus	92-96
19951702-4	2010	However, significant increase in the mRNA expression of these isoenzymes as well as AhR and ARNT in lymphocytes following pretreatment with 3-methylcholanthrene (MC) have demonstrated that responsiveness is retained in the blood lymphocytes, though the magnitude of increase is several fold lower when compared to liver.	Methylcholanthrene	162-164	aryl hydrocarbon receptor	Rattus norvegicus	84-87
19951702-4	2010	However, significant increase in the mRNA expression of these isoenzymes as well as AhR and ARNT in lymphocytes following pretreatment with 3-methylcholanthrene (MC) have demonstrated that responsiveness is retained in the blood lymphocytes, though the magnitude of increase is several fold lower when compared to liver.	Methylcholanthrene	162-164	aryl hydrocarbon receptor nuclear translocator	Rattus norvegicus	92-96
20398272-0	2010	Correction: Transformation of SV40-immortalized human uroepithelial cells by 3-methylcholanthrene increases IFN- and Large T Antigen-induced transcripts.	Methylcholanthrene	77-97	interferon alpha 1	Homo sapiens	108-112
20202668-8	2010	Additionally, the attack on the benzene ring of Adda side chain was exclusively observed during MC-RR degradation.	Methylcholanthrene	96-98	adducin 1	Homo sapiens	48-52
20051482-2	2010	In this investigation, we tested the hypothesis that MC elicits persistent induction of CYP1A1 expression in human hepatoma cells (HepG2) and that this phenomenon is mediated by sustained transcriptional activation of the CYP1A1 promoter.	Methylcholanthrene	53-55	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	88-94
20051482-2	2010	In this investigation, we tested the hypothesis that MC elicits persistent induction of CYP1A1 expression in human hepatoma cells (HepG2) and that this phenomenon is mediated by sustained transcriptional activation of the CYP1A1 promoter.	Methylcholanthrene	53-55	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	222-228
20051482-7	2010	In conclusion, the results of this study support the hypothesis that MC causes persistent induction of CYP1A1 in human hepatoma cells by mechanisms entailing sustained transcriptional activation of the CYP1A1 promoter via AHR-independent mechanisms.	Methylcholanthrene	69-71	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	202-208
20051482-3	2010	Treatment of HepG2 cells with MC resulted in marked induction (8-20-fold) of ethoxyresorufin O-de-ethylase activities, CYP1A1 apoprotein contents, and mRNA levels, which persisted for up to 96 h. MC also caused sustained transcriptional activation of the human CYP1A1 promoter for up to 96 h, as inferred from transient transfection experiments.	Methylcholanthrene	30-32	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	119-125
20051482-3	2010	Treatment of HepG2 cells with MC resulted in marked induction (8-20-fold) of ethoxyresorufin O-de-ethylase activities, CYP1A1 apoprotein contents, and mRNA levels, which persisted for up to 96 h. MC also caused sustained transcriptional activation of the human CYP1A1 promoter for up to 96 h, as inferred from transient transfection experiments.	Methylcholanthrene	30-32	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	261-267
20051482-7	2010	In conclusion, the results of this study support the hypothesis that MC causes persistent induction of CYP1A1 in human hepatoma cells by mechanisms entailing sustained transcriptional activation of the CYP1A1 promoter via AHR-independent mechanisms.	Methylcholanthrene	69-71	aryl hydrocarbon receptor	Homo sapiens	222-225
20371965-4	2010	Cotreatment with benzo[a]pyrene (BaP) or 3-methylchoranthrene (3-MC) decreased MDA-LDL-induced THP-1 cell growth, whereas treatment with benzo[e]pyrene (BeP) or pyrene, which is not a ligand for the arylhydrocarbon receptor (AhR), did not decrease THP-1 cell growth.	Methylcholanthrene	63-67	aryl hydrocarbon receptor	Homo sapiens	199-223
20371965-4	2010	Cotreatment with benzo[a]pyrene (BaP) or 3-methylchoranthrene (3-MC) decreased MDA-LDL-induced THP-1 cell growth, whereas treatment with benzo[e]pyrene (BeP) or pyrene, which is not a ligand for the arylhydrocarbon receptor (AhR), did not decrease THP-1 cell growth.	Methylcholanthrene	63-67	aryl hydrocarbon receptor	Homo sapiens	225-228
20067910-3	2010	Herein, we analysed the modulating role of BMP-7 on EMT of MC in vitro and its protective effects in a rat PD model.	Methylcholanthrene	59-61	bone morphogenetic protein 7	Rattus norvegicus	43-48
20026404-6	2010	After stimulation of MC with the cytokines TNF-alpha, IL-1beta and IFN-gamma alone or in combination to simulate a proinflammatory milieu as would occur during immune-mediated inflammatory disease, an upregulation of TLR3 is seen.	Methylcholanthrene	21-23	tumor necrosis factor	Homo sapiens	43-52
20026404-6	2010	After stimulation of MC with the cytokines TNF-alpha, IL-1beta and IFN-gamma alone or in combination to simulate a proinflammatory milieu as would occur during immune-mediated inflammatory disease, an upregulation of TLR3 is seen.	Methylcholanthrene	21-23	interleukin 1 beta	Homo sapiens	54-62
20026404-6	2010	After stimulation of MC with the cytokines TNF-alpha, IL-1beta and IFN-gamma alone or in combination to simulate a proinflammatory milieu as would occur during immune-mediated inflammatory disease, an upregulation of TLR3 is seen.	Methylcholanthrene	21-23	interferon gamma	Homo sapiens	67-76
20026404-6	2010	After stimulation of MC with the cytokines TNF-alpha, IL-1beta and IFN-gamma alone or in combination to simulate a proinflammatory milieu as would occur during immune-mediated inflammatory disease, an upregulation of TLR3 is seen.	Methylcholanthrene	21-23	toll like receptor 3	Homo sapiens	217-221
20067910-11	2010	RESULTS: MC constitutively expressed BMP-7, and its expression was downregulated during EMT.	Methylcholanthrene	9-11	bone morphogenetic protein 7	Rattus norvegicus	37-42
20067910-12	2010	Treatment with recombinant BMP-7 resulted in blockade of TGF-beta1-induced EMT of MC.	Methylcholanthrene	82-84	bone morphogenetic protein 7	Rattus norvegicus	27-32
20067910-12	2010	Treatment with recombinant BMP-7 resulted in blockade of TGF-beta1-induced EMT of MC.	Methylcholanthrene	82-84	transforming growth factor, beta 1	Rattus norvegicus	57-66
20067910-15	2010	Administration of BMP-7 decreased the number of invading MC and reduced fibrosis and angiogenesis.	Methylcholanthrene	57-59	bone morphogenetic protein 7	Rattus norvegicus	18-23
20067464-2	2010	The results from real time RT-PCR analysis demonstrated that Nic could induce CYP1 mRNAs and enhance the MC-mediated induction of the CYP1 mRNAs.	Methylcholanthrene	105-107	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	134-138
20157230-8	2010	The MLC leaf sequence defined by the planning system for each patient was exported and used as input into the MC system.	Methylcholanthrene	110-112	modulator of VRAC current 1	Homo sapiens	4-7
20067464-6	2010	The present findings demonstrate that Nic can enhance the MC-mediated induction of CYP1s, especially CYP1A1, and the formation of MC-DNA adduct in HepG2 cells.	Methylcholanthrene	58-60	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	101-107
20048044-3	2010	Alveolar macrophages (AMs) isolated from SM- and MC-infected mice exhibited differences in gene and surface expression of PD-L1, PD-L2, and major histocompatibility class II (MHC-II).	Methylcholanthrene	49-51	CD274 antigen	Mus musculus	122-127
20821494-8	2010	These results indicate that fish resistant to CYP1A induction also exhibit decreased sensitivity to PCB126 and 3-MC-induced ROS production and teratogenesis.	Methylcholanthrene	111-115	cytochrome P450 1A1	Fundulus heteroclitus	46-51
20048044-3	2010	Alveolar macrophages (AMs) isolated from SM- and MC-infected mice exhibited differences in gene and surface expression of PD-L1, PD-L2, and major histocompatibility class II (MHC-II).	Methylcholanthrene	49-51	programmed cell death 1 ligand 2	Mus musculus	129-134
19282292-5	2010	EGFR-positivity was found in 88% of evaluated cases, consistent with the proposed basaloid phenotype for all MC.	Methylcholanthrene	109-111	epidermal growth factor receptor	Homo sapiens	0-4
19831498-1	2010	Differential induction of rat-liver microsomal uridine diphospho-glucuronosyltransferase (UGT) activities by 3-methylcholanthrene or phenobarbital provided the model to separate and purify the corresponding UGT enzymes, initially termed GT1 and GT2, respectively.	Methylcholanthrene	109-129	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-93
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	19-21	complement C5a receptor 1	Homo sapiens	99-103
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	19-21	complement C5a receptor 1	Homo sapiens	105-110
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	19-21	transforming growth factor beta 1	Homo sapiens	113-150
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	19-21	renin	Homo sapiens	156-161
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	29-31	complement C5a receptor 1	Homo sapiens	99-103
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	29-31	complement C5a receptor 1	Homo sapiens	105-110
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	29-31	transforming growth factor beta 1	Homo sapiens	113-150
19926870-9	2010	In COPD lungs, the MC(T) and MC(TC) populations showed alterations in morphology and expression of CD88 (C5a-R), transforming growth factor (TGF)-beta, and renin.	Methylcholanthrene	29-31	renin	Homo sapiens	156-161
19950919-4	2010	The rate constants are in good agreement with the experimental data and are found to be k(1) = 2.87 x 10(-21)T(2.80) exp(-1328.60/T) and k(2) = 3.26 x 10(-16)T(1.65) exp(-4642.76/T) cm(3) molecule(-1) s(-1) over the temperature range 220-2000 K. The standard enthalpies of formation for the reactant CF(3)CHFOCF(3) and product radical CF(3)CFOCF(3) are evaluated via group-balanced isodesmic reactions, and the corresponding values are -454.06 +/- 0.2 and -402.74 +/- 0.2 kcal/mol, respectively, evaluated by MC-QCISD theory based on the BH&amp;H-LYP/6-311G(d, p) geometries.	Methylcholanthrene	509-511	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	547-550
19883719-4	2010	CYP2S1 mRNA levels were increased in lung, stomach, jejunum and ileum following treatment with 3-MC and in lung, liver and kidney tissues following treatment with TCDD.	Methylcholanthrene	95-99	cytochrome P450, family 2, subfamily s, polypeptide 1	Rattus norvegicus	0-6
19883719-5	2010	Induction of CYP2S1 mRNA was greater with TCDD than 3-MC treatment and was more pronounced in lung than other tissues.	Methylcholanthrene	52-56	cytochrome P450, family 2, subfamily s, polypeptide 1	Rattus norvegicus	13-19
19619075-8	2010	The coculture with SDSCs yielded MC-based tissue constructs with greater cell survival and differentiation into chondrogenic phenotypes, which exhibited higher glycosaminoglycan, collagen II, and Sox 9 but relatively low collagen I, resulting in the concomitant increase in equilibrium modulus.	Methylcholanthrene	33-35	SRY-box transcription factor 9	Homo sapiens	196-201
20564045-3	2010	The overexpression of melanocortin-1 receptors (MC1R) in isolated melanoma cells and melanoma tissues led to the radiolabeling of several linear and cyclic MC analogs for melanoma imaging or therapy.	Methylcholanthrene	48-50	melanocortin 1 receptor	Mus musculus	22-46
20412709-2	2010	Anti-CD20 monoclonal antibody, rituximab (RTX) has already been used with good results in MC in preliminary studies.	Methylcholanthrene	90-92	keratin 20	Homo sapiens	5-9
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	aryl hydrocarbon receptor	Homo sapiens	0-25
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	aryl hydrocarbon receptor	Homo sapiens	27-30
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	aryl hydrocarbon receptor	Homo sapiens	310-313
20201778-4	2010	Aryl hydrocarbon receptor (AhR) ligands a-naphthoflavone (a-Naph), b-naphthoflavone (b-Naph) and 3-methylchloranthene (3-MC) increased UGT1A1 luciferase activity in a concentration dependent manner resulting in 17.2, 11.3 and 6.1 fold, respectively, at their highest concentrations, suggesting that endogenous AhR is also involved in the regulation of the UGT1A1 reporter construct in HepG2 cells.	Methylcholanthrene	119-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	356-362
19297138-8	2010	MC residents exhibited OB endothelial hyperplasia, neuronal accumulation of particles (2/35), and immunoreactivity to beta amyloid betaA(42) (29/35) and/or alpha-synuclein (4/35) in neurons, glial cells and/or blood vessels.	Methylcholanthrene	0-2	synuclein alpha	Homo sapiens	156-171
19915937-4	2010	Following exposure of PICM-19H cells to either 3-methylcholanthrene, rifampicin or phenobarbital, the induced activities of cytochrome P450 (CYP450) isozymes CYP-1A, -2, and-3A were assessed.	Methylcholanthrene	47-67	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	124-139
19915937-4	2010	Following exposure of PICM-19H cells to either 3-methylcholanthrene, rifampicin or phenobarbital, the induced activities of cytochrome P450 (CYP450) isozymes CYP-1A, -2, and-3A were assessed.	Methylcholanthrene	47-67	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	141-147
19900403-0	2009	Persistent induction of cytochrome P450 (CYP)1A enzymes by 3-methylcholanthrene in vivo in mice is mediated by sustained transcriptional activation of the corresponding promoters.	Methylcholanthrene	59-79	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	24-47
19900403-4	2009	In this study, we tested the hypothesis that MC elicits persistent induction of CYP1A1 and 1A2 in vivo by mechanisms entailing sustained transcriptional activation of the corresponding promoters.	Methylcholanthrene	45-47	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	80-94
19900403-7	2009	The major findings were that MC elicited marked enhancement in the luciferase expression in the CYP1A1-luc as well CYP1A2-luc transgenic mice that was sustained for up to 22days, the magnitude of induction being more pronounced in the CYP1A1-luc mice.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	96-102
19900403-7	2009	The major findings were that MC elicited marked enhancement in the luciferase expression in the CYP1A1-luc as well CYP1A2-luc transgenic mice that was sustained for up to 22days, the magnitude of induction being more pronounced in the CYP1A1-luc mice.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	115-121
19900403-7	2009	The major findings were that MC elicited marked enhancement in the luciferase expression in the CYP1A1-luc as well CYP1A2-luc transgenic mice that was sustained for up to 22days, the magnitude of induction being more pronounced in the CYP1A1-luc mice.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	235-241
19900403-8	2009	MC also caused persistent induction of endogenous CYP1A1 and 1A2 expression in the WT, CYP1A1-luc, and 1A2-luc mice for up to 22days.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	50-64
19900403-8	2009	MC also caused persistent induction of endogenous CYP1A1 and 1A2 expression in the WT, CYP1A1-luc, and 1A2-luc mice for up to 22days.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	50-56
19900403-9	2009	In conclusion, our results support the hypothesis that MC elicits sustained CYP1A1 and 1A2 expression by sustained transcriptional activation of the corresponding promoters.	Methylcholanthrene	55-57	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	76-90
20456834-4	2010	RESULTS: Compared to controls, in rats pretreated with 3-methylcholanthrene, orphenadrine, and dexamethasone (main inducers of CYP1A1/2, 2B1/2, and 3A1/2, respectively), the non-renal clearances (CLNRs) of mirodenafil were significantly faster (by 39.4%, 59.3%, and 63.9%, respectively).	Methylcholanthrene	55-75	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	127-133
19772856-0	2009	Hyper- and hypo-induction of cytochrome P450 activities with Aroclor 1254 and 3-methylcholanthrene in Cyp1a2(-/-) mice.	Methylcholanthrene	78-98	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	29-44
19950277-7	2009	If the importance of IL-1beta and IL-6 in the pathogenesis of MC is confirmed, these results will open the way for the evaluation of new therapies for MC.	Methylcholanthrene	62-64	interleukin 6	Homo sapiens	34-38
19772856-0	2009	Hyper- and hypo-induction of cytochrome P450 activities with Aroclor 1254 and 3-methylcholanthrene in Cyp1a2(-/-) mice.	Methylcholanthrene	78-98	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	102-108
19772856-9	2009	Activity changes varied across gender and genotype, with 3-methylcholanthrene and Aroclor 1254 inducing in male Cyp1a2(-/-), and Aroclor 1254 inducing in female wild-type.	Methylcholanthrene	57-77	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	112-118
19772856-12	2009	Induction changes with 3-methylcholanthrene were greater in wild-type mice, a 60% increase in concentration and approximately 2 nm hypsochromic shift versus a 10% increase and approximately 1nm hypsochromic shift in Cyp1a2(-/-) mice.	Methylcholanthrene	23-43	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	216-222
19889059-9	2009	3-MC and BaP treatment increased the gene expression of CYP1A1, CYP1B1, CYP2E1, CYP4F4, CYP4F5 and soluble epoxide hydrolase.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	56-62
19889059-9	2009	3-MC and BaP treatment increased the gene expression of CYP1A1, CYP1B1, CYP2E1, CYP4F4, CYP4F5 and soluble epoxide hydrolase.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	64-70
19889059-9	2009	3-MC and BaP treatment increased the gene expression of CYP1A1, CYP1B1, CYP2E1, CYP4F4, CYP4F5 and soluble epoxide hydrolase.	Methylcholanthrene	0-4	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	72-78
19889059-9	2009	3-MC and BaP treatment increased the gene expression of CYP1A1, CYP1B1, CYP2E1, CYP4F4, CYP4F5 and soluble epoxide hydrolase.	Methylcholanthrene	0-4	cytochrome P450, family 4, subfamily f, polypeptide 4	Rattus norvegicus	80-86
19889059-9	2009	3-MC and BaP treatment increased the gene expression of CYP1A1, CYP1B1, CYP2E1, CYP4F4, CYP4F5 and soluble epoxide hydrolase.	Methylcholanthrene	0-4	cytochrome P450, family 4, subfamily f, polypeptide 5	Rattus norvegicus	88-94
19615983-1	2009	The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the effects of aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene (MC); the prototypical response is induction of drug-metabolizing enzymes.	Methylcholanthrene	179-199	aryl hydrocarbon receptor	Rattus norvegicus	4-29
19615983-1	2009	The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the effects of aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene (MC); the prototypical response is induction of drug-metabolizing enzymes.	Methylcholanthrene	179-199	aryl hydrocarbon receptor	Rattus norvegicus	31-34
19615983-1	2009	The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the effects of aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene (MC); the prototypical response is induction of drug-metabolizing enzymes.	Methylcholanthrene	201-203	aryl hydrocarbon receptor	Rattus norvegicus	4-29
19615983-1	2009	The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the effects of aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene (MC); the prototypical response is induction of drug-metabolizing enzymes.	Methylcholanthrene	201-203	aryl hydrocarbon receptor	Rattus norvegicus	31-34
19615983-6	2009	To assess whether the observed AHR depletion affected aromatic hydrocarbon responsiveness, the induction of hepatic cytochrome P450 1B1 (CYP1B1) mRNA by MC was measured as an AHR-mediated adaptive response.	Methylcholanthrene	153-155	aryl hydrocarbon receptor	Rattus norvegicus	31-34
19615983-6	2009	To assess whether the observed AHR depletion affected aromatic hydrocarbon responsiveness, the induction of hepatic cytochrome P450 1B1 (CYP1B1) mRNA by MC was measured as an AHR-mediated adaptive response.	Methylcholanthrene	153-155	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	116-135
19615983-6	2009	To assess whether the observed AHR depletion affected aromatic hydrocarbon responsiveness, the induction of hepatic cytochrome P450 1B1 (CYP1B1) mRNA by MC was measured as an AHR-mediated adaptive response.	Methylcholanthrene	153-155	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	137-143
19615983-6	2009	To assess whether the observed AHR depletion affected aromatic hydrocarbon responsiveness, the induction of hepatic cytochrome P450 1B1 (CYP1B1) mRNA by MC was measured as an AHR-mediated adaptive response.	Methylcholanthrene	153-155	aryl hydrocarbon receptor	Rattus norvegicus	175-178
19615983-7	2009	MC-induced hepatic CYP1B1 mRNA was reduced by 50% in ADX rats relative to SHAM-ADX.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	19-25
19615983-9	2009	These data demonstrate that: (1) adrenal-dependent factors contribute to the physiological maintenance of hepatic AHR protein levels; (2) the depletion of hepatic AHR protein in ADX rats coincided with a diminished adaptive response to MC; and (3) exogenous glucocorticoid treatment increases hepatic ARNT mRNA levels regardless of adrenal status.	Methylcholanthrene	236-238	aryl hydrocarbon receptor	Rattus norvegicus	163-166
19889059-0	2009	3-methylcholanthrene and benzo(a)pyrene modulate cardiac cytochrome P450 gene expression and arachidonic acid metabolism in male Sprague Dawley rats.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-72
19822660-7	2009	Together with the result that administration of the AhR ligand 3-methylcholanthrene partially protected mice with wild-type AhR from endotoxin-induced death, these results raise the possibility that an appropriate AhR ligand may be useful for treating patients with inflammatory disorders.	Methylcholanthrene	63-83	aryl-hydrocarbon receptor	Mus musculus	52-55
19822660-7	2009	Together with the result that administration of the AhR ligand 3-methylcholanthrene partially protected mice with wild-type AhR from endotoxin-induced death, these results raise the possibility that an appropriate AhR ligand may be useful for treating patients with inflammatory disorders.	Methylcholanthrene	63-83	aryl-hydrocarbon receptor	Mus musculus	124-127
19822660-7	2009	Together with the result that administration of the AhR ligand 3-methylcholanthrene partially protected mice with wild-type AhR from endotoxin-induced death, these results raise the possibility that an appropriate AhR ligand may be useful for treating patients with inflammatory disorders.	Methylcholanthrene	63-83	aryl-hydrocarbon receptor	Mus musculus	124-127
19752373-10	2009	Finally, Western blot showed MC express &gt;50% higher HIF-1alpha level than regular plasmid.	Methylcholanthrene	29-31	hypoxia inducible factor 1, alpha subunit	Mus musculus	55-65
19915059-4	2009	We found intact immune surveillance toward methylcholanthrene-induced sarcomas in IL-21(-/-) and IL-21R(-/-) mice compared with wild-type mice and B16 melanomas showed equal growth kinetics and development of lung metastases.	Methylcholanthrene	43-61	interleukin 21	Mus musculus	82-87
19845486-8	2009	In conclusion, this study demonstrates the effectiveness of MC intracellular delivery of the naturally occurring antioxidant catalase in improving animal survival.	Methylcholanthrene	60-62	catalase	Rattus norvegicus	125-133
19625371-9	2009	These observations demonstrate that HuMC store and secrete ANG to a variety of stimuli and suggest that MC-derived ANG is available in the subsequent inflammatory response.	Methylcholanthrene	38-40	angiogenin	Homo sapiens	59-62
20069924-13	2009	There was a significant relationship in a negative direction between the concentration of YKL-40 and cartilage thickness of MC (front access) (r = -0.249; p = 0.019).	Methylcholanthrene	124-126	chitinase 3 like 1	Homo sapiens	90-96
19666990-8	2009	RT-PCR and Western immunoblotting analysis showed that the inducibility of Cyp1a, Cyp2b, and Cyp3a by 3-methylcholanthrene, phenobarbital, and dexamethasone, respectively, was similar between nontumor- and tumor-bearing mice.	Methylcholanthrene	102-122	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	82-87
19666990-8	2009	RT-PCR and Western immunoblotting analysis showed that the inducibility of Cyp1a, Cyp2b, and Cyp3a by 3-methylcholanthrene, phenobarbital, and dexamethasone, respectively, was similar between nontumor- and tumor-bearing mice.	Methylcholanthrene	102-122	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	93-98
19649566-0	2009	Aryl-hydrocarbon receptor-dependent alteration of FAK/RhoA in the inhibition of HUVEC motility by 3-methylcholanthrene.	Methylcholanthrene	98-118	aryl hydrocarbon receptor	Homo sapiens	0-25
19649566-0	2009	Aryl-hydrocarbon receptor-dependent alteration of FAK/RhoA in the inhibition of HUVEC motility by 3-methylcholanthrene.	Methylcholanthrene	98-118	protein tyrosine kinase 2	Homo sapiens	50-53
19649566-0	2009	Aryl-hydrocarbon receptor-dependent alteration of FAK/RhoA in the inhibition of HUVEC motility by 3-methylcholanthrene.	Methylcholanthrene	98-118	ras homolog family member A	Homo sapiens	54-58
19649566-1	2009	We previously demonstrated the antiproliferative and antiangiogenic effects of 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, in human umbilical vascular endothelial cells (HUVECs).	Methylcholanthrene	79-99	aryl hydrocarbon receptor	Homo sapiens	110-135
19649566-1	2009	We previously demonstrated the antiproliferative and antiangiogenic effects of 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, in human umbilical vascular endothelial cells (HUVECs).	Methylcholanthrene	79-99	aryl hydrocarbon receptor	Homo sapiens	137-140
19649566-1	2009	We previously demonstrated the antiproliferative and antiangiogenic effects of 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, in human umbilical vascular endothelial cells (HUVECs).	Methylcholanthrene	101-104	aryl hydrocarbon receptor	Homo sapiens	110-135
19649566-1	2009	We previously demonstrated the antiproliferative and antiangiogenic effects of 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, in human umbilical vascular endothelial cells (HUVECs).	Methylcholanthrene	101-104	aryl hydrocarbon receptor	Homo sapiens	137-140
19649566-3	2009	3MC down-regulated FAK, but up-regulated RhoA, which was rescued by AhR knockdown.	Methylcholanthrene	0-3	protein tyrosine kinase 2	Homo sapiens	19-22
19649566-3	2009	3MC down-regulated FAK, but up-regulated RhoA, which was rescued by AhR knockdown.	Methylcholanthrene	0-3	ras homolog family member A	Homo sapiens	41-45
19649566-3	2009	3MC down-regulated FAK, but up-regulated RhoA, which was rescued by AhR knockdown.	Methylcholanthrene	0-3	aryl hydrocarbon receptor	Homo sapiens	68-71
19649566-5	2009	Additionally, 3MC increased RhoA activity via suppression of a negative feedback pathway of FAK/p190RhoGAP.	Methylcholanthrene	14-17	ras homolog family member A	Homo sapiens	28-32
19649566-5	2009	Additionally, 3MC increased RhoA activity via suppression of a negative feedback pathway of FAK/p190RhoGAP.	Methylcholanthrene	14-17	protein tyrosine kinase 2	Homo sapiens	92-95
19649566-5	2009	Additionally, 3MC increased RhoA activity via suppression of a negative feedback pathway of FAK/p190RhoGAP.	Methylcholanthrene	14-17	Rho GTPase activating protein 35	Homo sapiens	96-106
19649566-6	2009	With an increase in membrane-bound RhoA, subsequent stress fiber and focal adhesion complex formation was observed in 3MC-treated cells, and this was reversed by a RhoA inhibitor and AhR antagonists.	Methylcholanthrene	118-121	ras homolog family member A	Homo sapiens	35-39
19649566-6	2009	With an increase in membrane-bound RhoA, subsequent stress fiber and focal adhesion complex formation was observed in 3MC-treated cells, and this was reversed by a RhoA inhibitor and AhR antagonists.	Methylcholanthrene	118-121	ras homolog family member A	Homo sapiens	164-168
19649566-6	2009	With an increase in membrane-bound RhoA, subsequent stress fiber and focal adhesion complex formation was observed in 3MC-treated cells, and this was reversed by a RhoA inhibitor and AhR antagonists.	Methylcholanthrene	118-121	aryl hydrocarbon receptor	Homo sapiens	183-186
19649566-9	2009	Collectively, AhR"s genomic regulation of FAK/RhoA, together with RhoA activation, is ascribable to the anti-migration effect of 3MC in HUVECs.	Methylcholanthrene	129-132	aryl hydrocarbon receptor	Homo sapiens	14-17
19649566-9	2009	Collectively, AhR"s genomic regulation of FAK/RhoA, together with RhoA activation, is ascribable to the anti-migration effect of 3MC in HUVECs.	Methylcholanthrene	129-132	protein tyrosine kinase 2	Homo sapiens	42-45
19649566-9	2009	Collectively, AhR"s genomic regulation of FAK/RhoA, together with RhoA activation, is ascribable to the anti-migration effect of 3MC in HUVECs.	Methylcholanthrene	129-132	ras homolog family member A	Homo sapiens	46-50
19649566-9	2009	Collectively, AhR"s genomic regulation of FAK/RhoA, together with RhoA activation, is ascribable to the anti-migration effect of 3MC in HUVECs.	Methylcholanthrene	129-132	ras homolog family member A	Homo sapiens	66-70
19788401-2	2009	SAN treated control (CON) and ethanol (ET), 3- methylcholantherene (MC) or dexamethasone (DEX) pre-exposed rats, resulted in 48, 64, 47 and 33% decrease in CYP content.	Methylcholanthrene	68-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	156-159
19788401-3	2009	SAN exposure to CON, and DEX, MC or ET pre-treated animals caused a decrease (22-37%) in glutathione-S-transferase (GST) activity, however, quinone reductase (QR) activity decreased (26-45%) in the MC pre-exposed group.	Methylcholanthrene	30-32	hematopoietic prostaglandin D synthase	Rattus norvegicus	89-114
19788401-3	2009	SAN exposure to CON, and DEX, MC or ET pre-treated animals caused a decrease (22-37%) in glutathione-S-transferase (GST) activity, however, quinone reductase (QR) activity decreased (26-45%) in the MC pre-exposed group.	Methylcholanthrene	30-32	hematopoietic prostaglandin D synthase	Rattus norvegicus	116-119
19788401-4	2009	Similarly, western-blot analysis of hepatic CYP1A1 and CYP1A2 showed a decrease (27-37%) in MC pre-treated SAN exposed animals.	Methylcholanthrene	92-94	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	44-50
19788401-4	2009	Similarly, western-blot analysis of hepatic CYP1A1 and CYP1A2 showed a decrease (27-37%) in MC pre-treated SAN exposed animals.	Methylcholanthrene	92-94	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	55-61
19706774-12	2009	These data suggest that MT1-MMP activity may be key to ovarian carcinoma metastatic success by promoting both formation and dissemination of MCAs.	Methylcholanthrene	141-145	matrix metallopeptidase 14	Homo sapiens	24-31
19477508-7	2009	Immunohistochemistry of fibers incorporated with MC-3T3 ECM reveal the presence of the ECM components, collagen type I, collagen type IV, fibronectin and heparan sulfate, on their surface.	Methylcholanthrene	49-51	fibronectin 1	Mus musculus	138-149
19525444-10	2009	3MC slightly induced CYP2B10 mRNA only in the wild-type mice.	Methylcholanthrene	0-3	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	21-28
19537720-7	2009	The kinetic parameters for decay and results from density functional theory (DFT) calculations of the triplet state are consistent with a nonradiative process involving Ir-N (Ir-C for fac-Ir(pmb)(3)) bond rupture leading to a five-coordinate species that has triplet metal-centered ((3)MC) character.	Methylcholanthrene	286-288	FA complementation group C	Homo sapiens	184-187
19672312-4	2009	Using transgenic mice, we demonstrated that conditional deletion of Foxm1 from lung epithelial cells (epFoxm1(-/-) mice) prior to tumor initiation caused a striking reduction in the number and size of lung tumors, induced by either urethane or 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT).	Methylcholanthrene	244-264	forkhead box M1	Mus musculus	68-73
19451401-7	2009	LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene.	Methylcholanthrene	233-253	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-127
19398718-6	2009	MC recruitment in the skin is impaired, correlating with defective PDGFR-beta and transforming growth factor-beta (TGF-beta)-SMAD signaling.	Methylcholanthrene	0-2	platelet derived growth factor receptor beta	Homo sapiens	67-77
19672312-4	2009	Using transgenic mice, we demonstrated that conditional deletion of Foxm1 from lung epithelial cells (epFoxm1(-/-) mice) prior to tumor initiation caused a striking reduction in the number and size of lung tumors, induced by either urethane or 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT).	Methylcholanthrene	266-269	forkhead box M1	Mus musculus	68-73
19609788-6	2009	The MC at concentrations of 10 and 1 microM, without toxicity to PBMC in 24 h, showed obvious inhibitory activity on IL-18 secretion.	Methylcholanthrene	4-6	interleukin 18	Homo sapiens	117-122
19537720-9	2009	The energy level for the (3)MC state is estimated to lie between 21,700 and 24,000 cm(-1) for the fac-Ir(C--N)(3) complexes and at 28,000 cm(-1) for fac-Ir(pmb)(3).	Methylcholanthrene	28-30	FA complementation group C	Homo sapiens	98-101
19537720-9	2009	The energy level for the (3)MC state is estimated to lie between 21,700 and 24,000 cm(-1) for the fac-Ir(C--N)(3) complexes and at 28,000 cm(-1) for fac-Ir(pmb)(3).	Methylcholanthrene	28-30	FA complementation group C	Homo sapiens	149-152
19023562-6	2009	Accordingly, UGT1A6 mRNA expression, measured by RT-PCR, was 2.3-fold higher after 3-MC treatment and 2.1-fold higher after PQ administration.	Methylcholanthrene	83-87	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	13-19
19584540-2	2009	In this study, we found that oral administration of kaempferol or ginkgo biloba extract (EGb) containing 24% flavonol at 100 mg/kg body weight suppressed AhR transformation induced by 3-methylcholanthrene at 10 mg/kg body weight in the liver of mice.	Methylcholanthrene	184-204	aryl-hydrocarbon receptor	Mus musculus	154-157
19842478-3	2009	The observed thermal relaxation of SO within ionic liquids was slower than that of molecular solvents with similar polarity, indicating a greater degree of interactions between the ionic liquid ions and the zwitterionic MC isomer, which led to increased lifetimes for the MC-ion complexes (19.6 s in acetonitrile and 90.9 s in [P6,6,6,14][NTf2]).	Methylcholanthrene	220-222	nuclear transport factor 2	Homo sapiens	339-343
19842478-5	2009	Activation parameters found MC --&gt; SO relaxation was more temperature dependent in polar protic ILs such as [bmIm]+ than aprotic ILs such as [P6,6,6,14][NTf2] with deltaS++ values of 40 J K mol(-1) and -8.6 J K mol(-1), respectively.	Methylcholanthrene	28-33	nuclear transport factor 2	Homo sapiens	156-160
19465936-4	2009	The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1).	Methylcholanthrene	17-37	aryl hydrocarbon receptor	Homo sapiens	4-7
19465936-4	2009	The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1).	Methylcholanthrene	17-37	aryl hydrocarbon receptor	Homo sapiens	47-50
19465936-4	2009	The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1).	Methylcholanthrene	17-37	aryl hydrocarbon receptor	Homo sapiens	47-50
19465936-4	2009	The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1).	Methylcholanthrene	17-37	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	125-144
19465936-4	2009	The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1).	Methylcholanthrene	17-37	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	146-152
19358839-7	2009	Hepatic NTCP, OATP1a1, 1a4, 1b2 and 2b1; and OAT 2 and 3 mRNA levels were significantly decreased in high-fat and MC- diet rats when compared to control.	Methylcholanthrene	114-116	solute carrier family 10 member 1	Rattus norvegicus	8-12
19358839-7	2009	Hepatic NTCP, OATP1a1, 1a4, 1b2 and 2b1; and OAT 2 and 3 mRNA levels were significantly decreased in high-fat and MC- diet rats when compared to control.	Methylcholanthrene	114-116	solute carrier family 22 (organic anion transporter), member 7, pseudogene 1	Rattus norvegicus	45-56
19358839-9	2009	Liver tissue from high-fat and MC- rats stained positive for IL-1beta, a pro-inflammatory cytokine known to decrease expression of NTCP, OATP and OAT transporters, suggesting a plausible mechanism for the observed transporter alterations.	Methylcholanthrene	31-33	interleukin 1 beta	Rattus norvegicus	61-69
19358839-9	2009	Liver tissue from high-fat and MC- rats stained positive for IL-1beta, a pro-inflammatory cytokine known to decrease expression of NTCP, OATP and OAT transporters, suggesting a plausible mechanism for the observed transporter alterations.	Methylcholanthrene	31-33	solute carrier family 10 member 1	Rattus norvegicus	131-135
19497445-10	2009	Patients with DM + MC were more insulin resistant than DM patients and had an elevated whole blood viscosity that correlated with plasma glucose (p = 0.001) and C-reactive protein (p = 0.003).	Methylcholanthrene	19-21	insulin	Homo sapiens	32-39
19497445-10	2009	Patients with DM + MC were more insulin resistant than DM patients and had an elevated whole blood viscosity that correlated with plasma glucose (p = 0.001) and C-reactive protein (p = 0.003).	Methylcholanthrene	19-21	C-reactive protein	Homo sapiens	161-179
19513187-6	2009	PAF or its stabilized analog, methyl carbamyl (mc)PAF (EC(50)=0.8 nM), rapidly mobilized [Ca(2+)](i), which peaked within 30-60 s and remained elevated for 3 min.	Methylcholanthrene	47-50	PCNA clamp associated factor	Homo sapiens	0-3
19492158-4	2009	MC express the viral receptors Toll-like receptor 3 (TLR3), RIG-I and MDA5.	Methylcholanthrene	0-2	toll like receptor 3	Homo sapiens	53-57
19609245-10	2009	Finally, DCs transduced with both Ad5hCD40L and an adenoviral vector encoding the melanoma antigen MelanA/MART-1 and treated with MC and IFN-gamma efficiently primed naive autologous CD8+ T cells into antigen-specific cytotoxic T lymphocyte.	Methylcholanthrene	130-132	melan-A	Homo sapiens	106-112
19492158-4	2009	MC express the viral receptors Toll-like receptor 3 (TLR3), RIG-I and MDA5.	Methylcholanthrene	0-2	DExD/H-box helicase 58	Homo sapiens	60-65
19492158-4	2009	MC express the viral receptors Toll-like receptor 3 (TLR3), RIG-I and MDA5.	Methylcholanthrene	0-2	interferon induced with helicase C domain 1	Homo sapiens	70-74
19022236-5	2009	In contrast, dexamethasone significantly augmented transcriptional activation of CYP1A2 mRNA but not CYP1A1 gene by prototype AhR ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene (3MC).	Methylcholanthrene	185-205	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	81-87
19022236-5	2009	In contrast, dexamethasone significantly augmented transcriptional activation of CYP1A2 mRNA but not CYP1A1 gene by prototype AhR ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene (3MC).	Methylcholanthrene	207-210	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	81-87
19270430-8	2009	Co-immunoprecipitation assay showed that DHT significantly facilitated the complex formation between AR and AhR in 3MC-treated cells.	Methylcholanthrene	115-118	aryl hydrocarbon receptor	Homo sapiens	108-111
19342666-1	2009	Using IL-1/IL-1Ra knockout BALB/c mice, we showed that 3-methylcholatrene (3-MCA)-induced carcinogenesis is dependent on IL-1beta-induced inflammatory responses.	Methylcholanthrene	75-80	interleukin 1 complex	Mus musculus	6-10
19342666-1	2009	Using IL-1/IL-1Ra knockout BALB/c mice, we showed that 3-methylcholatrene (3-MCA)-induced carcinogenesis is dependent on IL-1beta-induced inflammatory responses.	Methylcholanthrene	75-80	interleukin 1 receptor antagonist	Mus musculus	11-17
19342666-1	2009	Using IL-1/IL-1Ra knockout BALB/c mice, we showed that 3-methylcholatrene (3-MCA)-induced carcinogenesis is dependent on IL-1beta-induced inflammatory responses.	Methylcholanthrene	75-80	interleukin 1 beta	Mus musculus	121-129
19336894-3	2009	CYP1A1 and CYP3A8 mRNAs were significantly induced by 3-methylcholanthrene and rifampicin, respectively.	Methylcholanthrene	54-74	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
18434450-5	2009	CD19+ BLyS binding and BLyS receptor 3 (BR3) staining showed a stepwise decrease with highest values in healthy controls and who were HCV+ without MC, and lowest in B-NHL (p&lt;0.05, p&lt;0.0001, respectively) with a further decrease in VH1-69+ clonal B cells.	Methylcholanthrene	147-149	CD19 molecule	Homo sapiens	0-4
18434450-5	2009	CD19+ BLyS binding and BLyS receptor 3 (BR3) staining showed a stepwise decrease with highest values in healthy controls and who were HCV+ without MC, and lowest in B-NHL (p&lt;0.05, p&lt;0.0001, respectively) with a further decrease in VH1-69+ clonal B cells.	Methylcholanthrene	147-149	TNF superfamily member 13b	Homo sapiens	6-10
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	aryl hydrocarbon receptor	Homo sapiens	119-122
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	140-146
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	148-154
19141685-5	2009	CSE markedly induced activation of AhR, and AhR agonists (2,3,7,8-tetrachlorodibenzo-p-dioxin, benzo[a]pyrene and 3-methylcholanthrene) reproduced the inhibitory effect of CSE on adipocyte differentiation.	Methylcholanthrene	114-134	aryl hydrocarbon receptor	Homo sapiens	44-47
18956144-8	2009	CYP1A2 levels and methoxyresorufin O-demethylase (MROD) activities, the CYP1A2-mediated reaction, were markedly induced in the livers of both ND and IDD mice treated with MC and ALA.	Methylcholanthrene	171-173	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	0-6
18956144-8	2009	CYP1A2 levels and methoxyresorufin O-demethylase (MROD) activities, the CYP1A2-mediated reaction, were markedly induced in the livers of both ND and IDD mice treated with MC and ALA.	Methylcholanthrene	171-173	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	72-78
19131451-9	2009	Renin content was high in vascular MC(TC) but markedly lower in MC(TC) in other compartments.	Methylcholanthrene	35-37	renin	Homo sapiens	0-5
19298395-2	2009	Here, we addressed whether the naturally occurring acylphloroglucinol myrtucommulone (MC) from Myrtus communis L. (myrtle) affected mPGES-1.	Methylcholanthrene	86-88	prostaglandin E synthase	Mus musculus	132-139
19298395-5	2009	KEY RESULTS: MC concentration-dependently inhibited cell-free mPGES-1-mediated conversion of PGH(2) to PGE(2) (IC(50) = 1 micromol x L(-1)).	Methylcholanthrene	13-15	prostaglandin E synthase	Mus musculus	62-69
19298395-8	2009	CONCLUSIONS AND IMPLICATIONS: MC is the first natural product to inhibit mPGES-1 that efficiently suppresses PGE(2) formation without significant inhibition of the COX enzymes.	Methylcholanthrene	30-32	prostaglandin E synthase	Mus musculus	73-80
19074972-4	2009	When comparing results from incubations with liver microsomes from 3-methylcholanthrene-treated rats (inducing CYP1A1 and CYP1B1) with those from noninduced rats, a 6-fold increase of the aldehyde metabolite was observed in the rat liver microsomes after 3-methylcholanthrene treatment.	Methylcholanthrene	67-87	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	111-117
19074972-4	2009	When comparing results from incubations with liver microsomes from 3-methylcholanthrene-treated rats (inducing CYP1A1 and CYP1B1) with those from noninduced rats, a 6-fold increase of the aldehyde metabolite was observed in the rat liver microsomes after 3-methylcholanthrene treatment.	Methylcholanthrene	67-87	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	122-128
19074972-4	2009	When comparing results from incubations with liver microsomes from 3-methylcholanthrene-treated rats (inducing CYP1A1 and CYP1B1) with those from noninduced rats, a 6-fold increase of the aldehyde metabolite was observed in the rat liver microsomes after 3-methylcholanthrene treatment.	Methylcholanthrene	255-275	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	111-117
19147448-7	2009	Further, in sham rats, MC was increased by a sub-threshold concentration of angiotensin II and reversed by both AT(1)- as well as EGF-receptor inhibition.	Methylcholanthrene	23-25	angiotensinogen	Rattus norvegicus	76-90
19147448-9	2009	CONCLUSION: These findings provide the first evidence that decreased SMC caveolae numbers are involved in enhanced MC in small mesenteric arteries, by affecting AT(1)- and EGF-receptor function.	Methylcholanthrene	70-72	angiotensin II receptor, type 1a	Rattus norvegicus	161-184
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	156-162
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	aryl hydrocarbon receptor repressor	Homo sapiens	168-181
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	aryl hydrocarbon receptor repressor	Homo sapiens	183-187
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	androgen receptor	Homo sapiens	260-277
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	androgen receptor	Homo sapiens	279-281
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	67-87	aryl hydrocarbon receptor	Homo sapiens	168-171
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	aryl hydrocarbon receptor	Homo sapiens	119-122
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	140-146
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	148-154
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	156-162
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	aryl hydrocarbon receptor repressor	Homo sapiens	168-181
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	aryl hydrocarbon receptor repressor	Homo sapiens	183-187
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	androgen receptor	Homo sapiens	260-277
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	androgen receptor	Homo sapiens	279-281
19270430-3	2009	In this study, we investigated the mechanism for the repression of 3-methylcholanthrene (3MC)-induced transcription of AhR-regulated genes, CYP1A1, CYP1A2, CYP1B1, and AhR repressor (AhRR), by 5alpha-dihydroteststerone (DHT) in LNCaP and T47D cells, which are androgen receptor (AR)- and AhR-positive.	Methylcholanthrene	89-92	aryl hydrocarbon receptor	Homo sapiens	168-171
19270430-9	2009	These results suggest that complex formation between activated AR and AhR plays an important role in the suppression of 3MC-induced transcription of CYP1 family genes by DHT.	Methylcholanthrene	120-123	androgen receptor	Homo sapiens	63-65
19270430-4	2009	Real-time PCR analysis showed that DHT repressed 3MC-induced mRNA expression of the CYP1 family and AhRR genes.	Methylcholanthrene	49-52	aryl hydrocarbon receptor repressor	Homo sapiens	100-104
19270430-5	2009	DHT repressed 3MC-induced luciferase activity in an AhR response element-driven luciferase reporter assay in LNCaP and T47D cells.	Methylcholanthrene	14-17	aryl hydrocarbon receptor	Homo sapiens	52-55
19270430-8	2009	Co-immunoprecipitation assay showed that DHT significantly facilitated the complex formation between AR and AhR in 3MC-treated cells.	Methylcholanthrene	115-118	androgen receptor	Homo sapiens	101-103
19270430-9	2009	These results suggest that complex formation between activated AR and AhR plays an important role in the suppression of 3MC-induced transcription of CYP1 family genes by DHT.	Methylcholanthrene	120-123	aryl hydrocarbon receptor	Homo sapiens	70-73
19159466-0	2009	The human Ago2 MC region does not contain an eIF4E-like mRNA cap binding motif.	Methylcholanthrene	15-17	argonaute RISC catalytic component 2	Homo sapiens	10-14
19280519-5	2009	Additionally, treatment of the Huh7 cells with 3-methylcholanthrene induced cytochrome P450 (CYP) 1A1 expression.	Methylcholanthrene	47-67	MIR7-3 host gene	Homo sapiens	31-35
19280519-5	2009	Additionally, treatment of the Huh7 cells with 3-methylcholanthrene induced cytochrome P450 (CYP) 1A1 expression.	Methylcholanthrene	47-67	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	76-101
19005739-6	2009	MC exhibit an expression of TLR3, RIG-I and MDA5.	Methylcholanthrene	0-2	toll like receptor 3	Homo sapiens	28-32
19005739-6	2009	MC exhibit an expression of TLR3, RIG-I and MDA5.	Methylcholanthrene	0-2	DExD/H-box helicase 58	Homo sapiens	34-39
19005739-6	2009	MC exhibit an expression of TLR3, RIG-I and MDA5.	Methylcholanthrene	0-2	interferon induced with helicase C domain 1	Homo sapiens	44-48
19144517-1	2009	We identified a series of 4-hydroxyquinolines bearing a C1 to C15 alkyl chain at the C2 position and a carbethoxy/carboxy group at the C3 position of the quinoline nucleus (MC compounds), endowed with selective inhibitory activity against the p300/CBP HAT enzymes.	Methylcholanthrene	173-175	E1A binding protein p300	Homo sapiens	243-247
19144517-1	2009	We identified a series of 4-hydroxyquinolines bearing a C1 to C15 alkyl chain at the C2 position and a carbethoxy/carboxy group at the C3 position of the quinoline nucleus (MC compounds), endowed with selective inhibitory activity against the p300/CBP HAT enzymes.	Methylcholanthrene	173-175	CREB binding protein	Homo sapiens	248-251
19159466-7	2009	RESULTS: A number of sequence-based and structure-based bioinformatics methods reveal the reported similarity between the Ago2 MC sequence region and the eIF4E cap-binding motif to be spurious.	Methylcholanthrene	127-129	argonaute RISC catalytic component 2	Homo sapiens	122-126
19159466-7	2009	RESULTS: A number of sequence-based and structure-based bioinformatics methods reveal the reported similarity between the Ago2 MC sequence region and the eIF4E cap-binding motif to be spurious.	Methylcholanthrene	127-129	eukaryotic translation initiation factor 4E	Homo sapiens	154-159
19159466-9	2009	Confident mapping of the Ago2 MC sequence region to the piwi mid domain results in a homology-based structure model that positions the identified aromatic residues over 20 A apart, with one of the aromatic side chains (F450) contributing instead to the hydrophobic core of the domain.	Methylcholanthrene	30-32	argonaute RISC catalytic component 2	Homo sapiens	25-29
19159466-12	2009	Mapping of the MC sequence to the mid domain structure reveals Ago2 aromatics that are incompatible with eIF4E-like mRNA cap-binding, yet display some limited local structure similarities that cause the chance sequence match to eIF4E.	Methylcholanthrene	15-17	argonaute RISC catalytic component 2	Homo sapiens	63-67
19159466-12	2009	Mapping of the MC sequence to the mid domain structure reveals Ago2 aromatics that are incompatible with eIF4E-like mRNA cap-binding, yet display some limited local structure similarities that cause the chance sequence match to eIF4E.	Methylcholanthrene	15-17	eukaryotic translation initiation factor 4E	Homo sapiens	105-110
19159466-12	2009	Mapping of the MC sequence to the mid domain structure reveals Ago2 aromatics that are incompatible with eIF4E-like mRNA cap-binding, yet display some limited local structure similarities that cause the chance sequence match to eIF4E.	Methylcholanthrene	15-17	eukaryotic translation initiation factor 4E	Homo sapiens	228-233
19129741-4	2009	AIMS: : To study gene transfer of MC DNA, expressing the human vascular endothelial growth factor (hVEGF), to mouse heart and skeletal muscles and to compare it with one of the efficient plasmids used in cardiovascular trials, the phVEGF165 containing the same expression cassette as the MC.	Methylcholanthrene	34-36	vascular endothelial growth factor A	Homo sapiens	63-97
18621517-0	2009	Cyclin A expression is associated with apoptosis and mitosis in murine 3-methylcholanthrene-induced fibrosarcomas.	Methylcholanthrene	71-91	cyclin A2	Mus musculus	0-8
19129741-4	2009	AIMS: : To study gene transfer of MC DNA, expressing the human vascular endothelial growth factor (hVEGF), to mouse heart and skeletal muscles and to compare it with one of the efficient plasmids used in cardiovascular trials, the phVEGF165 containing the same expression cassette as the MC.	Methylcholanthrene	34-36	vascular endothelial growth factor A	Homo sapiens	99-104
19738401-3	2009	RESULTS: Over 6 weeks of treatment, patients with melancholic depression and MC had poorer treatment response on the HAM-D scale and a worse functional outcome (GAF) as opposed to their counterparts without MC, which was first detected after 4 weeks of treatment (p = 0.02).	Methylcholanthrene	77-79	fibroblast growth factor 9	Homo sapiens	161-164
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	4-22	CD226 antigen	Mus musculus	81-87
18817362-8	2008	This new aromaticity index, ACE(MC), may be seen as the enthalpy of a hyperhomodesmotic chemical equation.	Methylcholanthrene	32-34	angiotensin I converting enzyme	Homo sapiens	28-31
18817362-9	2008	In contrast to the index ACE(DC) previously defined from a double cut of the ring, the multiple-cut ACE(MC) exhibits the expected asymptotic disappearance of the cyclic energy as the ring size tends to infinity.	Methylcholanthrene	104-106	angiotensin I converting enzyme	Homo sapiens	100-103
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	4-22	poliovirus receptor	Mus musculus	95-100
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	4-22	CD226 antigen	Mus musculus	106-112
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	24-27	CD226 antigen	Mus musculus	81-87
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	24-27	poliovirus receptor	Mus musculus	95-100
19029379-5	2008	The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1-deficient mice showed increased tumor development and mortality after transplantation of Meth A cells.	Methylcholanthrene	24-27	CD226 antigen	Mus musculus	106-112
21791387-3	2008	The same suppressive effect by ALLN was observed for ethoxyresorufin O-deethylase (EROD) activity induced by an AhR ligand, 3-methylcholanthrene (3MC).	Methylcholanthrene	124-144	aryl hydrocarbon receptor	Homo sapiens	112-115
18626632-9	2008	A strong CYP1A1 signal is found in liver microsomes of 3-methylcholanthrene-treated rats, while it is (nearly) absent in liver microsomes of rats treated with isonocotinic acid hydrazide (isoniazid).	Methylcholanthrene	55-75	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	9-15
18981100-4	2008	Late donor T cell transfer to MC was associated with marked accumulation of anti-host CD8 cells within the spleen, but delayed kinetics of differentiation, reduced expression of effector molecules including IFN-gamma, impaired cytotoxicity, and higher rates of sustained apoptosis.	Methylcholanthrene	30-32	CD8a molecule	Homo sapiens	86-89
18981100-4	2008	Late donor T cell transfer to MC was associated with marked accumulation of anti-host CD8 cells within the spleen, but delayed kinetics of differentiation, reduced expression of effector molecules including IFN-gamma, impaired cytotoxicity, and higher rates of sustained apoptosis.	Methylcholanthrene	30-32	interferon gamma	Homo sapiens	207-216
18928297-5	2008	CPE suppressed the MC-induced transformation to the control level by inhibiting the formation of a heterodimer between AhR and an aryl hydrocarbon receptor nuclear translocator in the liver at 3 h postadministration.	Methylcholanthrene	19-21	aryl-hydrocarbon receptor	Mus musculus	119-122
18928297-5	2008	CPE suppressed the MC-induced transformation to the control level by inhibiting the formation of a heterodimer between AhR and an aryl hydrocarbon receptor nuclear translocator in the liver at 3 h postadministration.	Methylcholanthrene	19-21	aryl hydrocarbon receptor nuclear translocator	Mus musculus	130-176
18928297-6	2008	It also suppressed MC-induced cytochrome P4501A1 expression and NAD(P)H:quinone-oxidoreductase activity, whereas it increased glutathione S-transferase activity at 25 h. CPE constituents and their metabolites might contribute, at least in part, to the suppression of AhR transformation.	Methylcholanthrene	19-21	aryl-hydrocarbon receptor	Mus musculus	267-270
21791387-3	2008	The same suppressive effect by ALLN was observed for ethoxyresorufin O-deethylase (EROD) activity induced by an AhR ligand, 3-methylcholanthrene (3MC).	Methylcholanthrene	146-149	aryl hydrocarbon receptor	Homo sapiens	112-115
18598703-10	2008	We show that MC-TRBD exhibits improved enzymatic activity and can effectively substitute the MetRS-Arc1p binary complex in vivo.	Methylcholanthrene	13-15	methionyl-tRNA synthetase 2, mitochondrial	Homo sapiens	93-98
18664595-6	2008	In 3T3-L1 cells, treatment with AhR agonists including benzo[a]pyrene and 3-methylcholanthrene reproduced the antiadipogenic effect of C. militaris.	Methylcholanthrene	74-94	aryl-hydrocarbon receptor	Mus musculus	32-35
18809969-3	2008	Here, we tested h1F6-maleimidocaproyl (mc) MMAF conjugates, consisting of an uncleavable mc linker, for their ability to interfere with the growth of CD70-positive carcinomas.	Methylcholanthrene	39-41	CD70 antigen	Mus musculus	150-154
19144265-4	2008	In patients with SM, bm MC expressed significantly higher amounts of CD203c compared to normal bm MC (median MFI in controls: 260 versus median MFI in SM: 516, p&lt;0.05).	Methylcholanthrene	24-26	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	69-75
19144265-5	2008	Slightly lower amounts of CD203c were detected on MC in SM-AHNMD and ASM compared to ISM.	Methylcholanthrene	50-52	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	26-32
19144265-7	2008	Cross-linking of the IgE receptor on MC resulted in a substantial upregulation of CD203c, whereas the KIT-ligand stem cell factor (SCF) showed no significant effects.	Methylcholanthrene	37-39	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	82-88
19144265-8	2008	In conclusion, CD203c is a novel activation-linked surface antigen on MC that is upregulated in response to IgE receptor cross-linking and is overexpressed on neoplastic MC in patients with SM.	Methylcholanthrene	70-72	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	15-21
19144265-8	2008	In conclusion, CD203c is a novel activation-linked surface antigen on MC that is upregulated in response to IgE receptor cross-linking and is overexpressed on neoplastic MC in patients with SM.	Methylcholanthrene	170-172	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	15-21
18598759-9	2008	These results show that exogenous NO can increase COX-2-dependent PGD(2) and IL-6 production by MC in inflammatory environments through the p38 MAPK pathway.	Methylcholanthrene	96-98	cytochrome c oxidase II, mitochondrial	Mus musculus	50-55
18598759-9	2008	These results show that exogenous NO can increase COX-2-dependent PGD(2) and IL-6 production by MC in inflammatory environments through the p38 MAPK pathway.	Methylcholanthrene	96-98	interleukin 6	Mus musculus	77-81
18598759-9	2008	These results show that exogenous NO can increase COX-2-dependent PGD(2) and IL-6 production by MC in inflammatory environments through the p38 MAPK pathway.	Methylcholanthrene	96-98	mitogen-activated protein kinase 14	Mus musculus	140-143
18598703-10	2008	We show that MC-TRBD exhibits improved enzymatic activity and can effectively substitute the MetRS-Arc1p binary complex in vivo.	Methylcholanthrene	13-15	Arc1p	Saccharomyces cerevisiae S288C	99-104
18598703-11	2008	Moreover, MC-TRBD, being exclusively cytoplasmic, also mimics the MetRS-Arc1p complex in terms of subcellular localization.	Methylcholanthrene	10-12	methionyl-tRNA synthetase 2, mitochondrial	Homo sapiens	66-71
18598703-11	2008	Moreover, MC-TRBD, being exclusively cytoplasmic, also mimics the MetRS-Arc1p complex in terms of subcellular localization.	Methylcholanthrene	10-12	Arc1p	Saccharomyces cerevisiae S288C	72-77
18954002-1	2008	A multiconformational study of substrates of cytochrome P450 3A4 has been carried out within the BiS/MC algorithm.	Methylcholanthrene	101-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-64
18591227-5	2008	The objective of this study was to compare survival rates and characterize the host responses of SM- and MC-infected IL-10-depleted (IL-10(-/-)) mice, which exhibit a Th1-polarized immune response and are considered resistant hosts.	Methylcholanthrene	105-107	negative elongation factor complex member C/D, Th1l	Mus musculus	167-170
18559486-9	2008	Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin.	Methylcholanthrene	17-37	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	72-78
18559486-9	2008	Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin.	Methylcholanthrene	17-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	84-90
18524872-0	2008	Cytochrome P450 2C11 5"-flanking region and promoter mediate in vivo suppression by 3-methylcholanthrene.	Methylcholanthrene	84-104	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	0-20
18524872-1	2008	Aromatic hydrocarbons such as 3-methylcholanthrene (MC) elicit toxic and adaptive responses through the aryl hydrocarbon receptor (AHR).	Methylcholanthrene	30-50	aryl hydrocarbon receptor	Rattus norvegicus	104-129
18524872-1	2008	Aromatic hydrocarbons such as 3-methylcholanthrene (MC) elicit toxic and adaptive responses through the aryl hydrocarbon receptor (AHR).	Methylcholanthrene	30-50	aryl hydrocarbon receptor	Rattus norvegicus	131-134
18524872-1	2008	Aromatic hydrocarbons such as 3-methylcholanthrene (MC) elicit toxic and adaptive responses through the aryl hydrocarbon receptor (AHR).	Methylcholanthrene	52-54	aryl hydrocarbon receptor	Rattus norvegicus	104-129
18524872-1	2008	Aromatic hydrocarbons such as 3-methylcholanthrene (MC) elicit toxic and adaptive responses through the aryl hydrocarbon receptor (AHR).	Methylcholanthrene	52-54	aryl hydrocarbon receptor	Rattus norvegicus	131-134
18524872-6	2008	As a positive control for AHR activation, MC dramatically induced the luciferase activity of a Cyp1a1-driven luciferase plasmid under AHR control.	Methylcholanthrene	42-44	aryl hydrocarbon receptor	Rattus norvegicus	26-29
18524872-6	2008	As a positive control for AHR activation, MC dramatically induced the luciferase activity of a Cyp1a1-driven luciferase plasmid under AHR control.	Methylcholanthrene	42-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	95-101
18524872-6	2008	As a positive control for AHR activation, MC dramatically induced the luciferase activity of a Cyp1a1-driven luciferase plasmid under AHR control.	Methylcholanthrene	42-44	aryl hydrocarbon receptor	Rattus norvegicus	134-137
18524872-7	2008	Modulation of reporter gene activity by MC was accompanied by induction of endogenous CYP1A1 and suppression of endogenous CYP2C11 mRNA/protein.	Methylcholanthrene	40-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	86-92
18524872-7	2008	Modulation of reporter gene activity by MC was accompanied by induction of endogenous CYP1A1 and suppression of endogenous CYP2C11 mRNA/protein.	Methylcholanthrene	40-42	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	123-130
18591227-3	2008	The host responses mounted against the SM and MC variants differ, and lower tissue interleukin 10 (IL-10) levels are consistently observed in lungs of MC-infected C57BL/6 and BALB/c mice.	Methylcholanthrene	151-153	interleukin 10	Mus musculus	83-97
18591227-3	2008	The host responses mounted against the SM and MC variants differ, and lower tissue interleukin 10 (IL-10) levels are consistently observed in lungs of MC-infected C57BL/6 and BALB/c mice.	Methylcholanthrene	151-153	interleukin 10	Mus musculus	99-104
18591227-5	2008	The objective of this study was to compare survival rates and characterize the host responses of SM- and MC-infected IL-10-depleted (IL-10(-/-)) mice, which exhibit a Th1-polarized immune response and are considered resistant hosts.	Methylcholanthrene	105-107	interleukin 10	Mus musculus	117-131
18591227-6	2008	As expected, SM-infected IL-10(-/-) mice survived longer than wild-type mice, whereas MC-infected IL-10(-/-) mice did not exhibit a survival benefit.	Methylcholanthrene	86-88	interleukin 10	Mus musculus	98-103
18591227-7	2008	Consistent with this observation, we demonstrated marked differences in the inflammatory responses of SM- and MC-infected IL-10(-/-) and wild-type mice.	Methylcholanthrene	110-112	interleukin 10	Mus musculus	122-127
18591227-10	2008	Lung tissue levels of IL-21, IL-6, IL-4, transforming growth factor beta, IL-12, and gamma interferon were higher in MC-infected IL-10(-/-) and wild-type mice than in SM-infected mice, whereas tumor necrosis factor alpha levels were higher in SM-infected IL-10(-/-) mice.	Methylcholanthrene	117-119	interleukin 21	Mus musculus	22-27
18591227-10	2008	Lung tissue levels of IL-21, IL-6, IL-4, transforming growth factor beta, IL-12, and gamma interferon were higher in MC-infected IL-10(-/-) and wild-type mice than in SM-infected mice, whereas tumor necrosis factor alpha levels were higher in SM-infected IL-10(-/-) mice.	Methylcholanthrene	117-119	interleukin 10	Mus musculus	129-134
18591227-10	2008	Lung tissue levels of IL-21, IL-6, IL-4, transforming growth factor beta, IL-12, and gamma interferon were higher in MC-infected IL-10(-/-) and wild-type mice than in SM-infected mice, whereas tumor necrosis factor alpha levels were higher in SM-infected IL-10(-/-) mice.	Methylcholanthrene	117-119	tumor necrosis factor	Mus musculus	193-220
18591227-10	2008	Lung tissue levels of IL-21, IL-6, IL-4, transforming growth factor beta, IL-12, and gamma interferon were higher in MC-infected IL-10(-/-) and wild-type mice than in SM-infected mice, whereas tumor necrosis factor alpha levels were higher in SM-infected IL-10(-/-) mice.	Methylcholanthrene	117-119	interleukin 10	Mus musculus	255-260
18591227-11	2008	In conclusion, the MC variant elicits an excessive inflammatory response in a Th1-polarized host environment, and therefore, the outcome is negatively affected by the absence of IL-10.	Methylcholanthrene	19-21	negative elongation factor complex member C/D, Th1l	Mus musculus	78-81
18591227-11	2008	In conclusion, the MC variant elicits an excessive inflammatory response in a Th1-polarized host environment, and therefore, the outcome is negatively affected by the absence of IL-10.	Methylcholanthrene	19-21	interleukin 10	Mus musculus	178-183
18702954-4	2008	CXCL10 was significantly higher (1) in control 2 than in control 1 (P &lt; .001), (2) in MC than in control 1, and (3) in MC + AT than in controls 1 and 2 and in MC (P = .002).	Methylcholanthrene	89-91	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
18702954-4	2008	CXCL10 was significantly higher (1) in control 2 than in control 1 (P &lt; .001), (2) in MC than in control 1, and (3) in MC + AT than in controls 1 and 2 and in MC (P = .002).	Methylcholanthrene	122-124	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
18702954-4	2008	CXCL10 was significantly higher (1) in control 2 than in control 1 (P &lt; .001), (2) in MC than in control 1, and (3) in MC + AT than in controls 1 and 2 and in MC (P = .002).	Methylcholanthrene	122-124	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
18702954-5	2008	A high CXCL10 level (&gt;mean + SD control 1; &gt;167 pg/mL) was present in 7% control 1, 21% control 2, 49% MC, and 78% MC + AT (P &lt; .0001).	Methylcholanthrene	109-111	C-X-C motif chemokine ligand 10	Homo sapiens	7-13
18702954-5	2008	A high CXCL10 level (&gt;mean + SD control 1; &gt;167 pg/mL) was present in 7% control 1, 21% control 2, 49% MC, and 78% MC + AT (P &lt; .0001).	Methylcholanthrene	121-125	C-X-C motif chemokine ligand 10	Homo sapiens	7-13
18702954-6	2008	CCL2 was significantly higher in MC and in MC + AT than in control 1 or in control 2 (P &lt; .01).	Methylcholanthrene	33-35	C-C motif chemokine ligand 2	Homo sapiens	0-4
18702954-6	2008	CCL2 was significantly higher in MC and in MC + AT than in control 1 or in control 2 (P &lt; .01).	Methylcholanthrene	43-47	C-C motif chemokine ligand 2	Homo sapiens	0-4
18702954-7	2008	A high CCL2 level (&gt;mean + SD control 1; &gt;730 pg/mL) was present in 2% control 1, 1% control 2, 18% MC, and 21% MC + AT (P &lt; .0001).	Methylcholanthrene	106-108	C-C motif chemokine ligand 2	Homo sapiens	7-11
18702954-7	2008	A high CCL2 level (&gt;mean + SD control 1; &gt;730 pg/mL) was present in 2% control 1, 1% control 2, 18% MC, and 21% MC + AT (P &lt; .0001).	Methylcholanthrene	118-122	C-C motif chemokine ligand 2	Homo sapiens	7-11
18702954-8	2008	The study demonstrates high CXCL10 and CCL2 serum levels in patients with MC; CXCL10 in MC + AT is significantly higher than that in MC.	Methylcholanthrene	74-76	C-X-C motif chemokine ligand 10	Homo sapiens	28-34
18702954-8	2008	The study demonstrates high CXCL10 and CCL2 serum levels in patients with MC; CXCL10 in MC + AT is significantly higher than that in MC.	Methylcholanthrene	74-76	C-C motif chemokine ligand 2	Homo sapiens	39-43
18702954-8	2008	The study demonstrates high CXCL10 and CCL2 serum levels in patients with MC; CXCL10 in MC + AT is significantly higher than that in MC.	Methylcholanthrene	74-76	C-X-C motif chemokine ligand 10	Homo sapiens	78-84
18702954-8	2008	The study demonstrates high CXCL10 and CCL2 serum levels in patients with MC; CXCL10 in MC + AT is significantly higher than that in MC.	Methylcholanthrene	88-90	C-X-C motif chemokine ligand 10	Homo sapiens	78-84
18502397-3	2008	However, its precise molecular mechanism remains unknown because the chemical activates AHR without its direct binding in contrast to typical AHR ligands such as 3-methylcholanthrene (3MC) and beta-naphthoflavone (BNF).	Methylcholanthrene	162-182	aryl hydrocarbon receptor	Homo sapiens	142-145
18502397-10	2008	The present results suggest that omeprazole as well as BNF and 3MC activates both human CYP1A1 and CYP1A2 expression through the common regulatory region despite that omeprazole may involve a different cellular signal(s) from BNF and 3MC.	Methylcholanthrene	63-66	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	88-94
18502397-10	2008	The present results suggest that omeprazole as well as BNF and 3MC activates both human CYP1A1 and CYP1A2 expression through the common regulatory region despite that omeprazole may involve a different cellular signal(s) from BNF and 3MC.	Methylcholanthrene	63-66	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	99-105
18502397-10	2008	The present results suggest that omeprazole as well as BNF and 3MC activates both human CYP1A1 and CYP1A2 expression through the common regulatory region despite that omeprazole may involve a different cellular signal(s) from BNF and 3MC.	Methylcholanthrene	234-237	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	88-94
18502397-10	2008	The present results suggest that omeprazole as well as BNF and 3MC activates both human CYP1A1 and CYP1A2 expression through the common regulatory region despite that omeprazole may involve a different cellular signal(s) from BNF and 3MC.	Methylcholanthrene	234-237	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	99-105
18651167-7	2008	On the basis of MC, RI-PTH monitoring would have resulted in five FP results, with a specificity of 50%.	Methylcholanthrene	16-18	parathyroid hormone	Homo sapiens	23-26
18699723-7	2008	C57BL/6NHsd mice received intraoral mc-MnSOD-PL, mc-DsRed-PL control, full-length MnSOD-PL, or blank-PL and then were irradiated 24 hr later with 31 Gy to the esophagus.	Methylcholanthrene	36-38	superoxide dismutase 2, mitochondrial	Mus musculus	39-44
18345025-4	2008	Tumors from MCA/BHT-treated Rosa26-Foxm1 mice displayed a significant increase in the number, size and DNA replication compared to wild-type mice.	Methylcholanthrene	12-15	gene trap ROSA 26, Philippe Soriano	Mus musculus	28-34
18345025-4	2008	Tumors from MCA/BHT-treated Rosa26-Foxm1 mice displayed a significant increase in the number, size and DNA replication compared to wild-type mice.	Methylcholanthrene	12-15	forkhead box M1	Mus musculus	35-40
18502397-3	2008	However, its precise molecular mechanism remains unknown because the chemical activates AHR without its direct binding in contrast to typical AHR ligands such as 3-methylcholanthrene (3MC) and beta-naphthoflavone (BNF).	Methylcholanthrene	184-187	aryl hydrocarbon receptor	Homo sapiens	142-145
18502397-7	2008	Reporter assays with deletion constructs have demonstrated that the omeprazole-induced expression of both CYP1A1 and CYP1A2 is mediated via the common regulatory region containing multiple AHR-binding motifs (the nucleotides from -464 to -1829 of human CYP1A1), which is identical with the region for BNF and 3MC induction.	Methylcholanthrene	309-312	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	106-112
18502397-7	2008	Reporter assays with deletion constructs have demonstrated that the omeprazole-induced expression of both CYP1A1 and CYP1A2 is mediated via the common regulatory region containing multiple AHR-binding motifs (the nucleotides from -464 to -1829 of human CYP1A1), which is identical with the region for BNF and 3MC induction.	Methylcholanthrene	309-312	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	117-123
18973019-6	2008	RESULTS: The positive rate of IKK-alpha in MC group was significantly higher than that in NC group (P &lt; 0.01).	Methylcholanthrene	43-45	component of inhibitor of nuclear factor kappa B kinase complex	Rattus norvegicus	30-39
18422734-8	2008	However, when measuring the Th2 cytokine-production capacity post-stimulation, a significant increase in the percentage of IL-4-producing T cells was observed in the IS groups, compared with the MC group, resulting in a significantly lower ratio of IFN-gamma-/IL-4-producing T cells.	Methylcholanthrene	195-197	interferon gamma	Homo sapiens	249-258
18440119-5	2008	Suppression of CYP2C11 constructs was not observed upon treatment of transfected rat 5L, BP8 or mouse Hepa-1 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylcholanthrene.	Methylcholanthrene	166-186	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	15-22
18448146-6	2008	As assessed by immunostaining, neoplastic MC were found to exhibit CD117 and CD25 but did not display CD5 or CD20, whereas SLL cells were found to coexpress CD5 and CD20 but did not express MC antigens.	Methylcholanthrene	42-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
18448146-6	2008	As assessed by immunostaining, neoplastic MC were found to exhibit CD117 and CD25 but did not display CD5 or CD20, whereas SLL cells were found to coexpress CD5 and CD20 but did not express MC antigens.	Methylcholanthrene	42-44	interferon stimulated exonuclease gene 20	Homo sapiens	77-81
18096572-4	2008	In contrast, activation of the AHR with 3-methylcholanthrene or benzo[a]pyrene resulted in predominant formation of AHR*ARNT complexes.	Methylcholanthrene	40-60	aryl-hydrocarbon receptor	Mus musculus	31-34
18096572-4	2008	In contrast, activation of the AHR with 3-methylcholanthrene or benzo[a]pyrene resulted in predominant formation of AHR*ARNT complexes.	Methylcholanthrene	40-60	aryl-hydrocarbon receptor	Mus musculus	116-119
18096572-4	2008	In contrast, activation of the AHR with 3-methylcholanthrene or benzo[a]pyrene resulted in predominant formation of AHR*ARNT complexes.	Methylcholanthrene	40-60	aryl hydrocarbon receptor nuclear translocator	Mus musculus	120-124
18282714-2	2008	CXCL10 was assayed in 50 MC patients without AT, in 40 MC patients with AT (MC+AT), in 2 gender- and age-matched control groups [50 healthy controls (without HCV or AT; control); 40 controls with AT (without HCV and MC; control+AT)].	Methylcholanthrene	25-27	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
18282714-3	2008	CXCL10 was significantly higher: (1) in control+AT than in control (p&lt;0.001); (2) in MC patients than in control (p&lt;0.001); (3) in MC+AT patients than in control (p&lt;0.001), control+AT (p&lt;0.001), or in MC (p=0.002).	Methylcholanthrene	88-90	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
18282714-6	2008	In conclusion, our study is the first to demonstrate high serum levels of CXCL10 in MC and that CXCL10 in MC+AT patients are significantly higher compared to MC patients.	Methylcholanthrene	84-86	C-X-C motif chemokine ligand 10	Homo sapiens	74-80
18282714-6	2008	In conclusion, our study is the first to demonstrate high serum levels of CXCL10 in MC and that CXCL10 in MC+AT patients are significantly higher compared to MC patients.	Methylcholanthrene	106-108	C-X-C motif chemokine ligand 10	Homo sapiens	96-102
18455014-8	2008	The mean AFP level among MC patients was 150.2 ng/mL with vascular invasion detected in 7.7% of explants, and 47.4% with incidental tumors.	Methylcholanthrene	25-27	alpha fetoprotein	Homo sapiens	9-12
18314503-4	2008	To help interpret the kinetic data, we structurally characterized the SLV mutants by NMR spectroscopy and generated a three-dimensional model of the SLI/SLV complex by homology modeling with MC-Sym.	Methylcholanthrene	191-194	SHC adaptor protein 2	Homo sapiens	149-152
18314503-4	2008	To help interpret the kinetic data, we structurally characterized the SLV mutants by NMR spectroscopy and generated a three-dimensional model of the SLI/SLV complex by homology modeling with MC-Sym.	Methylcholanthrene	191-194	solute carrier family 50 member 1	Homo sapiens	153-156
18203689-8	2008	Therefore, in this investigation, we tested the hypothesis that MC elicits persistent induction of CYP1B1 and phase II genes, which are in part regulated by the Ah receptor (AHR).	Methylcholanthrene	64-66	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	99-105
18203689-8	2008	Therefore, in this investigation, we tested the hypothesis that MC elicits persistent induction of CYP1B1 and phase II genes, which are in part regulated by the Ah receptor (AHR).	Methylcholanthrene	64-66	aryl hydrocarbon receptor	Rattus norvegicus	161-172
18203689-8	2008	Therefore, in this investigation, we tested the hypothesis that MC elicits persistent induction of CYP1B1 and phase II genes, which are in part regulated by the Ah receptor (AHR).	Methylcholanthrene	64-66	aryl hydrocarbon receptor	Rattus norvegicus	174-177
18203689-10	2008	The major finding was that MC persistently induced (3- to 10-fold) the expression of several phase II enzymes, including GST-alpha, NQO1, UGT1A1, ALDH, and epoxide hydrolase in both tissues for up to 28 days.	Methylcholanthrene	27-29	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	132-136
18203689-10	2008	The major finding was that MC persistently induced (3- to 10-fold) the expression of several phase II enzymes, including GST-alpha, NQO1, UGT1A1, ALDH, and epoxide hydrolase in both tissues for up to 28 days.	Methylcholanthrene	27-29	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	138-144
18203689-10	2008	The major finding was that MC persistently induced (3- to 10-fold) the expression of several phase II enzymes, including GST-alpha, NQO1, UGT1A1, ALDH, and epoxide hydrolase in both tissues for up to 28 days.	Methylcholanthrene	27-29	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	146-150
18203689-12	2008	Our results thus support the hypothesis that MC elicits coordinated and sustained induction of phase II genes presumably via persistent activation of the AHR, a phenomenon that may have implications for chemical-induced carcinogenesis and chemopreventive strategies in humans.	Methylcholanthrene	45-47	aryl hydrocarbon receptor	Homo sapiens	154-157
18022818-0	2008	Molecular mechanisms of p21 and p27 induction by 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, involved in antiproliferation of human umbilical vascular endothelial cells.	Methylcholanthrene	49-69	H3 histone pseudogene 16	Homo sapiens	24-27
18022818-0	2008	Molecular mechanisms of p21 and p27 induction by 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, involved in antiproliferation of human umbilical vascular endothelial cells.	Methylcholanthrene	49-69	interferon alpha inducible protein 27	Homo sapiens	32-35
18022818-0	2008	Molecular mechanisms of p21 and p27 induction by 3-methylcholanthrene, an aryl-hydrocarbon receptor agonist, involved in antiproliferation of human umbilical vascular endothelial cells.	Methylcholanthrene	49-69	aryl hydrocarbon receptor	Homo sapiens	74-99
18022818-1	2008	We previously reported that 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, inhibits the proliferation of human umbilical vascular endothelial cells (HUVECs; Juan et al., 2006, Eur J Pharmacol 530: 1-8).	Methylcholanthrene	28-48	aryl hydrocarbon receptor	Homo sapiens	59-84
18022818-1	2008	We previously reported that 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, inhibits the proliferation of human umbilical vascular endothelial cells (HUVECs; Juan et al., 2006, Eur J Pharmacol 530: 1-8).	Methylcholanthrene	28-48	aryl hydrocarbon receptor	Homo sapiens	86-89
18022818-1	2008	We previously reported that 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, inhibits the proliferation of human umbilical vascular endothelial cells (HUVECs; Juan et al., 2006, Eur J Pharmacol 530: 1-8).	Methylcholanthrene	50-53	aryl hydrocarbon receptor	Homo sapiens	59-84
18022818-1	2008	We previously reported that 3-methylcholanthrene (3MC), an aryl-hydrocarbon receptor (AhR) agonist, inhibits the proliferation of human umbilical vascular endothelial cells (HUVECs; Juan et al., 2006, Eur J Pharmacol 530: 1-8).	Methylcholanthrene	50-53	aryl hydrocarbon receptor	Homo sapiens	86-89
18022818-2	2008	Herein, pretreatment of HUVECs with p21 or p27 small interfering (si)RNA reduced 3MC-induced elimination of [(3)H]thymidine incorporation, demonstrating their essential roles in the antiproliferation of HUVECs.	Methylcholanthrene	81-84	H3 histone pseudogene 16	Homo sapiens	36-39
18022818-2	2008	Herein, pretreatment of HUVECs with p21 or p27 small interfering (si)RNA reduced 3MC-induced elimination of [(3)H]thymidine incorporation, demonstrating their essential roles in the antiproliferation of HUVECs.	Methylcholanthrene	81-84	interferon alpha inducible protein 27	Homo sapiens	43-46
18022818-3	2008	The molecular mechanisms of p21 and p27 involved in the antiproliferative effects of 3MC were elucidated in this study.	Methylcholanthrene	85-88	H3 histone pseudogene 16	Homo sapiens	28-31
18022818-3	2008	The molecular mechanisms of p21 and p27 involved in the antiproliferative effects of 3MC were elucidated in this study.	Methylcholanthrene	85-88	interferon alpha inducible protein 27	Homo sapiens	36-39
18022818-5	2008	Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA.	Methylcholanthrene	15-18	H3 histone pseudogene 16	Homo sapiens	28-31
18022818-5	2008	Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA.	Methylcholanthrene	15-18	interferon alpha inducible protein 27	Homo sapiens	36-39
18022818-5	2008	Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA.	Methylcholanthrene	15-18	aryl hydrocarbon receptor	Homo sapiens	86-89
18022818-5	2008	Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA.	Methylcholanthrene	15-18	aryl hydrocarbon receptor	Homo sapiens	119-122
18022818-5	2008	Interestingly, 3MC-mediated p21 and p27 inductions were eliminated by resveratrol, an AhR antagonist, suggesting their AhR dependency, further confirmed by AhR siRNA.	Methylcholanthrene	15-18	aryl hydrocarbon receptor	Homo sapiens	119-122
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Methylcholanthrene	95-98	H3 histone pseudogene 16	Homo sapiens	72-75
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Methylcholanthrene	95-98	interferon alpha inducible protein 27	Homo sapiens	80-83
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Methylcholanthrene	95-98	aryl hydrocarbon receptor	Homo sapiens	124-127
18022818-7	2008	3MC concentration-dependently enhanced not only the consensus dioxin-responsive element (DRE)-driven luciferase activity, but also the binding activity of the AhR to the putative DRE derived from the p21 and p27 promoters.	Methylcholanthrene	0-3	aryl hydrocarbon receptor	Homo sapiens	159-162
18022818-7	2008	3MC concentration-dependently enhanced not only the consensus dioxin-responsive element (DRE)-driven luciferase activity, but also the binding activity of the AhR to the putative DRE derived from the p21 and p27 promoters.	Methylcholanthrene	0-3	H3 histone pseudogene 16	Homo sapiens	200-203
18022818-7	2008	3MC concentration-dependently enhanced not only the consensus dioxin-responsive element (DRE)-driven luciferase activity, but also the binding activity of the AhR to the putative DRE derived from the p21 and p27 promoters.	Methylcholanthrene	0-3	interferon alpha inducible protein 27	Homo sapiens	208-211
18022818-8	2008	A deletion of the DRE (-285/-270) in p21 (-2,300/+8) only partially alleviated the 3MC-induced luciferase activity unless NAC was added, suggesting that there may be a DRE-independent mechanism associated with oxidative stress.	Methylcholanthrene	83-86	H3 histone pseudogene 16	Homo sapiens	37-40
18022818-10	2008	Our study demonstrated that both the functional DRE and the phosphorylation of p38MAPK are essential for the induction of p21 and p27, resulting in the antiproliferative action of 3MC in HUVECs.	Methylcholanthrene	180-183	H3 histone pseudogene 16	Homo sapiens	122-125
18022818-10	2008	Our study demonstrated that both the functional DRE and the phosphorylation of p38MAPK are essential for the induction of p21 and p27, resulting in the antiproliferative action of 3MC in HUVECs.	Methylcholanthrene	180-183	interferon alpha inducible protein 27	Homo sapiens	130-133
18438460-6	2008	3-MC caused a 15-fold increase in mutant frequency and an increase in transversion type mutations; a very early occurrence of this type of mutation in lung tissue was previously identified in Ki-ras oncogenes of lung tumors from 3-MC exposed mice.	Methylcholanthrene	0-4	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	192-198
18334960-15	2008	The MC-L phenotype has thus been defined as MC-L(CD105, CD106, CD54, CD166, CD90, CD29, CD71, pax -6 +/ p75, SSEA1, Tra-1-61, Tra-1-81, CD31, CD34, CD45, CD11a, CD11c, CD14, CD138, Flk1, Flt1, VE-Cadherin -).	Methylcholanthrene	4-6	paired box 6	Homo sapiens	94-100
18438460-6	2008	3-MC caused a 15-fold increase in mutant frequency and an increase in transversion type mutations; a very early occurrence of this type of mutation in lung tissue was previously identified in Ki-ras oncogenes of lung tumors from 3-MC exposed mice.	Methylcholanthrene	229-233	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	192-198
18003862-0	2008	3-Methylcholanthrene displays dual effects on estrogen receptor (ER) alpha and ER beta signaling in a cell-type specific fashion.	Methylcholanthrene	0-20	estrogen receptor 1	Homo sapiens	46-74
18257902-7	2008	IFN-gamma and IL-10 levels in response to PHA in supernatants of MC of neonates were significantly lower compared to that in adults (p &lt; 0.05, Wilcoxon two-sample test).	Methylcholanthrene	65-67	interferon gamma	Bos taurus	0-9
18257902-7	2008	IFN-gamma and IL-10 levels in response to PHA in supernatants of MC of neonates were significantly lower compared to that in adults (p &lt; 0.05, Wilcoxon two-sample test).	Methylcholanthrene	65-67	interleukin-10	Bos taurus	14-19
18257902-12	2008	IFN-gamma and IL-13 levels in WB and MC supernatants revealed significant differences.	Methylcholanthrene	37-39	interleukin 13	Bos taurus	14-19
18086550-3	2008	In a cell-free system, indigoids induced the transformation dose-dependently, but suppressed the transformation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin and the binding of 3-methylcholanthrene to the AhR.	Methylcholanthrene	178-198	aryl-hydrocarbon receptor	Mus musculus	206-209
18438341-7	2008	CONCLUSION: To elevate antitumor activity of LAK toward MC-rhabdomyosarcoma and B16 melanoma cells, low doses of doxorubicin could be used at certain conditions of LAK generation.	Methylcholanthrene	56-58	alpha-kinase 1	Mus musculus	45-48
18003862-0	2008	3-Methylcholanthrene displays dual effects on estrogen receptor (ER) alpha and ER beta signaling in a cell-type specific fashion.	Methylcholanthrene	0-20	estrogen receptor 2	Homo sapiens	79-86
18003862-4	2008	Here, we study the effect of the combustion byproduct 3-methylcholanthrene (3-MC) on ERalpha and ERbeta.	Methylcholanthrene	54-74	estrogen receptor 1	Homo sapiens	85-92
17680691-2	2008	Isothermal titration calorimetry shows that (i) the separated MC, M, and C domains of human eRF1 bind to eRF3; (ii) GTP binding to eRF3 requires complex formation with either the MC or M + C domains; (iii) the M domain interacts with the N and C domains; (iv) the MC domain and Mg2+ induce GTPase activity of eRF3 in the ribosome.	Methylcholanthrene	62-64	eukaryotic translation termination factor 1	Homo sapiens	92-96
18003862-4	2008	Here, we study the effect of the combustion byproduct 3-methylcholanthrene (3-MC) on ERalpha and ERbeta.	Methylcholanthrene	54-74	estrogen receptor 2	Homo sapiens	97-103
18003862-4	2008	Here, we study the effect of the combustion byproduct 3-methylcholanthrene (3-MC) on ERalpha and ERbeta.	Methylcholanthrene	76-80	estrogen receptor 1	Homo sapiens	85-92
18003862-4	2008	Here, we study the effect of the combustion byproduct 3-methylcholanthrene (3-MC) on ERalpha and ERbeta.	Methylcholanthrene	76-80	estrogen receptor 2	Homo sapiens	97-103
18003862-5	2008	3-MC is a compound identified previously as an activator of the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	0-4	aryl hydrocarbon receptor	Homo sapiens	64-89
18003862-5	2008	3-MC is a compound identified previously as an activator of the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	0-4	aryl hydrocarbon receptor	Homo sapiens	91-94
18003862-8	2008	We show that 3-MC acts as a repressor in some cells, presumably via the AhR, whereas it is a potent activator of ER activity in other cells.	Methylcholanthrene	13-17	aryl hydrocarbon receptor	Homo sapiens	72-75
18003862-10	2008	In summary, our results suggest that exposure to AhR ligands like 3-MC can lead to either activation or repression of E(2) signaling, depending on the cellular context.	Methylcholanthrene	66-70	aryl hydrocarbon receptor	Homo sapiens	49-52
17680691-2	2008	Isothermal titration calorimetry shows that (i) the separated MC, M, and C domains of human eRF1 bind to eRF3; (ii) GTP binding to eRF3 requires complex formation with either the MC or M + C domains; (iii) the M domain interacts with the N and C domains; (iv) the MC domain and Mg2+ induce GTPase activity of eRF3 in the ribosome.	Methylcholanthrene	179-181	eukaryotic translation termination factor 1	Homo sapiens	92-96
18178624-4	2008	Unexpectedly, however, fewer MyD88-/- mice formed sarcomas than WT controls when exposed to MCA.	Methylcholanthrene	92-95	myeloid differentiation primary response gene 88	Mus musculus	29-34
17955373-3	2008	MC potently induced cell death of different cancer cell lines (EC(50) 3-8 microM) with characteristics of apoptosis, visualized by the activation of caspase-3, -8 and -9, cleavage of poly(ADP-ribose)polymerase (PARP), release of nucleosomes into the cytosol, and DNA fragmentation.	Methylcholanthrene	0-2	caspase 3	Homo sapiens	149-169
17955373-3	2008	MC potently induced cell death of different cancer cell lines (EC(50) 3-8 microM) with characteristics of apoptosis, visualized by the activation of caspase-3, -8 and -9, cleavage of poly(ADP-ribose)polymerase (PARP), release of nucleosomes into the cytosol, and DNA fragmentation.	Methylcholanthrene	0-2	poly(ADP-ribose) polymerase 1	Homo sapiens	183-209
17955373-3	2008	MC potently induced cell death of different cancer cell lines (EC(50) 3-8 microM) with characteristics of apoptosis, visualized by the activation of caspase-3, -8 and -9, cleavage of poly(ADP-ribose)polymerase (PARP), release of nucleosomes into the cytosol, and DNA fragmentation.	Methylcholanthrene	0-2	poly(ADP-ribose) polymerase 1	Homo sapiens	211-215
17955373-4	2008	MC was much less cytotoxic for non-transformed human peripheral blood mononuclear cells (PBMC) or foreskin fibroblasts (EC(50) cell death = 20-50 microM), and MC up to 30 microM hardly caused processing of PARP, caspase-3, -8 and -9 in human PBMC.	Methylcholanthrene	0-2	poly(ADP-ribose) polymerase 1	Homo sapiens	206-210
17955373-4	2008	MC was much less cytotoxic for non-transformed human peripheral blood mononuclear cells (PBMC) or foreskin fibroblasts (EC(50) cell death = 20-50 microM), and MC up to 30 microM hardly caused processing of PARP, caspase-3, -8 and -9 in human PBMC.	Methylcholanthrene	0-2	caspase 3	Homo sapiens	212-232
17955373-6	2008	Thus, MC caused loss of the mitochondrial membrane potential in MM6 cells and evoked release of cytochrome c from mitochondria.	Methylcholanthrene	6-8	cytochrome c, somatic	Homo sapiens	96-108
17955373-7	2008	Interestingly, Jurkat cells deficient in caspase-9 were resistant to MC-induced cell death and no processing of PARP or caspase-8 was evident.	Methylcholanthrene	69-71	caspase 9	Homo sapiens	41-50
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	Fas cell surface death receptor	Homo sapiens	34-38
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	Fas cell surface death receptor	Homo sapiens	45-50
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	Fas associated via death domain	Homo sapiens	64-68
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	caspase 8	Homo sapiens	72-81
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	poly(ADP-ribose) polymerase 1	Homo sapiens	135-139
17955373-9	2008	Conclusively, MC induces apoptosis in cancer cell lines, with marginal cytotoxicity for non-transformed cells, via the mitochondrial cytochrome c/Apaf-1/caspase-9 pathway.	Methylcholanthrene	14-16	cytochrome c, somatic	Homo sapiens	133-145
17955373-9	2008	Conclusively, MC induces apoptosis in cancer cell lines, with marginal cytotoxicity for non-transformed cells, via the mitochondrial cytochrome c/Apaf-1/caspase-9 pathway.	Methylcholanthrene	14-16	apoptotic peptidase activating factor 1	Homo sapiens	146-152
17955373-9	2008	Conclusively, MC induces apoptosis in cancer cell lines, with marginal cytotoxicity for non-transformed cells, via the mitochondrial cytochrome c/Apaf-1/caspase-9 pathway.	Methylcholanthrene	14-16	caspase 9	Homo sapiens	153-162
18098063-6	2008	reverse transcriptase-polymerase chain reaction (RT-PCR) analysis clearly showed that the hepatic CYP1A1 and CYP1A2 mRNA levels substantially increased after treatment with MC, which was suppressed by Urtica supplementation.	Methylcholanthrene	173-175	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	98-104
18078454-5	2008	In addition, decreased Bax expression, increased Bcl-2 expression and a decreased release of cytochrome c into the cytosol were observed in the melatonin-pretreated SK-N-MC cells.	Methylcholanthrene	170-172	cytochrome c, somatic	Homo sapiens	93-105
18088504-4	2008	In rats pretreated with 3-methylcholanthrene (3-MC), orphenadrine or dexamethasone (main inducers of CYP1A1/2, CYP2B1/2 and CYP3A1/2, respectively, in rats), the time-averaged non-renal clearance (CLNR) of theophylline was significantly faster than in their respective controls (1260, 42.7 and 69.0% increases, respectively).	Methylcholanthrene	24-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-107
18088504-4	2008	In rats pretreated with 3-methylcholanthrene (3-MC), orphenadrine or dexamethasone (main inducers of CYP1A1/2, CYP2B1/2 and CYP3A1/2, respectively, in rats), the time-averaged non-renal clearance (CLNR) of theophylline was significantly faster than in their respective controls (1260, 42.7 and 69.0% increases, respectively).	Methylcholanthrene	24-44	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	111-117
18612618-5	2008	Chymase is present in more moderate amounts in a subpopulation of mast cells (MC(TC)).	Methylcholanthrene	78-81	chymase 1	Homo sapiens	0-7
18088504-4	2008	In rats pretreated with 3-methylcholanthrene (3-MC), orphenadrine or dexamethasone (main inducers of CYP1A1/2, CYP2B1/2 and CYP3A1/2, respectively, in rats), the time-averaged non-renal clearance (CLNR) of theophylline was significantly faster than in their respective controls (1260, 42.7 and 69.0% increases, respectively).	Methylcholanthrene	24-44	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	124-132
18098063-6	2008	reverse transcriptase-polymerase chain reaction (RT-PCR) analysis clearly showed that the hepatic CYP1A1 and CYP1A2 mRNA levels substantially increased after treatment with MC, which was suppressed by Urtica supplementation.	Methylcholanthrene	173-175	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	109-115
17880909-5	2007	In a cell-free system, curcumin inhibited the binding of 3-methylcholanthrene, an AhR agonist, to the receptor.	Methylcholanthrene	57-77	aryl-hydrocarbon receptor	Mus musculus	82-85
17963696-5	2007	3-Methylcholanthrene (a potent AhR agonist) increased the expression (mRNA) of the major inflammatory targets IL-1beta and MMP9.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	31-34
17963696-5	2007	3-Methylcholanthrene (a potent AhR agonist) increased the expression (mRNA) of the major inflammatory targets IL-1beta and MMP9.	Methylcholanthrene	0-20	interleukin 1 beta	Homo sapiens	110-118
17963696-5	2007	3-Methylcholanthrene (a potent AhR agonist) increased the expression (mRNA) of the major inflammatory targets IL-1beta and MMP9.	Methylcholanthrene	0-20	matrix metallopeptidase 9	Homo sapiens	123-127
18199982-7	2007	All applied variants of therapy - adoptive LAK-therapy, vaccine therapy and their combination were effective for treatment of mice bearing Dox-sensitive and Dox-resistant transplantable murine MC-rhabdomyosarcoma.	Methylcholanthrene	193-195	alpha-kinase 1	Mus musculus	43-46
17879099-3	2007	On treatment with the AhR ligands 3-methylcholanthrene (MC), beta-naphthoflavone (betaNF), and indigo, the transgenic tobacco plants exhibited enhanced GUS activity, presumably by inducible expression of the reporter gene.	Methylcholanthrene	34-54	glucuronidase, beta	Mus musculus	152-155
17879099-3	2007	On treatment with the AhR ligands 3-methylcholanthrene (MC), beta-naphthoflavone (betaNF), and indigo, the transgenic tobacco plants exhibited enhanced GUS activity, presumably by inducible expression of the reporter gene.	Methylcholanthrene	56-58	glucuronidase, beta	Mus musculus	152-155
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	108-110	glucuronidase, beta	Mus musculus	35-38
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	108-110	glucuronidase, beta	Mus musculus	112-115
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	146-148	glucuronidase, beta	Mus musculus	35-38
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	146-148	glucuronidase, beta	Mus musculus	112-115
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	146-148	glucuronidase, beta	Mus musculus	35-38
17879099-5	2007	Plants carrying AhRV expressed the GUS reporter gene in a dose- and time-dependent manner when treated with MC; GUS activity was detected at 5 nM MC on solid medium and at 12 h after soaking in 25 microM MC.	Methylcholanthrene	146-148	glucuronidase, beta	Mus musculus	112-115
17935295-1	2007	Ginsenoside bioactive compounds, namely, compound K (C-K), compound Mx (C-Mx), and ginsenoside Mc (G-Mc), were the metabolites of ginsenosides Rb 1, Rb 2, Rb 3, and Rc by intestinal microflora of humans or rats, microorganisms, and enzymes, and C-K showed beneficial effects in vitro and in vivo as an antitumoral agent.	Methylcholanthrene	95-97	RB transcriptional corepressor 1	Homo sapiens	143-147
18282411-10	2007	Expression of costimulatory molecules such as CD40 in MC was analyzed by flow cytometry.	Methylcholanthrene	54-56	CD40 molecule	Homo sapiens	46-50
18282411-14	2007	(3) Expression of costimulatory molecule CD40 in MC increased significantly during acute phase of KD [(6.19 +/- 2.25)% vs. (2.00 +/- 1.37)%, P &lt; 0.05], while the protein levels of CD40 in KD-coronary artery lesion (CAL)(+) group was found to be significantly higher than that of KD-CAL-group [KD-CAL, (9.63 +/- 2.96)% vs. (4.12 +/- 1.91)%, P &lt; 0.05].	Methylcholanthrene	49-51	CD40 molecule	Homo sapiens	41-45
18282411-14	2007	(3) Expression of costimulatory molecule CD40 in MC increased significantly during acute phase of KD [(6.19 +/- 2.25)% vs. (2.00 +/- 1.37)%, P &lt; 0.05], while the protein levels of CD40 in KD-coronary artery lesion (CAL)(+) group was found to be significantly higher than that of KD-CAL-group [KD-CAL, (9.63 +/- 2.96)% vs. (4.12 +/- 1.91)%, P &lt; 0.05].	Methylcholanthrene	49-51	CD40 molecule	Homo sapiens	183-187
18057719-6	2007	Pretreatment with 3-methylcholanthrene (MC) resulted in remarkable increases of both M-1 and M-4 (3 to 9-fold that of untreated).	Methylcholanthrene	18-38	cholinergic receptor, muscarinic 4	Rattus norvegicus	93-96
18057719-6	2007	Pretreatment with 3-methylcholanthrene (MC) resulted in remarkable increases of both M-1 and M-4 (3 to 9-fold that of untreated).	Methylcholanthrene	40-42	cholinergic receptor, muscarinic 4	Rattus norvegicus	93-96
18257284-3	2007	The recombinant expression plasmid pEGFP-N1/MnSOD was transfected into MC by lipofectamine 2000-mediated gene transfer method, which were observed through co-Focus Fluorescence microscopy.	Methylcholanthrene	71-73	superoxide dismutase 2	Rattus norvegicus	44-49
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	Fc epsilon receptor Ia	Homo sapiens	31-43
17845420-9	2007	A significantly decreased expression of BDNF protein was found in atopic dermatitis lesional MCs when compared with control MC expression.	Methylcholanthrene	93-95	brain derived neurotrophic factor	Homo sapiens	40-44
17586480-5	2007	PCB 77 was more potent than PCB 47 or PCB 52 at inhibiting MROD and EROD activities in hepatic microsomes from MC-treated rats, while no inhibition of either activity was observed with PCB 54.	Methylcholanthrene	111-113	pyruvate carboxylase	Rattus norvegicus	0-3
17560542-4	2007	Flavone, flavonol, and flavanone but not catechin inhibited the specific binding between the AhR and 3-methylcholanthrene dose-dependently, indicating that the former three subclasses possibly act as competitive antagonists of the AhR.	Methylcholanthrene	101-121	aryl hydrocarbon receptor	Homo sapiens	93-96
17560542-4	2007	Flavone, flavonol, and flavanone but not catechin inhibited the specific binding between the AhR and 3-methylcholanthrene dose-dependently, indicating that the former three subclasses possibly act as competitive antagonists of the AhR.	Methylcholanthrene	101-121	aryl hydrocarbon receptor	Homo sapiens	231-234
17559912-9	2007	Additionally, in asthmatic patients the number of MC(TC) was significantly related to the vascular area (r(s) = 0.74, P &lt; .01) and to the number of VEGF(+) cells (r(s) = 0.78, P &lt; .01).	Methylcholanthrene	50-52	vascular endothelial growth factor A	Homo sapiens	151-155
17559912-12	2007	CONCLUSION: MC(TC) can play a role in the vascular component of airway remodeling in asthma, possibly through induction of VEGF.	Methylcholanthrene	12-14	vascular endothelial growth factor A	Homo sapiens	123-127
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	Fc epsilon receptor Ia	Homo sapiens	110-122
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	colony stimulating factor 2	Homo sapiens	179-185
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	interleukin 6	Homo sapiens	187-191
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	interleukin 13	Homo sapiens	193-198
17617628-5	2007	MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.	Methylcholanthrene	0-2	tumor necrosis factor	Homo sapiens	204-213
17395225-4	2007	With regard to its mechanism of action, MC suppressed the activating phosphorylation of Syk, a key enzyme in mast-cell signaling processes and that of Akt in a dose-dependent manner.	Methylcholanthrene	40-42	spleen tyrosine kinase	Mus musculus	88-91
17435107-8	2007	Hepatic deletion of POR and the subsequent increase in P450 expression were dependent on inducer dose, with maximal POR deletion occurring at a single dose of 3-methylcholanthrene of 40 mg/kg.	Methylcholanthrene	159-179	cytochrome p450 oxidoreductase	Mus musculus	20-23
17435107-8	2007	Hepatic deletion of POR and the subsequent increase in P450 expression were dependent on inducer dose, with maximal POR deletion occurring at a single dose of 3-methylcholanthrene of 40 mg/kg.	Methylcholanthrene	159-179	cytochrome p450 oxidoreductase	Mus musculus	116-119
17576390-4	2007	The BCL-6 gene (area B) was cloned and sequenced from peripheral blood mononuclear cells (PBMC) of 21 chronically HCV-infected patients with or without MC and B-NHL, and six healthy controls.	Methylcholanthrene	92-94	BCL6 transcription repressor	Homo sapiens	4-9
17524464-3	2007	Here we identify a motif (MC) within the Mid domain of Ago proteins, which bears significant similarity to the m(7)G cap-binding domain of eIF4E, an essential translation initiation factor.	Methylcholanthrene	26-28	eukaryotic translation initiation factor 4E	Homo sapiens	139-144
17524464-4	2007	We identify conserved aromatic residues within the MC motif of human Ago2 that are required for binding to the m(7)G cap and for translational repression but do not affect the assembly of Ago2 with miRNA or its catalytic activity.	Methylcholanthrene	51-53	argonaute RISC catalytic component 2	Homo sapiens	69-73
17395225-4	2007	With regard to its mechanism of action, MC suppressed the activating phosphorylation of Syk, a key enzyme in mast-cell signaling processes and that of Akt in a dose-dependent manner.	Methylcholanthrene	40-42	thymoma viral proto-oncogene 1	Mus musculus	151-154
17395225-6	2007	Taken together, these results suggest that the anti-allergic activity of MC may be due to the inhibition of histamine secretion and cytokine expression through the Syk inhibition in mast cells.	Methylcholanthrene	73-75	spleen tyrosine kinase	Mus musculus	164-167
17187281-11	2007	In addition, no significant differences in gene expressions of MMPs were seen in either ligament, except that gene expression of MMP-13 was significantly lower at 7 days in Group MH than in Group MC (P&lt;0.05).	Methylcholanthrene	196-198	matrix metallopeptidase 13	Rattus norvegicus	129-135
17727064-10	2007	RESULTS: It was found that the concentrations of IFN-gamma was significantly lower in cultures with the drug-containing serum taken at 1-1.5 h after the treatment than that in cultures with the MC control serum (P &lt; 0.01).	Methylcholanthrene	194-196	interferon gamma	Mus musculus	49-58
17255103-8	2007	MC-elicited currents from zSMCTe were similar to hSMCT currents.	Methylcholanthrene	0-2	solute carrier family 5 member 8, like	Danio rerio	26-32
17371978-4	2007	It was found that MCA-induced tumor incidence and growth were significantly attenuated in IL-5 transgenic mice of both the BALB/c and C57BL/6 backgrounds.	Methylcholanthrene	18-21	interleukin 5	Mus musculus	90-94
17132692-8	2007	CD95-ligation was obtained by treatment of cultured MC with the anti-CD95 Ab CH11.	Methylcholanthrene	52-54	Fas cell surface death receptor	Homo sapiens	0-4
17132692-8	2007	CD95-ligation was obtained by treatment of cultured MC with the anti-CD95 Ab CH11.	Methylcholanthrene	52-54	Fas cell surface death receptor	Homo sapiens	69-73
17227672-5	2007	The Leu-substituted mutant, AhR(Phe318Leu), activated the luciferase activity to the level comparable to wild type in the cells treated with 3-methylcholanthrene (MC) but not at all with beta-naphthoflavone (beta-NF).	Methylcholanthrene	141-161	aryl hydrocarbon receptor	Homo sapiens	28-31
17276403-0	2007	3-Methylcholanthrene elicits DNA adduct formation in the CYP1A1 promoter region and attenuates reporter gene expression in rat H4IIE cells.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-63
17276403-2	2007	Here, we tested the hypothesis that CYP1A2 catalyzes formation of MC-DNA adducts that are preferentially formed in the promoter region of CYP1A1, resulting in modulation of CYP1A1 gene expression.	Methylcholanthrene	66-68	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	36-42
17276403-2	2007	Here, we tested the hypothesis that CYP1A2 catalyzes formation of MC-DNA adducts that are preferentially formed in the promoter region of CYP1A1, resulting in modulation of CYP1A1 gene expression.	Methylcholanthrene	66-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	138-144
17276403-2	2007	Here, we tested the hypothesis that CYP1A2 catalyzes formation of MC-DNA adducts that are preferentially formed in the promoter region of CYP1A1, resulting in modulation of CYP1A1 gene expression.	Methylcholanthrene	66-68	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	173-179
17276403-3	2007	MC bound covalently to plasmid DNA (50 micro g) containing human CYP1A1 promoter (pGL3-1A1), when incubated with wild-type (WT) liver microsomes (2 mg) and NAPPH 37 degrees C for 2h, giving rise to 9 adducts, as determined by (32)P-postlabeling.	Methylcholanthrene	0-2	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	65-71
17276403-6	2007	Our results suggest that CYP1A2 plays a key role in sequence-specific MC-DNA adduct formation in the CYP1A1 promoter region, leading to attenuation of CYP1A1 gene expression.	Methylcholanthrene	70-72	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	25-31
17276403-6	2007	Our results suggest that CYP1A2 plays a key role in sequence-specific MC-DNA adduct formation in the CYP1A1 promoter region, leading to attenuation of CYP1A1 gene expression.	Methylcholanthrene	70-72	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-107
17276403-6	2007	Our results suggest that CYP1A2 plays a key role in sequence-specific MC-DNA adduct formation in the CYP1A1 promoter region, leading to attenuation of CYP1A1 gene expression.	Methylcholanthrene	70-72	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	151-157
17227672-5	2007	The Leu-substituted mutant, AhR(Phe318Leu), activated the luciferase activity to the level comparable to wild type in the cells treated with 3-methylcholanthrene (MC) but not at all with beta-naphthoflavone (beta-NF).	Methylcholanthrene	163-165	aryl hydrocarbon receptor	Homo sapiens	28-31
17227672-8	2007	[3H]MC bound by AhR(Phe318Leu) was competed with unlabeled MC but not with beta-NF.	Methylcholanthrene	4-6	aryl hydrocarbon receptor	Homo sapiens	16-19
17227672-8	2007	[3H]MC bound by AhR(Phe318Leu) was competed with unlabeled MC but not with beta-NF.	Methylcholanthrene	59-61	aryl hydrocarbon receptor	Homo sapiens	16-19
17151192-0	2007	Constitutive and 3-methylcholanthrene-induced rat ALDH3A1 expression is mediated by multiple xenobiotic response elements.	Methylcholanthrene	17-37	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	50-57
17230597-3	2007	In order to determine whether 5-fluorouracil is metabolized via CYP1A2 in male Sprague-Dawley rats, the rats were pretreated with 3-methylcholanthrene (a main inducer of CYP1A1/2 in rats).	Methylcholanthrene	130-150	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	64-70
17230597-3	2007	In order to determine whether 5-fluorouracil is metabolized via CYP1A2 in male Sprague-Dawley rats, the rats were pretreated with 3-methylcholanthrene (a main inducer of CYP1A1/2 in rats).	Methylcholanthrene	130-150	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	170-176
17151192-9	2007	We also demonstrate that 3-methylcholanthrene induces ALDH3A1 expression above high constitutive background in corneal epithelial cells.	Methylcholanthrene	25-45	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	54-61
16950798-7	2007	3-MC induced a 4-fold increase of the mutant frequency of the lacI gene in the liver.	Methylcholanthrene	0-4	tissue factor pathway inhibitor	Rattus norvegicus	62-66
17927507-0	2007	Effect of oral administration of Butyrivibrio fibrisolvens MDT-1, a gastrointestinal bacterium, on 3-methylcholanthrene-induced tumor in mice.	Methylcholanthrene	99-119	retinol dehydrogenase 11	Mus musculus	59-64
17584130-10	2007	The non-specific "superpotent" MC agonist, PT-141, which is the carboxylate derivative of MT-II, has reached phase II human trials.	Methylcholanthrene	31-33	metallothionein 2A	Homo sapiens	90-95
17377406-7	2007	RESULTS: Vitamin A exerted an in vitro inhibitory effect on the production of the anti-inflammatory cytokine IL-1ra by MC of preterm newborns and adults, but did not affect the secretion of the pro-inflammatory cytokines IL-1beta, IL-6 and IFNgamma.	Methylcholanthrene	119-121	interleukin 1 receptor antagonist	Homo sapiens	109-115
17679024-4	2007	Carcinomas with MC commonly possessed the MUC2+ phenotype (90.9-100%), and 76.6-83.3% possessed either the MUC2+/MUC5AC+/MUC1+ or the MUC2+/MUC5AC-/MUC1+ phenotype.	Methylcholanthrene	16-18	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	42-46
17679024-6	2007	Frequencies of p53 overexpression of carcinomas with MC were significantly lower compared to those without MC (21-27% vs. 55%).	Methylcholanthrene	53-55	tumor protein p53	Homo sapiens	15-18
17679024-8	2007	These results indicate that colorectal carcinomas with MC can be grouped together as goblet cell type (MUC2+) carcinoma.	Methylcholanthrene	55-57	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	103-107
17927507-2	2007	Oral administration of MDT-1 (10(9) cfu/dose, 3 times a wk for 15 wk) delayed the onset of tumors induced by 3-methylcholanthrene and also reduced tumor incidence in mice.	Methylcholanthrene	109-129	retinol dehydrogenase 11	Mus musculus	23-28
17222212-0	2006	Immunohistochemical detection of myogenin and p21 in methylcholanthrene-induced mouse rhabdomyosarcomas.	Methylcholanthrene	53-71	myogenin	Mus musculus	33-41
17539306-4	2007	RESULTS: Relative gene expression of TLR2/4 in MC group were significantly higher than that in NC group (P &lt; 0.01).	Methylcholanthrene	47-49	toll-like receptor 2	Rattus norvegicus	37-43
17539306-5	2007	Relative gene expression of TLR2 in KMD and KHD group was significantly lower than that in MC group (P &lt; 0.05).	Methylcholanthrene	91-93	toll-like receptor 2	Rattus norvegicus	28-32
17069994-8	2006	Expression of AhR mRNA and of the markers of its activation, CYP1A1 and NQO1, was significantly increased by administration of TCDD, 3-MC and, to lower extent, BNF.	Methylcholanthrene	133-137	aryl hydrocarbon receptor	Rattus norvegicus	14-17
17069994-8	2006	Expression of AhR mRNA and of the markers of its activation, CYP1A1 and NQO1, was significantly increased by administration of TCDD, 3-MC and, to lower extent, BNF.	Methylcholanthrene	133-137	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	61-67
17069994-8	2006	Expression of AhR mRNA and of the markers of its activation, CYP1A1 and NQO1, was significantly increased by administration of TCDD, 3-MC and, to lower extent, BNF.	Methylcholanthrene	133-137	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	72-76
16782735-8	2007	BLyS serum levels tended to be higher in HCV-infected patients than in healthy controls (1.8 +/- 0.9 vs 1.5 +/- 0.2 ng/ml), were higher in patients with MC than without (2.03 +/- 1.02 vs 1.5 +/- 0.5 ng/ml; P = 0.008), and even higher in type II than type III MC (2.3 +/- 1.2 vs 1.7 +/- 0.6 ng/ml; P = 0.03).	Methylcholanthrene	153-155	TNF superfamily member 13b	Homo sapiens	0-4
16782735-8	2007	BLyS serum levels tended to be higher in HCV-infected patients than in healthy controls (1.8 +/- 0.9 vs 1.5 +/- 0.2 ng/ml), were higher in patients with MC than without (2.03 +/- 1.02 vs 1.5 +/- 0.5 ng/ml; P = 0.008), and even higher in type II than type III MC (2.3 +/- 1.2 vs 1.7 +/- 0.6 ng/ml; P = 0.03).	Methylcholanthrene	259-261	TNF superfamily member 13b	Homo sapiens	0-4
16782735-9	2007	There was a correlation between BLyS and MC serum levels (R = 0.4; P = 0.004).	Methylcholanthrene	41-43	TNF superfamily member 13b	Homo sapiens	32-36
17006743-2	2006	The purpose of this in vivo study was to investigate intestinal glutamine transport and expression of glutamine transporter ATB(0) in methyl-cholanthrene (MCA)-sarcoma bearing rats.	Methylcholanthrene	134-153	solute carrier family 6 member 14	Rattus norvegicus	124-130
17006743-2	2006	The purpose of this in vivo study was to investigate intestinal glutamine transport and expression of glutamine transporter ATB(0) in methyl-cholanthrene (MCA)-sarcoma bearing rats.	Methylcholanthrene	155-158	solute carrier family 6 member 14	Rattus norvegicus	124-130
17222212-0	2006	Immunohistochemical detection of myogenin and p21 in methylcholanthrene-induced mouse rhabdomyosarcomas.	Methylcholanthrene	53-71	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	46-49
17032394-10	2006	VEGF-positive and bFGF-positive MC and GC were found in nearly all lesions and in less than half of the lesions, respectively.	Methylcholanthrene	32-34	fibroblast growth factor 2	Homo sapiens	18-22
17256436-6	2006	Clinicopathologically, the MC type showed higher rates of venous invasion, lymph node metastasis, liver metastasis, and peritoneal dissemination and higher frequencies of TNM stage III and IV cancers than the PT type.	Methylcholanthrene	27-29	teneurin transmembrane protein 1	Homo sapiens	171-174
17116258-13	2006	In one (6.7%) MC cancer two different pathways were found, each of them affering to a different SLN.	Methylcholanthrene	14-16	sarcolipin	Homo sapiens	96-99
16945501-1	2006	During the conduct of a study designed to determine the effect of 3-methylcholanthrene (3-MC), a synthetic polycyclic aromatic hydrocarbon (PAH) that acts through the aryl hydrocarbon receptor (AhR), on uterine contractility in Wistar rats, uterine tumors were identified in both vehicle and 3-MC-treated animals.	Methylcholanthrene	88-92	aryl hydrocarbon receptor	Rattus norvegicus	194-197
17032394-7	2006	Immunoreactivity of the MC and GC was assessed as the percentage of VEGF- and bFGF-positive cells from the total number of the respective cell type.	Methylcholanthrene	24-26	vascular endothelial growth factor A	Homo sapiens	68-72
17032394-7	2006	Immunoreactivity of the MC and GC was assessed as the percentage of VEGF- and bFGF-positive cells from the total number of the respective cell type.	Methylcholanthrene	24-26	fibroblast growth factor 2	Homo sapiens	78-82
16945501-1	2006	During the conduct of a study designed to determine the effect of 3-methylcholanthrene (3-MC), a synthetic polycyclic aromatic hydrocarbon (PAH) that acts through the aryl hydrocarbon receptor (AhR), on uterine contractility in Wistar rats, uterine tumors were identified in both vehicle and 3-MC-treated animals.	Methylcholanthrene	292-296	aryl hydrocarbon receptor	Rattus norvegicus	194-197
16945501-1	2006	During the conduct of a study designed to determine the effect of 3-methylcholanthrene (3-MC), a synthetic polycyclic aromatic hydrocarbon (PAH) that acts through the aryl hydrocarbon receptor (AhR), on uterine contractility in Wistar rats, uterine tumors were identified in both vehicle and 3-MC-treated animals.	Methylcholanthrene	66-86	aryl hydrocarbon receptor	Rattus norvegicus	167-192
16945501-1	2006	During the conduct of a study designed to determine the effect of 3-methylcholanthrene (3-MC), a synthetic polycyclic aromatic hydrocarbon (PAH) that acts through the aryl hydrocarbon receptor (AhR), on uterine contractility in Wistar rats, uterine tumors were identified in both vehicle and 3-MC-treated animals.	Methylcholanthrene	66-86	aryl hydrocarbon receptor	Rattus norvegicus	194-197
16945501-1	2006	During the conduct of a study designed to determine the effect of 3-methylcholanthrene (3-MC), a synthetic polycyclic aromatic hydrocarbon (PAH) that acts through the aryl hydrocarbon receptor (AhR), on uterine contractility in Wistar rats, uterine tumors were identified in both vehicle and 3-MC-treated animals.	Methylcholanthrene	88-92	aryl hydrocarbon receptor	Rattus norvegicus	167-192
16956241-5	2006	In addition, the possible mechanism for generating BN film via B(N3)(3) was discussed based on MC-SCF calculation results.	Methylcholanthrene	95-97	KIT ligand	Homo sapiens	98-101
16868070-6	2006	Significant expression of CYP1A1/2 and 3A2 in the cells treated with Matrigel was induced by 3-MC and PCN, respectively.	Methylcholanthrene	93-97	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	26-32
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	24-44	estrogen receptor 1	Homo sapiens	65-82
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	24-44	estrogen receptor 1	Homo sapiens	84-86
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	178-181	estrogen receptor 1	Homo sapiens	211-218
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	24-44	aryl hydrocarbon receptor	Homo sapiens	100-103
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	46-49	estrogen receptor 1	Homo sapiens	65-82
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	46-49	estrogen receptor 1	Homo sapiens	84-86
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	46-49	aryl hydrocarbon receptor	Homo sapiens	100-103
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	178-181	estrogen receptor 1	Homo sapiens	65-82
16972788-2	2006	One study reported that 3-methylcholanthrene (3MC) activated the estrogen receptor (ER) through the AhR, which acts as co-regulatory protein, whereas a recent report showed that 3MC directly bound and activated ERalpha.	Methylcholanthrene	178-181	estrogen receptor 1	Homo sapiens	84-86
16782765-0	2006	Regulation of constitutive mouse hepatic cytochromes P450 and growth hormone signaling components by 3-methylcholanthrene.	Methylcholanthrene	101-121	growth hormone	Mus musculus	62-76
16968971-6	2006	Exposure to the prototypical Cyp1A1 inducer, 3-methylcholanthrene, 3-MC, resulted in the translocation of SPT1 from a primarily cytoplasmic domain to sites of focal adhesion complexes.	Methylcholanthrene	45-65	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	29-35
16968971-6	2006	Exposure to the prototypical Cyp1A1 inducer, 3-methylcholanthrene, 3-MC, resulted in the translocation of SPT1 from a primarily cytoplasmic domain to sites of focal adhesion complexes.	Methylcholanthrene	45-65	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	106-110
16968971-6	2006	Exposure to the prototypical Cyp1A1 inducer, 3-methylcholanthrene, 3-MC, resulted in the translocation of SPT1 from a primarily cytoplasmic domain to sites of focal adhesion complexes.	Methylcholanthrene	67-71	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	29-35
16968971-6	2006	Exposure to the prototypical Cyp1A1 inducer, 3-methylcholanthrene, 3-MC, resulted in the translocation of SPT1 from a primarily cytoplasmic domain to sites of focal adhesion complexes.	Methylcholanthrene	67-71	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	106-110
16968971-8	2006	When compared to the wild type, cells transfected with recombinant SPT1-GFP vectors had significantly attenuated levels of 3-MC-induced Cyp1A1 mRNA, as determined by quantitative reverse transcription PCR.	Methylcholanthrene	123-127	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	67-71
16968971-8	2006	When compared to the wild type, cells transfected with recombinant SPT1-GFP vectors had significantly attenuated levels of 3-MC-induced Cyp1A1 mRNA, as determined by quantitative reverse transcription PCR.	Methylcholanthrene	123-127	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	136-142
16968971-9	2006	Although all the Glioma cell lines exhibited mitogenic proliferative response in dose response assay with the potent Cyp1A1 inducers 3-MC, 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and benzo [k] fluoranthene, BKF, only the recombinant cell line designated - 75SPT1-GFP, which was transfected with a mutant deletion of SPT1, retained its proliferative capacity at the highest PAH doses used in this study.	Methylcholanthrene	133-137	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	117-123
16782765-1	2006	3-Methylcholanthrene (MC) activates the aryl hydrocarbon receptor and increases expression of cytochrome P450 (P450) enzymes such as CYP1A1.	Methylcholanthrene	0-20	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	94-115
16782765-1	2006	3-Methylcholanthrene (MC) activates the aryl hydrocarbon receptor and increases expression of cytochrome P450 (P450) enzymes such as CYP1A1.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	133-139
16782765-1	2006	3-Methylcholanthrene (MC) activates the aryl hydrocarbon receptor and increases expression of cytochrome P450 (P450) enzymes such as CYP1A1.	Methylcholanthrene	22-24	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	94-115
16782765-1	2006	3-Methylcholanthrene (MC) activates the aryl hydrocarbon receptor and increases expression of cytochrome P450 (P450) enzymes such as CYP1A1.	Methylcholanthrene	22-24	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	133-139
16782765-2	2006	MC also decreases expression of CYP2C11, the major hepatic P450 in male rats that is regulated by pulsatile growth hormone (GH) secretion via a pathway partially dependent on signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	32-39
16782765-2	2006	MC also decreases expression of CYP2C11, the major hepatic P450 in male rats that is regulated by pulsatile growth hormone (GH) secretion via a pathway partially dependent on signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	gonadotropin releasing hormone receptor	Rattus norvegicus	108-122
16782765-2	2006	MC also decreases expression of CYP2C11, the major hepatic P450 in male rats that is regulated by pulsatile growth hormone (GH) secretion via a pathway partially dependent on signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	gonadotropin releasing hormone receptor	Rattus norvegicus	124-126
16782765-2	2006	MC also decreases expression of CYP2C11, the major hepatic P450 in male rats that is regulated by pulsatile growth hormone (GH) secretion via a pathway partially dependent on signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	signal transducer and activator of transcription 5B	Rattus norvegicus	175-226
16782765-2	2006	MC also decreases expression of CYP2C11, the major hepatic P450 in male rats that is regulated by pulsatile growth hormone (GH) secretion via a pathway partially dependent on signal transducer and activator of transcription 5b (STAT5b).	Methylcholanthrene	0-2	signal transducer and activator of transcription 5B	Rattus norvegicus	228-234
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	60-62	growth hormone	Mus musculus	22-24
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	60-62	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	85-92
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	60-62	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	181-187
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	60-62	growth hormone	Mus musculus	212-214
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	60-62	signal transducer and activator of transcription 5B	Mus musculus	220-226
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	128-130	growth hormone	Mus musculus	22-24
16782765-3	2006	If disruption of this GH signaling pathway is important for MC"s ability to suppress CYP2C11 transcription, we hypothesize that MC suppresses other male-specific genes (e.g., mouse Cyp2d9) regulated by pulsatile GH with STAT5b dependence.	Methylcholanthrene	128-130	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	181-187
16782765-4	2006	We examined the time course of MC"s effects on hepatic P450s and GH signaling components in male C57BL/6 mice.	Methylcholanthrene	31-33	growth hormone	Mus musculus	65-67
16917891-8	2006	Examination of a representative region in exon 12 (and also in exon 7) in the PAH gene shows that 5 mC is restricted to cytosines in CpG dinucleotides in the hypermutable codons.	Methylcholanthrene	100-102	phenylalanine hydroxylase	Homo sapiens	78-81
16782765-6	2006	MC dramatically induced CYP1A1 mRNA, protein, and catalytic activity.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	24-30
16782765-7	2006	MC caused a 42% decrease in CYP2D9 protein, a 28% decrease in CYP2D9 mRNA, and a 27% decrease in testosterone 16alpha-hydroxylation activity.	Methylcholanthrene	0-2	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	28-34
16782765-7	2006	MC caused a 42% decrease in CYP2D9 protein, a 28% decrease in CYP2D9 mRNA, and a 27% decrease in testosterone 16alpha-hydroxylation activity.	Methylcholanthrene	0-2	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	62-68
16782765-8	2006	MC caused a pronounced decrease in CYP3A protein; however, there was no apparent change in testosterone 6beta-hydroxylation activity, and changes in mRNA levels for CYP3A forms were relatively small.	Methylcholanthrene	0-2	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	35-40
16782765-9	2006	Expression of GH receptor and major urinary protein 2, a gene regulated by GH with STAT5b dependence, was decreased by MC at the mRNA level.	Methylcholanthrene	119-121	growth hormone	Mus musculus	14-16
16782765-9	2006	Expression of GH receptor and major urinary protein 2, a gene regulated by GH with STAT5b dependence, was decreased by MC at the mRNA level.	Methylcholanthrene	119-121	signal transducer and activator of transcription 5B	Mus musculus	83-89
16782765-10	2006	These results show that MC suppresses mouse Cyp2d9, a pulsatile GH- and STAT5b-dependent male-specific gene, via a pretranslational mechanism that may involve disrupted GH signaling.	Methylcholanthrene	24-26	cytochrome P450, family 2, subfamily d, polypeptide 9	Mus musculus	44-50
16782765-10	2006	These results show that MC suppresses mouse Cyp2d9, a pulsatile GH- and STAT5b-dependent male-specific gene, via a pretranslational mechanism that may involve disrupted GH signaling.	Methylcholanthrene	24-26	growth hormone	Mus musculus	64-66
16782765-10	2006	These results show that MC suppresses mouse Cyp2d9, a pulsatile GH- and STAT5b-dependent male-specific gene, via a pretranslational mechanism that may involve disrupted GH signaling.	Methylcholanthrene	24-26	signal transducer and activator of transcription 5B	Mus musculus	72-78
16782765-10	2006	These results show that MC suppresses mouse Cyp2d9, a pulsatile GH- and STAT5b-dependent male-specific gene, via a pretranslational mechanism that may involve disrupted GH signaling.	Methylcholanthrene	24-26	growth hormone	Mus musculus	169-171
16782765-11	2006	Mouse CYP3A protein levels are dramatically decreased by MC via a mechanism that is not yet understood.	Methylcholanthrene	57-59	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	6-11
16867264-0	2006	Influences of 3-methylcholanthrene, phenobarbital and dexamethasone on xenobiotic metabolizing-related cytochrome P450 enzymes and steroidogenesis in human fetal adrenal cortical cells.	Methylcholanthrene	14-34	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	103-118
16867264-11	2006	CONCLUSION: 3-Methylcholanthrene, phenobarbital or dexamethasone could interfere with the synthesis of cortisol, aldosterone and progesterone in primary human fetal adrenal cortical cells, which likely act through xenobiotic metabolizing-related cytochrome P450 isoform activation.	Methylcholanthrene	12-32	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	246-261
16608922-5	2006	TPA, 3-MC, BHA, and PB reduced HNF1alpha mRNA levels in preconfluent and confluent cells and caused marked reductions in luciferase activity in pGSTA1-1591-luc transfectants.	Methylcholanthrene	5-9	HNF1 homeobox A	Homo sapiens	31-40
16953078-6	2006	Caspase-3 activation was observed after retinoid treatment in CM-MC cells.	Methylcholanthrene	65-67	caspase 3	Canis lupus familiaris	0-9
16864695-4	2006	Here we tested the hypothesis that their generation of Mc-MPhi via IL-10 is also impaired.	Methylcholanthrene	55-57	interleukin 10	Homo sapiens	67-72
16723119-0	2006	Induction of 26S proteasome subunit PSMB5 by the bifunctional inducer 3-methylcholanthrene through the Nrf2-ARE, but not the AhR/Arnt-XRE, pathway.	Methylcholanthrene	70-90	proteasome (prosome, macropain) subunit, beta type 5	Mus musculus	36-41
16723119-0	2006	Induction of 26S proteasome subunit PSMB5 by the bifunctional inducer 3-methylcholanthrene through the Nrf2-ARE, but not the AhR/Arnt-XRE, pathway.	Methylcholanthrene	70-90	nuclear factor, erythroid derived 2, like 2	Mus musculus	103-107
16723119-4	2006	Expression of catalytic core subunits including PSMB5 and peptidase activities of the proteasome were elevated following incubation with 3-methylcholanthrene (3-MC).	Methylcholanthrene	137-157	proteasome (prosome, macropain) subunit, beta type 5	Mus musculus	48-53
16723119-4	2006	Expression of catalytic core subunits including PSMB5 and peptidase activities of the proteasome were elevated following incubation with 3-methylcholanthrene (3-MC).	Methylcholanthrene	159-163	proteasome (prosome, macropain) subunit, beta type 5	Mus musculus	48-53
16723119-5	2006	Studies using reporter genes containing the murine Psmb5 promoter showed that transcriptional activity of this gene was enhanced by 3-MC.	Methylcholanthrene	132-136	proteasome (prosome, macropain) subunit, beta type 5	Mus musculus	51-56
16723119-7	2006	However, mutation of the proximal AREs of the Psmb5 promoter largely abrogated its inducibility by 3-MC.	Methylcholanthrene	99-103	proteasome (prosome, macropain) subunit, beta type 5	Mus musculus	46-51
16723119-8	2006	In addition, this promoter showed a blunted response toward 3-MC in the absence of nrf2; 3-MC incubation increased nuclear levels of Nrf2 only in wild-type cells.	Methylcholanthrene	60-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	133-137
16723119-8	2006	In addition, this promoter showed a blunted response toward 3-MC in the absence of nrf2; 3-MC incubation increased nuclear levels of Nrf2 only in wild-type cells.	Methylcholanthrene	89-93	nuclear factor, erythroid derived 2, like 2	Mus musculus	133-137
16784979-9	2006	Cytokeratin 7 staining was occasionally observed in both MC (9.1%, 5/55 cases) and conventional adenocarcinoma (13.4%, 16/119 cases).	Methylcholanthrene	57-59	keratin 7	Homo sapiens	0-13
16723984-8	2006	In cultured MC and PTC, aldosterone induced significant increases in CTGF gene expression and protein synthesis associated with increased collagen synthesis, which was abolished by prior treatment with spironolactone.	Methylcholanthrene	12-14	cellular communication network factor 2	Rattus norvegicus	69-73
16891458-5	2006	In addition, MC exhibited much enhanced IL-12 gene transfer efficiency to dendritic cells rather than chitosan itself in terms of the induction of murine IL-12 p70 and murine IFN-gamma.	Methylcholanthrene	13-15	interferon gamma	Mus musculus	175-184
16808479-6	2006	The MC-ICPMS is run at a high mass resolution of &gt;/=10 000 to eliminate interference of mass 37 ArH with Cl.	Methylcholanthrene	4-6	low density lipoprotein receptor adaptor protein 1	Homo sapiens	99-102
16586464-6	2006	In rats pretreated with 3-methylcholanthrene and dexamethasone (main inducers of CYP1A1/2 and 3A1/2 in rats, respectively), the Cl(nr) values were significantly faster (43.8% and 26.3% increase, respectively).	Methylcholanthrene	24-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-87
16608922-8	2006	Immunoblot analysis of DNA binding studies indicate that variant (v)HNF1-C binding to HRE is increased in preconfluent cells treated with 3-MC, BHA, and PB.	Methylcholanthrene	138-142	HNF1 homeobox A	Homo sapiens	68-72
16608922-10	2006	Finally, treatment with 3-MC, BHA, and PB increased vHNF1-C mRNA levels in preconfluent cells.	Methylcholanthrene	24-28	HNF1 homeobox B	Homo sapiens	52-57
16651740-3	2006	mRNA expression in liver, duodenum, jejunum and ileum was examined in mice, which were treated with microsomal enzyme inducers-aryl hydrocarbon receptor (AhR) ligands 3-methylcholanthrene (3-MC) and pregnane-x-receptor (PXR) ligand pregenolone-16alpha-carbonitrile (PCN) and compared with control vehicle.	Methylcholanthrene	167-187	aryl-hydrocarbon receptor	Mus musculus	154-157
16825254-5	2006	Local production of VEGF by transitional MC appears to play a central role in the processes leading to peritoneal angiogenesis.	Methylcholanthrene	41-43	vascular endothelial growth factor A	Homo sapiens	20-24
16246473-4	2006	A factor analysis of the 18 different operational conditions under investigation indicated that the optimal operational conditions for degradation of PAHs occurred at MC 60%, S:GW 0.8:1 and T 38 degrees C. Thus, it is recommended to maintain operational conditions during in-vessel composting of PAH-solid waste close to these values.	Methylcholanthrene	167-169	phenylalanine hydroxylase	Homo sapiens	150-153
16257430-0	2006	Aryl hydrocarbon receptor-independent activation of estrogen receptor-dependent transcription by 3-methylcholanthrene.	Methylcholanthrene	97-117	aryl hydrocarbon receptor	Homo sapiens	0-25
16257430-3	2006	Presently, we investigate the effect of the AhR ligands 3-methylcholanthrene (3MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3,3",4,4",5-pentachlorobiphenyl (BZ126) on ERE-regulated luciferase reporter activity and endogenous ER target gene expression.	Methylcholanthrene	56-76	aryl hydrocarbon receptor	Homo sapiens	44-47
16257430-3	2006	Presently, we investigate the effect of the AhR ligands 3-methylcholanthrene (3MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3,3",4,4",5-pentachlorobiphenyl (BZ126) on ERE-regulated luciferase reporter activity and endogenous ER target gene expression.	Methylcholanthrene	78-81	aryl hydrocarbon receptor	Homo sapiens	44-47
16257430-4	2006	In MCF-7 human breast cancer cells, 3MC induced transcription of ER reporter genes containing native promoter sequences of the ER-responsive genes complement 3 and pS2 and heterologous promoters regulated by isolated EREs.	Methylcholanthrene	36-39	trefoil factor 1	Homo sapiens	164-167
16257430-6	2006	3MC also stimulated expression of the endogenous ER target genes amphiregulin, cathepsin D and progesterone receptor, albeit to a much lower extent than was achieved following stimulation with 17beta-estradiol.	Methylcholanthrene	0-3	amphiregulin	Homo sapiens	65-77
16257430-6	2006	3MC also stimulated expression of the endogenous ER target genes amphiregulin, cathepsin D and progesterone receptor, albeit to a much lower extent than was achieved following stimulation with 17beta-estradiol.	Methylcholanthrene	0-3	cathepsin D	Homo sapiens	79-90
16257430-6	2006	3MC also stimulated expression of the endogenous ER target genes amphiregulin, cathepsin D and progesterone receptor, albeit to a much lower extent than was achieved following stimulation with 17beta-estradiol.	Methylcholanthrene	0-3	progesterone receptor	Homo sapiens	95-116
16257430-8	2006	Finally, studies carried out in the AhR-positive rat hepatoma cell line 5L and the AhR-deficient variant BP8 demonstrated that ER reporter activity could be induced by 3MC in a manner that was independent of AhR and thus distinct from the AhR-ER "hijacking" mechanism described recently.	Methylcholanthrene	168-171	aryl hydrocarbon receptor	Rattus norvegicus	36-39
16257430-8	2006	Finally, studies carried out in the AhR-positive rat hepatoma cell line 5L and the AhR-deficient variant BP8 demonstrated that ER reporter activity could be induced by 3MC in a manner that was independent of AhR and thus distinct from the AhR-ER "hijacking" mechanism described recently.	Methylcholanthrene	168-171	aryl hydrocarbon receptor	Rattus norvegicus	83-86
16257430-8	2006	Finally, studies carried out in the AhR-positive rat hepatoma cell line 5L and the AhR-deficient variant BP8 demonstrated that ER reporter activity could be induced by 3MC in a manner that was independent of AhR and thus distinct from the AhR-ER "hijacking" mechanism described recently.	Methylcholanthrene	168-171	Blood pressure QTL 8	Rattus norvegicus	105-108
16257430-8	2006	Finally, studies carried out in the AhR-positive rat hepatoma cell line 5L and the AhR-deficient variant BP8 demonstrated that ER reporter activity could be induced by 3MC in a manner that was independent of AhR and thus distinct from the AhR-ER "hijacking" mechanism described recently.	Methylcholanthrene	168-171	aryl hydrocarbon receptor	Rattus norvegicus	83-86
16257430-8	2006	Finally, studies carried out in the AhR-positive rat hepatoma cell line 5L and the AhR-deficient variant BP8 demonstrated that ER reporter activity could be induced by 3MC in a manner that was independent of AhR and thus distinct from the AhR-ER "hijacking" mechanism described recently.	Methylcholanthrene	168-171	aryl hydrocarbon receptor	Rattus norvegicus	83-86
16651740-3	2006	mRNA expression in liver, duodenum, jejunum and ileum was examined in mice, which were treated with microsomal enzyme inducers-aryl hydrocarbon receptor (AhR) ligands 3-methylcholanthrene (3-MC) and pregnane-x-receptor (PXR) ligand pregenolone-16alpha-carbonitrile (PCN) and compared with control vehicle.	Methylcholanthrene	189-193	aryl-hydrocarbon receptor	Mus musculus	154-157
16651740-5	2006	Mrp2 mRNA was significantly increased by both PCN and 3-MC treatment.	Methylcholanthrene	54-58	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	0-4
16651740-7	2006	In summary, this study demonstrated that the expression of mrp2 mRNA is regulated by PCN and 3-MC, however, bcrp mRNA expression was not significantly affected by PCN and 3-MC.	Methylcholanthrene	93-97	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	59-63
16595894-2	2006	We sequenced full-length AhRR mRNA extracted from the heart of a male Wistar rat injected intraperitoneally with 3-methylcholanthrene (3-MC) 24 h before.	Methylcholanthrene	113-133	aryl-hydrocarbon receptor repressor	Rattus norvegicus	25-29
16467433-3	2006	Here we characterized a slow mGluR1-mediated potential that was evoked by high-frequency (100-Hz) olfactory nerve (ON) stimulation in the presence of NBQX and D-APV, blockers of ionotropic glutamate receptors, and that was associated with a local Ca2+ transient in the MC dendritic tuft.	Methylcholanthrene	269-271	glutamate receptor, metabotropic 1	Mus musculus	29-35
16467433-4	2006	High-frequency ON stimulation in the presence of NBQX and D-APV also evoked a slow, nearly 2-Hz oscillation of MC membrane potential that was abolished by the mGluR1 antagonist LY367385 (50 microM).	Methylcholanthrene	111-113	glutamate receptor, metabotropic 1	Mus musculus	159-165
16467433-7	2006	Imaging with the Na+ indicator SBFI revealed a Na+ transient in the MC dendrite accompanying the mGluR1 slow potential.	Methylcholanthrene	68-70	glutamate receptor, metabotropic 1	Mus musculus	97-103
16596202-4	2006	The aim of this study was to evaluate whether abnormalities in the blood levels of IL-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and human IL-1 accessory protein in HCV+ patients are associated with development of MC and/or NHL.	Methylcholanthrene	233-235	interleukin 1 alpha	Homo sapiens	83-87
16596202-4	2006	The aim of this study was to evaluate whether abnormalities in the blood levels of IL-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and human IL-1 accessory protein in HCV+ patients are associated with development of MC and/or NHL.	Methylcholanthrene	233-235	interleukin 1 alpha	Homo sapiens	92-96
16596202-4	2006	The aim of this study was to evaluate whether abnormalities in the blood levels of IL-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and human IL-1 accessory protein in HCV+ patients are associated with development of MC and/or NHL.	Methylcholanthrene	233-235	interleukin 1 alpha	Homo sapiens	92-96
16596202-5	2006	Relative to healthy controls, we observed: i) an increase in the circulating levels of IL-1beta in HCV+ patients simultaneously affected by NHL; ii) increased levels of IL-1 accessory protein in patients singly infected by HCV; iii) increase of IL-1 receptor antagonist in HCV+ patients and in those affected also by NHL with or without MC; iv) a homogeneous increase of sIL-1R type II in all the subgroup of patients.	Methylcholanthrene	337-339	interleukin 1 alpha	Homo sapiens	169-173
16731765-4	2006	In this work, we tested the ability of aspirin to activate the AKT survival pathway in methylcholanthrene-induced fibrosarcoma cells (Meth A) transplanted into BALB/c nude mice and the clinical effect of aspirin cotreatment during etoposide (VP-16)-based anticancer therapy.	Methylcholanthrene	87-105	thymoma viral proto-oncogene 1	Mus musculus	63-66
16640786-4	2006	CONCLUSION: These results are in line with studies reporting the role of p53 as a post-transcriptional regulator of cyclin B1 protein and confirm that dysregulation of cyclin B1 promote radiation-induced MC.	Methylcholanthrene	204-206	transformation related protein 53, pseudogene	Mus musculus	73-76
16640786-4	2006	CONCLUSION: These results are in line with studies reporting the role of p53 as a post-transcriptional regulator of cyclin B1 protein and confirm that dysregulation of cyclin B1 promote radiation-induced MC.	Methylcholanthrene	204-206	cyclin B1	Mus musculus	168-177
16595894-2	2006	We sequenced full-length AhRR mRNA extracted from the heart of a male Wistar rat injected intraperitoneally with 3-methylcholanthrene (3-MC) 24 h before.	Methylcholanthrene	135-139	aryl-hydrocarbon receptor repressor	Rattus norvegicus	25-29
16595894-5	2006	Although AhRR was ubiquitously expressed in all tissues tested, the levels of AhRR expression were higher in the small intestine, where the 3-MC-dependent induction of CYP1A1 transcription was less significant, than in the heart, lung, liver, and kidney.	Methylcholanthrene	140-144	aryl-hydrocarbon receptor repressor	Rattus norvegicus	78-82
16595894-5	2006	Although AhRR was ubiquitously expressed in all tissues tested, the levels of AhRR expression were higher in the small intestine, where the 3-MC-dependent induction of CYP1A1 transcription was less significant, than in the heart, lung, liver, and kidney.	Methylcholanthrene	140-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	168-174
16595894-6	2006	The dose-dependent suppression of AhR-dependent transcriptional activation in both the presence and absence of 3-MC was observed in rat liver-derived RL-34 cells transiently transfected with the expression plasmid for AhRR in combination with the reporter plasmid.	Methylcholanthrene	111-115	aryl hydrocarbon receptor	Rattus norvegicus	34-37
16595894-6	2006	The dose-dependent suppression of AhR-dependent transcriptional activation in both the presence and absence of 3-MC was observed in rat liver-derived RL-34 cells transiently transfected with the expression plasmid for AhRR in combination with the reporter plasmid.	Methylcholanthrene	111-115	aryl-hydrocarbon receptor repressor	Rattus norvegicus	218-222
16597362-4	2006	In rats pretreated with 3-methylcholanthrene and phenobarbital (main inducers of CYP1A1/2 and 2B1/2 in rats, respectively), the CL values were significantly higher (153 and 67.2% increases, respectively).	Methylcholanthrene	24-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-99
16688995-6	2006	RESULTS: Levels of MC-CD54 expression and sVCAM-1 in the ACI patients increased obviously (P &lt; 0.01), reached the peak on the 7th day, and declined obviously on the 14th day in both groups, however, the lowering in the SI group was more significant than that in the control group (P &lt; 0.01); and positive correlation was shown between these two indexes (P &lt; 0.01).	Methylcholanthrene	19-21	intercellular adhesion molecule 1	Homo sapiens	22-26
16581968-3	2006	We report here for the first time that the Rac-activating toxin CNF1 interferes with the occurrence of MC and leads to aneuploidy and multinucleation.	Methylcholanthrene	103-105	AKT serine/threonine kinase 1	Homo sapiens	43-46
16427050-2	2006	We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53.	Methylcholanthrene	83-85	tumor protein p53	Homo sapiens	189-192
16427050-5	2006	The protein expression of retinoid X receptor (RXR), a partner of LXR to form a heterodimer, was suppressed by MC and Dox in HepG2 cells.	Methylcholanthrene	111-113	retinoid X receptor alpha	Homo sapiens	26-45
16427050-5	2006	The protein expression of retinoid X receptor (RXR), a partner of LXR to form a heterodimer, was suppressed by MC and Dox in HepG2 cells.	Methylcholanthrene	111-113	retinoid X receptor alpha	Homo sapiens	47-50
16183705-6	2006	On the other hand, YC-1 inhibited hydrolysis of the fluorogenic quenching substrate Mca-Pro-Leu-Gly-Leu-Dpa-Ala-Arg-NH(2) by recombinant MMP-2 and MMP-9 with IC(50) values = 2.07 and 8.20 muM, respectively.	Methylcholanthrene	84-87	glutathione S-transferase alpha 1	Rattus norvegicus	19-23
16489053-0	2006	3-Methylcholanthrene and other aryl hydrocarbon receptor agonists directly activate estrogen receptor alpha.	Methylcholanthrene	0-20	estrogen receptor 1	Homo sapiens	84-107
16337070-7	2006	Anti-CYP3A4 antibody markedly inhibited MB(2), MB(4), and MC formation and also 6 beta-hydroxytestosterone formation from testosterone.	Methylcholanthrene	58-60	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	5-11
16393975-1	2006	In this study, we show that IFN-gamma or IFN-alpha reduce expression of H60 on 3"-methylcholanthrene (MCA) sarcomas from 129/Sv mice.	Methylcholanthrene	79-100	interferon gamma	Mus musculus	28-37
16393975-1	2006	In this study, we show that IFN-gamma or IFN-alpha reduce expression of H60 on 3"-methylcholanthrene (MCA) sarcomas from 129/Sv mice.	Methylcholanthrene	79-100	interferon alpha	Mus musculus	41-50
16393975-1	2006	In this study, we show that IFN-gamma or IFN-alpha reduce expression of H60 on 3"-methylcholanthrene (MCA) sarcomas from 129/Sv mice.	Methylcholanthrene	79-100	histocompatibility 60a	Mus musculus	72-75
16359657-5	2006	In this study, we used an aryl hydrocarbon receptor agonist, 3-methylcholanthrene (3-MC), to investigate its effect on the proliferation and angiogenesis of human umbilical vascular endothelial cells.	Methylcholanthrene	61-81	aryl hydrocarbon receptor	Homo sapiens	26-51
16359657-5	2006	In this study, we used an aryl hydrocarbon receptor agonist, 3-methylcholanthrene (3-MC), to investigate its effect on the proliferation and angiogenesis of human umbilical vascular endothelial cells.	Methylcholanthrene	83-87	aryl hydrocarbon receptor	Homo sapiens	26-51
16359657-7	2006	Interestingly, the inhibition of DNA synthesis by 3-MC was eliminated to a greater extent by aryl hydrocarbon receptor antagonists, alpha-NF (0.5 and 1 microM) and resveratrol (5 and 10 microM), than by the antioxidant, N-acetylcysteine (5 and 10 mM).	Methylcholanthrene	50-54	aryl hydrocarbon receptor	Homo sapiens	93-118
16359657-10	2006	Additionally, alpha-naphthoflavon (alpha-NF) ameliorated the effects of 3-MC on cell permeability, adhesion and tube formation, indicating the involvement of the aryl hydrocarbon receptor in angiogenesis.	Methylcholanthrene	72-76	aryl hydrocarbon receptor	Homo sapiens	162-187
16359657-11	2006	The results suggest that the adverse effects of 3-MC are mainly mediated by the aryl hydrocarbon receptor and not via increased oxidative stress.	Methylcholanthrene	48-52	aryl hydrocarbon receptor	Homo sapiens	80-105
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	33-58
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	60-63
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	0-20	aryl hydrocarbon receptor	Homo sapiens	144-147
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	0-20	estrogen receptor 1	Homo sapiens	148-171
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	0-20	estrogen receptor 1	Homo sapiens	173-181
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	22-25	aryl hydrocarbon receptor	Homo sapiens	33-58
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	22-25	aryl hydrocarbon receptor	Homo sapiens	60-63
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	22-25	aryl hydrocarbon receptor	Homo sapiens	144-147
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	22-25	estrogen receptor 1	Homo sapiens	148-171
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	22-25	estrogen receptor 1	Homo sapiens	173-181
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	104-107	aryl hydrocarbon receptor	Homo sapiens	33-58
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	104-107	aryl hydrocarbon receptor	Homo sapiens	60-63
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	104-107	aryl hydrocarbon receptor	Homo sapiens	144-147
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	104-107	estrogen receptor 1	Homo sapiens	148-171
16489053-1	2006	3-Methylcholanthrene (3MC) is an aryl hydrocarbon receptor (AhR) agonist, and it has been reported that 3MC induces estrogenic activity through AhR-estrogen receptor alpha (ER alpha) interactions.	Methylcholanthrene	104-107	estrogen receptor 1	Homo sapiens	173-181
16489053-2	2006	In this study, we used 3MC and 3,3",4,4",5-pentachlorobiphenyl (PCB) as prototypical AhR ligands, and both compounds activated estrogen-responsive reporter genes/gene products (cathepsin D) in MCF-7 breast cancer cells.	Methylcholanthrene	23-26	aryl hydrocarbon receptor	Homo sapiens	85-88
16489053-2	2006	In this study, we used 3MC and 3,3",4,4",5-pentachlorobiphenyl (PCB) as prototypical AhR ligands, and both compounds activated estrogen-responsive reporter genes/gene products (cathepsin D) in MCF-7 breast cancer cells.	Methylcholanthrene	23-26	cathepsin D	Homo sapiens	177-188
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	27-30	estrogen receptor 1	Homo sapiens	57-65
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	27-30	estrogen receptor 1	Homo sapiens	107-115
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	27-30	estrogen receptor 1	Homo sapiens	107-115
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	27-30	estrogen receptor 1	Homo sapiens	107-115
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	206-209	estrogen receptor 1	Homo sapiens	57-65
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	206-209	estrogen receptor 1	Homo sapiens	107-115
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	206-209	estrogen receptor 1	Homo sapiens	107-115
16489053-4	2006	These results suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance energy transfer experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.	Methylcholanthrene	206-209	estrogen receptor 1	Homo sapiens	107-115
16489053-5	2006	In a chromatin immunoprecipitation assay, PCB and 3MC enhanced ER alpha (but not AhR) association with the estrogen-responsive region of the pS2 gene promoter.	Methylcholanthrene	50-53	estrogen receptor 1	Homo sapiens	63-71
16489053-5	2006	In a chromatin immunoprecipitation assay, PCB and 3MC enhanced ER alpha (but not AhR) association with the estrogen-responsive region of the pS2 gene promoter.	Methylcholanthrene	50-53	trefoil factor 1	Homo sapiens	141-144
16489053-6	2006	Moreover, in AhR knockout mice, 3MC increased uterine weights and induced expression of cyclin D1 mRNA levels.	Methylcholanthrene	32-35	aryl-hydrocarbon receptor	Mus musculus	13-16
16489053-6	2006	Moreover, in AhR knockout mice, 3MC increased uterine weights and induced expression of cyclin D1 mRNA levels.	Methylcholanthrene	32-35	cyclin D1	Mus musculus	88-97
16489053-7	2006	These results show that PCB and 3MC directly activate ER alpha-dependent transactivation and extend the number of ligands that activate both AhR and ER alpha.	Methylcholanthrene	32-35	estrogen receptor 1	Homo sapiens	54-62
16489053-7	2006	These results show that PCB and 3MC directly activate ER alpha-dependent transactivation and extend the number of ligands that activate both AhR and ER alpha.	Methylcholanthrene	32-35	aryl hydrocarbon receptor	Homo sapiens	141-144
16489053-7	2006	These results show that PCB and 3MC directly activate ER alpha-dependent transactivation and extend the number of ligands that activate both AhR and ER alpha.	Methylcholanthrene	32-35	estrogen receptor 1	Homo sapiens	149-157
16115717-5	2006	Moreover, oral administration of the molokhia extract (100mg/kg body weight) decreased 3-methylcholanthrene-induced AhR transformation to the control level by inhibiting translocation of the AhR from cytosol into the nucleus in the liver of rats.	Methylcholanthrene	87-107	aryl hydrocarbon receptor	Rattus norvegicus	116-119
16115717-5	2006	Moreover, oral administration of the molokhia extract (100mg/kg body weight) decreased 3-methylcholanthrene-induced AhR transformation to the control level by inhibiting translocation of the AhR from cytosol into the nucleus in the liver of rats.	Methylcholanthrene	87-107	aryl hydrocarbon receptor	Rattus norvegicus	191-194
16191477-3	2006	Typical inducers of the cytochrome P4501A1 (CYP1A1), such as TCDD, benzo(a)pyrene (B(a)P) and 3-methylcholanthrene, have a planar molecular structure in common and bind to the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	94-114	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	24-42
16183705-6	2006	On the other hand, YC-1 inhibited hydrolysis of the fluorogenic quenching substrate Mca-Pro-Leu-Gly-Leu-Dpa-Ala-Arg-NH(2) by recombinant MMP-2 and MMP-9 with IC(50) values = 2.07 and 8.20 muM, respectively.	Methylcholanthrene	84-87	matrix metallopeptidase 2	Rattus norvegicus	137-142
16183705-6	2006	On the other hand, YC-1 inhibited hydrolysis of the fluorogenic quenching substrate Mca-Pro-Leu-Gly-Leu-Dpa-Ala-Arg-NH(2) by recombinant MMP-2 and MMP-9 with IC(50) values = 2.07 and 8.20 muM, respectively.	Methylcholanthrene	84-87	matrix metallopeptidase 9	Rattus norvegicus	147-152
16191477-3	2006	Typical inducers of the cytochrome P4501A1 (CYP1A1), such as TCDD, benzo(a)pyrene (B(a)P) and 3-methylcholanthrene, have a planar molecular structure in common and bind to the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	94-114	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	44-50
16137816-4	2005	The aim of this study was to evaluate, in a Caco-2 cell line, the effect of a coexposure to 3-methylcholanthrene (3MC, AhR ligand) and WY-14643 (WY, PPARalpha ligand) on CYP1A1 expression (enzymatic activity, mRNA level and promoter activity).	Methylcholanthrene	92-112	aryl hydrocarbon receptor	Homo sapiens	119-122
16191477-3	2006	Typical inducers of the cytochrome P4501A1 (CYP1A1), such as TCDD, benzo(a)pyrene (B(a)P) and 3-methylcholanthrene, have a planar molecular structure in common and bind to the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	94-114	aryl hydrocarbon receptor	Homo sapiens	176-201
16191477-3	2006	Typical inducers of the cytochrome P4501A1 (CYP1A1), such as TCDD, benzo(a)pyrene (B(a)P) and 3-methylcholanthrene, have a planar molecular structure in common and bind to the aryl hydrocarbon receptor (AhR).	Methylcholanthrene	94-114	aryl hydrocarbon receptor	Homo sapiens	203-206
16537294-7	2006	Increased expression of CD63 on MC (tissue biomarker of MC), of nitrotyrosine on MC and EC (an indirect indicator of NO in vivo), and of iNOS on MC and EC (source of NO) suggest that NO produced by activated and degranulated MC as well as activated EC play an important role in SK&amp;F 95654-induced mesenteric vascular injury.	Methylcholanthrene	32-34	Cd63 molecule	Rattus norvegicus	24-28
16137816-4	2005	The aim of this study was to evaluate, in a Caco-2 cell line, the effect of a coexposure to 3-methylcholanthrene (3MC, AhR ligand) and WY-14643 (WY, PPARalpha ligand) on CYP1A1 expression (enzymatic activity, mRNA level and promoter activity).	Methylcholanthrene	92-112	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	170-176
16137816-5	2005	An additive effect on CYP1A1 expression was shown in cells coexposed with 3MC (0.1 or 1 microM) and a low WY concentration (30 microM) whereas a potentiating effect was observed after coexposure with 3MC (0.1 or 1 microM) and a high WY concentration (200 microM).	Methylcholanthrene	74-77	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	22-28
16137816-7	2005	In conclusion, coexposure with 3MC and the PPARalpha agonist WY leads to an additive or potentiating effect on CYP1A1 inducibility, depending on the WY concentration.	Methylcholanthrene	31-34	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	111-117
16202979-4	2005	Thus, the aim of this study was to clarify the role of CYP1A1 in the suppression of LXR-mediated signal transductions by 3-methlychoranthrene (MC), one of the PAHs.	Methylcholanthrene	143-145	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	55-61
16135659-7	2005	All 23 single assays were validated by assessing the effects (induction or repression) of known inducers (ethanol, 3-methylcholanthrene, rifampicin, dexamethasone, phenobarbital) on P450 expression in human primary hepatocytes.	Methylcholanthrene	115-135	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	182-186
16120810-3	2005	We have now detected a low basal level of UGT1A5 expression in cultured human hepatocytes, and treatment with rifampicin or 3-methylcholanthrene increased the level of UGT1A5 mRNA.	Methylcholanthrene	124-144	UDP glucuronosyltransferase family 1 member A5	Homo sapiens	42-48
16120810-3	2005	We have now detected a low basal level of UGT1A5 expression in cultured human hepatocytes, and treatment with rifampicin or 3-methylcholanthrene increased the level of UGT1A5 mRNA.	Methylcholanthrene	124-144	UDP glucuronosyltransferase family 1 member A5	Homo sapiens	168-174
16202979-6	2005	The repression of LXR-mediated signal transductions by MC was restored by co-treatment of HepG2 cells with a CYP1A1 inhibitor, alpha-naphthoflavone, and by the transfection of short interference RNA for CYP1A1.	Methylcholanthrene	55-57	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	109-115
16202979-6	2005	The repression of LXR-mediated signal transductions by MC was restored by co-treatment of HepG2 cells with a CYP1A1 inhibitor, alpha-naphthoflavone, and by the transfection of short interference RNA for CYP1A1.	Methylcholanthrene	55-57	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	203-209
15885734-0	2005	Induction of Cyp1a1 and Cyp1b1 and formation of DNA adducts in C57BL/6, Balb/c, and F1 mice following in utero exposure to 3-methylcholanthrene.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	13-19
15885734-0	2005	Induction of Cyp1a1 and Cyp1b1 and formation of DNA adducts in C57BL/6, Balb/c, and F1 mice following in utero exposure to 3-methylcholanthrene.	Methylcholanthrene	123-143	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	24-30
15885734-2	2005	Previous studies from our laboratory demonstrated differences in the mutational spectrum induced in the Ki-ras gene from lung tumors isolated from [D2 x B6D2F1]F2 mice and Balb/c mice treated in utero with 3-methylcholanthrene (MC).	Methylcholanthrene	206-226	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	104-110
15885734-2	2005	Previous studies from our laboratory demonstrated differences in the mutational spectrum induced in the Ki-ras gene from lung tumors isolated from [D2 x B6D2F1]F2 mice and Balb/c mice treated in utero with 3-methylcholanthrene (MC).	Methylcholanthrene	228-230	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	104-110
15885734-5	2005	MC treatment caused maximal induction of Cyp1a1 and Cyp1b1 RNA 2-8 h after injection in both organs.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	41-47
15885734-5	2005	MC treatment caused maximal induction of Cyp1a1 and Cyp1b1 RNA 2-8 h after injection in both organs.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	52-58
15885734-6	2005	RNA levels for both genes then declined in both fetal organs, but a small biphasic, secondary increase in Cyp1a1 was observed specifically in the fetal lung 24-48 h after MC exposure in all four strains.	Methylcholanthrene	171-173	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	106-112
15885734-7	2005	Cyp1a1 induction by MC at 4 h was 2-5 times greater in fetal liver (7000- to 16,000-fold) than fetal lung (2000- to 6000-fold).	Methylcholanthrene	20-22	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-6
16196516-6	2005	On immunohistochemistry, only p53 reactivity was statistically different between MC and non-MC components in IMC cases.	Methylcholanthrene	81-83	tumor protein p53	Homo sapiens	30-33
16300371-3	2005	Here, we tested the hypothesis that MC elicits persistent induction of other genes that are regulated by the Ah receptor (AHR).	Methylcholanthrene	36-38	aryl hydrocarbon receptor	Rattus norvegicus	109-120
16300371-3	2005	Here, we tested the hypothesis that MC elicits persistent induction of other genes that are regulated by the Ah receptor (AHR).	Methylcholanthrene	36-38	aryl hydrocarbon receptor	Rattus norvegicus	122-125
16300371-6	2005	Several phase I (P4501A1, -1A2) and phase II [e.g., glutathione-S-transferase (GST)-M1, UDP-glucuronosyl transferases (UGT)] genes were persistently induced (3-10-fold) by MC for 15-28 days.	Methylcholanthrene	172-174	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	119-122
16385299-6	2005	The hypothesis was that resuscitation with MC-based fluids would be accompanied by MCT1 up-regulation and glial response.	Methylcholanthrene	43-45	solute carrier family 16 member 1	Rattus norvegicus	83-87
16385299-11	2005	RESULTS: Rats resuscitated with MC-containing fluids had increased levels of MCT1 in brain endothelial cells and neuropil compared with sham rats.	Methylcholanthrene	32-34	solute carrier family 16 member 1	Rattus norvegicus	77-81
16385299-14	2005	CONCLUSION: In hemorrhagic shock, resuscitation with MC-based fluids increased brain MCT1 level and led to activation of astrocytes.	Methylcholanthrene	53-55	solute carrier family 16 member 1	Rattus norvegicus	85-89
16196516-6	2005	On immunohistochemistry, only p53 reactivity was statistically different between MC and non-MC components in IMC cases.	Methylcholanthrene	92-94	tumor protein p53	Homo sapiens	30-33
16177085-6	2005	CD4+ CD25+ T cells from these IFN-gamma-treated mice failed to exhibit immunosuppressive activity as measured by 1) increased number of pulmonary metastasis, 2) enhanced development of 3-methylcholanthrene-induced primary tumors, 3) suppression of peptide-specific T cell proliferation, and 4) enhanced expression of Foxp3.	Methylcholanthrene	185-205	interferon gamma	Mus musculus	30-39
16271038-3	2005	GATA-6 and NF-Y were selectively activated with lung carcinogens 3-methylcholanthrene and nitrosoethylurea in mice of strains susceptible to lung tumorigenesis but not in animals of resistant strains.	Methylcholanthrene	65-85	GATA binding protein 6	Mus musculus	0-6
16142311-6	2005	MC (68%, 100%) also showed a higher frequency of the expression of MUC5AC and MUC2 compared to NMC (31%, p=0.001; 38%, p&lt;0.001), and TFF1 showed similar patterns of expression.	Methylcholanthrene	0-2	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	67-73
16142311-6	2005	MC (68%, 100%) also showed a higher frequency of the expression of MUC5AC and MUC2 compared to NMC (31%, p=0.001; 38%, p&lt;0.001), and TFF1 showed similar patterns of expression.	Methylcholanthrene	0-2	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	78-82
16142311-6	2005	MC (68%, 100%) also showed a higher frequency of the expression of MUC5AC and MUC2 compared to NMC (31%, p=0.001; 38%, p&lt;0.001), and TFF1 showed similar patterns of expression.	Methylcholanthrene	0-2	trefoil factor 1	Homo sapiens	136-140
16142311-8	2005	MC (68%, 100%) showed a higher frequency of expression of APC protein and p21 than NMC (19%, p&lt;0.001; 45%, p&lt;0.01).	Methylcholanthrene	0-2	H3 histone pseudogene 16	Homo sapiens	74-77
16142311-9	2005	Our results showed that MUC2 expression and de novo ectopic expression of MUC5AC and TFF1 are more frequent in HP, SA, TVA, VA, and MC than in TA and NMC.	Methylcholanthrene	132-134	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	24-28
16142311-9	2005	Our results showed that MUC2 expression and de novo ectopic expression of MUC5AC and TFF1 are more frequent in HP, SA, TVA, VA, and MC than in TA and NMC.	Methylcholanthrene	132-134	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	74-80
16142311-9	2005	Our results showed that MUC2 expression and de novo ectopic expression of MUC5AC and TFF1 are more frequent in HP, SA, TVA, VA, and MC than in TA and NMC.	Methylcholanthrene	132-134	trefoil factor 1	Homo sapiens	85-89
16393856-0	2005	CCAAT/enhancer binding protein activation by PD98059 contributes to the inhibition of AhR-mediated 3-methylcholanthrene induction of CYP1A1.	Methylcholanthrene	99-119	aryl hydrocarbon receptor	Homo sapiens	86-89
16210974-8	2005	Although acute GVHD was observed more often in patients with MC for DC1/DC2 and chronic GVHD occurred more often in patients with MC for DC2, there was no statistically significant correlation.	Methylcholanthrene	130-132	monoacylglycerol O-acyltransferase 1	Homo sapiens	137-140
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	166-170	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	36-42
16393856-0	2005	CCAAT/enhancer binding protein activation by PD98059 contributes to the inhibition of AhR-mediated 3-methylcholanthrene induction of CYP1A1.	Methylcholanthrene	99-119	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	133-139
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	166-170	mitogen-activated protein kinase kinase 1	Homo sapiens	106-110
16393856-2	2005	In view of the observations that PD98059 inhibits AhR-mediated CYP1A1 induction and has the capability to activate C/EBPbeta, the study investigated whether the inhibition by PD98059 of 3-MC induction of CYP1A1 results from C/EBP activation.	Methylcholanthrene	186-190	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	204-210
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	166-170	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	146-152
16393856-3	2005	3-MC induction of the CYP1A1 and the CYP1A1 promoter-luciferase gene were inhibited by treatment of H4IIE cells with PD98059.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	22-28
16393856-6	2005	The role of C/EBP activation by PD98059 in repressing CYP1A1 induction was supported by the observation that a dominant-negative mutant C/EBP abolished the ability of PD98059 to suppress 3-MC induction of CYP1A1.	Methylcholanthrene	187-191	CCAAT enhancer binding protein alpha	Homo sapiens	12-17
16393856-3	2005	3-MC induction of the CYP1A1 and the CYP1A1 promoter-luciferase gene were inhibited by treatment of H4IIE cells with PD98059.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-43
16393856-6	2005	The role of C/EBP activation by PD98059 in repressing CYP1A1 induction was supported by the observation that a dominant-negative mutant C/EBP abolished the ability of PD98059 to suppress 3-MC induction of CYP1A1.	Methylcholanthrene	187-191	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	54-60
16393856-4	2005	PD98059 treatment inhibited 3-MC-induced AhR binding to the XRE, but increased protein binding to the CYP1A1 C/EBP binding site.	Methylcholanthrene	28-32	aryl hydrocarbon receptor	Homo sapiens	41-44
16393856-6	2005	The role of C/EBP activation by PD98059 in repressing CYP1A1 induction was supported by the observation that a dominant-negative mutant C/EBP abolished the ability of PD98059 to suppress 3-MC induction of CYP1A1.	Methylcholanthrene	187-191	CCAAT enhancer binding protein alpha	Homo sapiens	136-141
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	18-22	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	36-42
16393856-6	2005	The role of C/EBP activation by PD98059 in repressing CYP1A1 induction was supported by the observation that a dominant-negative mutant C/EBP abolished the ability of PD98059 to suppress 3-MC induction of CYP1A1.	Methylcholanthrene	187-191	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	205-211
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	18-22	mitogen-activated protein kinase kinase 1	Homo sapiens	106-110
16393856-5	2005	PD98059 inhibited 3-MC induction of CYP1A1 in cells stably transfected with a dominant negative mutant of MKK1, indicating that PD98059 represses CYP1A1 induction by 3-MC irrespective of its MKK1 inhibition.	Methylcholanthrene	18-22	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	146-152
15936777-2	2005	Sustained increases in cytosolic free calcium, increased iNOS expression and elevated nitric oxide (NO) production are associated with MC apoptosis in vitro.	Methylcholanthrene	135-137	nitric oxide synthase 2	Rattus norvegicus	57-61
15926192-1	2005	In order to find what types of hepatic microsomal cytochrome P450 (CYP) isozymes are involved in the metabolism of DA-8159 and in the formation of DA-8164 in rats, enzyme inducers, such as dexamethasone, phenobarbital, 3-methylcholanthrene and isoniazid, and enzyme inhibitors, such as troleandomycin and quinine, were pretreated in rats.	Methylcholanthrene	219-239	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-65
15936777-8	2005	These reactive oxygen molecules and increased intracellular free calcium may mediate the increase in Jun-AP1 expression and JNK activation induced by G treatment in MC.	Methylcholanthrene	165-167	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
15936777-8	2005	These reactive oxygen molecules and increased intracellular free calcium may mediate the increase in Jun-AP1 expression and JNK activation induced by G treatment in MC.	Methylcholanthrene	165-167	mitogen-activated protein kinase 8	Rattus norvegicus	124-127
16129707-2	2005	We show that neutralization of NKG2D enhances the sensitivity of wild-type (WT) C57BL/6 and BALB/c mice to methylcholanthrene (MCA)-induced fibrosarcoma.	Methylcholanthrene	107-125	killer cell lectin-like receptor subfamily K, member 1	Mus musculus	31-36
16129707-2	2005	We show that neutralization of NKG2D enhances the sensitivity of wild-type (WT) C57BL/6 and BALB/c mice to methylcholanthrene (MCA)-induced fibrosarcoma.	Methylcholanthrene	127-130	killer cell lectin-like receptor subfamily K, member 1	Mus musculus	31-36
15926192-1	2005	In order to find what types of hepatic microsomal cytochrome P450 (CYP) isozymes are involved in the metabolism of DA-8159 and in the formation of DA-8164 in rats, enzyme inducers, such as dexamethasone, phenobarbital, 3-methylcholanthrene and isoniazid, and enzyme inhibitors, such as troleandomycin and quinine, were pretreated in rats.	Methylcholanthrene	219-239	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	67-70
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	33-53	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	7-14
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	33-53	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	19-26
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	33-53	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	8-14
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	33-53	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	20-26
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	55-59	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	7-14
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	55-59	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	19-26
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	55-59	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	8-14
16167840-7	2005	In the hCYP1A1 and hCYP1A2 mice, 3-methylcholanthrene (3-MC) induced both human CYP1A1 and CYP1A2 protein in the liver.	Methylcholanthrene	55-59	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	20-26
16210792-5	2005	However, the transformation frequency for HFEMF at SAR of more than 100 W/kg with MC or MC plus TPA was increased compared with MC alone or MC plus TPA.	Methylcholanthrene	88-90	sarcosinemia autosomal recessive	Mus musculus	51-54
16210792-5	2005	However, the transformation frequency for HFEMF at SAR of more than 100 W/kg with MC or MC plus TPA was increased compared with MC alone or MC plus TPA.	Methylcholanthrene	82-84	sarcosinemia autosomal recessive	Mus musculus	51-54
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	145-165	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	52-68
16210792-5	2005	However, the transformation frequency for HFEMF at SAR of more than 100 W/kg with MC or MC plus TPA was increased compared with MC alone or MC plus TPA.	Methylcholanthrene	88-90	sarcosinemia autosomal recessive	Mus musculus	51-54
16210792-5	2005	However, the transformation frequency for HFEMF at SAR of more than 100 W/kg with MC or MC plus TPA was increased compared with MC alone or MC plus TPA.	Methylcholanthrene	88-90	sarcosinemia autosomal recessive	Mus musculus	51-54
15860653-3	2005	The luciferase reporter assay using the CYP1A1 promoter reporter in HeLa cells treated with beta-naphthoflavone or 3-methylcholanthrene, which are known as typical agonists for AhR, showed that reporter activities of the K401R and N487D variants were reduced to 40 to 58% of those of wild-type (WT) but not of the other variants.	Methylcholanthrene	115-135	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	40-46
15860653-3	2005	The luciferase reporter assay using the CYP1A1 promoter reporter in HeLa cells treated with beta-naphthoflavone or 3-methylcholanthrene, which are known as typical agonists for AhR, showed that reporter activities of the K401R and N487D variants were reduced to 40 to 58% of those of wild-type (WT) but not of the other variants.	Methylcholanthrene	115-135	aryl hydrocarbon receptor	Homo sapiens	177-180
15963949-3	2005	We herein showed that genistein dose-dependently increased TGF-beta1 mRNA expression in mouse colon cancer MC-26 cells.	Methylcholanthrene	107-110	transforming growth factor, beta 1	Mus musculus	59-68
15895106-1	2005	We studied 7-ethoxyresorufin deethylase as an index of cytochrome P4501A1 (CYP1A1) activity in liver microsomes from rats pretreated with 3-methylcholanthrene.	Methylcholanthrene	138-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	55-73
15895106-1	2005	We studied 7-ethoxyresorufin deethylase as an index of cytochrome P4501A1 (CYP1A1) activity in liver microsomes from rats pretreated with 3-methylcholanthrene.	Methylcholanthrene	138-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	75-81
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	145-165	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	70-75
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	145-165	caspase 3	Rattus norvegicus	81-90
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	167-170	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	52-68
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	167-170	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	70-75
16255988-1	2005	OBJECTIVE: To investigate the dynamic expression of cyclooxygenase-2 (COX-2) and caspase-3 during the carcinogenesis, invasion and metastasis of 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN)-induced rat lung cancer and its significance.	Methylcholanthrene	167-170	caspase 3	Rattus norvegicus	81-90
15961541-1	2005	We examined the role of CD4+CD25+ regulatory T cells in the development of 3-methylcholanthrene (MCA)-induced tumors.	Methylcholanthrene	75-95	CD4 antigen	Mus musculus	24-27
15961541-1	2005	We examined the role of CD4+CD25+ regulatory T cells in the development of 3-methylcholanthrene (MCA)-induced tumors.	Methylcholanthrene	97-100	CD4 antigen	Mus musculus	24-27
15882963-3	2005	In the presence of 3-methylcholanthrene (MC), proliferation of the cells transfected with wild-type AhR was completely suppressed, whereas cells expressing AhR mutants proliferated in a manner equivalent to control TM3 cells, suggesting AhR-dependent growth inhibition.	Methylcholanthrene	19-39	aryl-hydrocarbon receptor	Mus musculus	100-103
15882963-3	2005	In the presence of 3-methylcholanthrene (MC), proliferation of the cells transfected with wild-type AhR was completely suppressed, whereas cells expressing AhR mutants proliferated in a manner equivalent to control TM3 cells, suggesting AhR-dependent growth inhibition.	Methylcholanthrene	41-43	aryl-hydrocarbon receptor	Mus musculus	100-103
15882963-3	2005	In the presence of 3-methylcholanthrene (MC), proliferation of the cells transfected with wild-type AhR was completely suppressed, whereas cells expressing AhR mutants proliferated in a manner equivalent to control TM3 cells, suggesting AhR-dependent growth inhibition.	Methylcholanthrene	41-43	aryl-hydrocarbon receptor	Mus musculus	156-159
15882963-3	2005	In the presence of 3-methylcholanthrene (MC), proliferation of the cells transfected with wild-type AhR was completely suppressed, whereas cells expressing AhR mutants proliferated in a manner equivalent to control TM3 cells, suggesting AhR-dependent growth inhibition.	Methylcholanthrene	41-43	aryl-hydrocarbon receptor	Mus musculus	156-159
15882963-5	2005	A p38 MAPK specific inhibitor, SB203580, blocked the increase of p21Cip1 mRNA in response to MC.	Methylcholanthrene	93-95	mitogen-activated protein kinase 14	Mus musculus	2-5
15882963-5	2005	A p38 MAPK specific inhibitor, SB203580, blocked the increase of p21Cip1 mRNA in response to MC.	Methylcholanthrene	93-95	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	65-72
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
16268500-5	2005	RESULTS: Cell proliferation assays showed that treatment with both NPPB (50 and 25 micromol x L(-1)) and in hypertonic media (100% increased osmolarity with D-mannitol ) significantly reduced the number of human MC and 3H-thymidine incorporation in a dose-dependent manner.	Methylcholanthrene	212-214	natriuretic peptide B	Homo sapiens	67-71
15769886-6	2005	In addition, the expression levels of human CYP1A2 mRNA and CYP1A2 protein were also increased 2- to 9- and 5-fold, respectively, by treatment with 3-MC.	Methylcholanthrene	148-152	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-50
15769886-6	2005	In addition, the expression levels of human CYP1A2 mRNA and CYP1A2 protein were also increased 2- to 9- and 5-fold, respectively, by treatment with 3-MC.	Methylcholanthrene	148-152	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	60-66
15976335-6	2005	Her-2 was only present in one MC with 1+ reactivity.	Methylcholanthrene	30-32	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-5
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	10-16
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	18-24
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 4, subfamily a, polypeptide 1	Rattus norvegicus	26-32
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Methylcholanthrene	77-97	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	38-44
15784688-5	2005	In patients with SM, MC also reacted with antibodies against SIRPalpha and CD47.	Methylcholanthrene	21-23	signal regulatory protein alpha	Homo sapiens	61-70
15514940-4	2005	Methylcholanthrene, an immunosuppressive polycyclic hydrocarbon carcinogen implicated as a causative agent in human cancers, has long been used to induce murine tumors with a high incidence of genetic alterations and sensitivity to wt p53-specific CTL.	Methylcholanthrene	0-18	transformation related protein 53, pseudogene	Mus musculus	235-238
15784688-5	2005	In patients with SM, MC also reacted with antibodies against SIRPalpha and CD47.	Methylcholanthrene	21-23	CD47 molecule	Homo sapiens	75-79
15784688-6	2005	By contrast, the levels of SHP-1 were low or undetectable in MC in most cases.	Methylcholanthrene	61-63	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	27-32
15784688-10	2005	In summary, our data show that MC express functional SIRPalpha and CD47 in SM, whereas expression of SHP-1 varies among donors and is low compared with LMC.	Methylcholanthrene	31-33	signal regulatory protein alpha	Homo sapiens	53-62
15784688-10	2005	In summary, our data show that MC express functional SIRPalpha and CD47 in SM, whereas expression of SHP-1 varies among donors and is low compared with LMC.	Methylcholanthrene	31-33	CD47 molecule	Homo sapiens	67-71
15784688-11	2005	It is hypothesized that CD172 and CD47 contribute to MC clustering and that the "lack" of SHP-1 in MC may facilitate KIT-dependent signaling in a subgroup of patients.	Methylcholanthrene	99-101	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	90-95
15784688-11	2005	It is hypothesized that CD172 and CD47 contribute to MC clustering and that the "lack" of SHP-1 in MC may facilitate KIT-dependent signaling in a subgroup of patients.	Methylcholanthrene	99-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
15849819-7	2005	The induction of hepatic microsomal cytochrome P450 2E1 (CYP2E1) was obviously seen in group ME and group FE, but was not detected in group MC and group FC.	Methylcholanthrene	140-142	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	57-63
15797623-2	2005	Here, we demonstrate that hWAPL transcription is induced by 3-methylcholanthrene (3-MC) in the cervical carcinoma-derived cell line SiHa.	Methylcholanthrene	60-80	WAPL cohesin release factor	Homo sapiens	26-31
15797623-2	2005	Here, we demonstrate that hWAPL transcription is induced by 3-methylcholanthrene (3-MC) in the cervical carcinoma-derived cell line SiHa.	Methylcholanthrene	82-86	WAPL cohesin release factor	Homo sapiens	26-31
15797623-6	2005	Interestingly, when the aryl hydrocarbon receptor (AhR) function was inhibited by alpha-naphthoflavone (ANF), the induction of hWAPL transcription by 3-MC was greater than that in AhR-functioning normal cells.	Methylcholanthrene	150-154	aryl-hydrocarbon receptor	Mus musculus	24-49
15797623-6	2005	Interestingly, when the aryl hydrocarbon receptor (AhR) function was inhibited by alpha-naphthoflavone (ANF), the induction of hWAPL transcription by 3-MC was greater than that in AhR-functioning normal cells.	Methylcholanthrene	150-154	aryl-hydrocarbon receptor	Mus musculus	51-54
15797623-6	2005	Interestingly, when the aryl hydrocarbon receptor (AhR) function was inhibited by alpha-naphthoflavone (ANF), the induction of hWAPL transcription by 3-MC was greater than that in AhR-functioning normal cells.	Methylcholanthrene	150-154	WAPL cohesin release factor	Homo sapiens	127-132
15797623-8	2005	Furthermore, mRNA level of a mouse homolog of hWAPL in mouse uterus was induced by 3-MC injection into the abdominal cavity.	Methylcholanthrene	83-87	WAPL cohesin release factor	Homo sapiens	46-51
15797623-9	2005	Thus, some effects from 3-MC exposure on uterus may be mediated by the unscheduled overexpression of hWAPL.	Methylcholanthrene	24-28	WAPL cohesin release factor	Homo sapiens	101-106
16708425-3	2005	Pristane exposure led to tissue specific differences in the CYP isozymes expressed and elicited increased CYP protein expression over 3-methylcholanthrene induced levels in microsomes isolated from liver, Peyer"s Patches, and thymus.	Methylcholanthrene	134-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-63
15657367-3	2005	The CYP2A5 mRNA up-regulation in these mouse strains showed a difference in response, typical for AHR-regulated genes, both by TCDD in cultured primary hepatocytes and by 3-methylcholanthrene in vivo.	Methylcholanthrene	171-191	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	4-10
15657367-3	2005	The CYP2A5 mRNA up-regulation in these mouse strains showed a difference in response, typical for AHR-regulated genes, both by TCDD in cultured primary hepatocytes and by 3-methylcholanthrene in vivo.	Methylcholanthrene	171-191	aryl-hydrocarbon receptor	Mus musculus	98-101
15914662-6	2005	Loss of cca-1 function decreases the chance that excitatory input from MC will successfully trigger an action potential, and reduces the ability of an animal to take in food.	Methylcholanthrene	71-73	Voltage-dependent T-type calcium channel subunit alpha	Caenorhabditis elegans	8-13
15797623-0	2005	Effects of 3-methylcholanthrene on the transcriptional activity and mRNA accumulation of the oncogene hWAPL.	Methylcholanthrene	11-31	WAPL cohesin release factor	Homo sapiens	102-107
15816502-4	2005	TGFbeta is a potent pro-fibrotic factor and induces epithelial-mesenchymal transition (EMT) of the MC.	Methylcholanthrene	99-101	transforming growth factor beta 1	Homo sapiens	0-7
15649379-4	2005	By optimization of assay conditions on cell number and serum concentration, the fast-track DRESSA enabled detection of 0.5 pM 2,3,7,8-tetrachlorodibenzo-p-dioxin within 6 h. It also enabled detection of 10 pM 3-methylcholanthrene, 100 pM benzo[a]pyrene, and 100 pM beta-naphthoflavone within 6-16 h. By combination with the AhR antagonist alpha-naphthoflavone, nonspecific, false-positive responses could be eliminated.	Methylcholanthrene	209-229	aryl hydrocarbon receptor	Homo sapiens	324-327
15711891-6	2005	We found that MC-26 cells expressed Smad2, Smad3, and Smad4 mRNAs by reverse transeription-polymerase chain reaction and confirmed that the TGF-beta signaling pathway is functional using a transient transfection assay with 3TP-Lux reporter plasmid.	Methylcholanthrene	14-17	SMAD family member 2	Mus musculus	36-41
15711891-6	2005	We found that MC-26 cells expressed Smad2, Smad3, and Smad4 mRNAs by reverse transeription-polymerase chain reaction and confirmed that the TGF-beta signaling pathway is functional using a transient transfection assay with 3TP-Lux reporter plasmid.	Methylcholanthrene	14-17	SMAD family member 3	Mus musculus	43-48
15711891-6	2005	We found that MC-26 cells expressed Smad2, Smad3, and Smad4 mRNAs by reverse transeription-polymerase chain reaction and confirmed that the TGF-beta signaling pathway is functional using a transient transfection assay with 3TP-Lux reporter plasmid.	Methylcholanthrene	14-17	SMAD family member 4	Mus musculus	54-59
15711891-6	2005	We found that MC-26 cells expressed Smad2, Smad3, and Smad4 mRNAs by reverse transeription-polymerase chain reaction and confirmed that the TGF-beta signaling pathway is functional using a transient transfection assay with 3TP-Lux reporter plasmid.	Methylcholanthrene	14-17	transforming growth factor, beta 1	Mus musculus	140-148
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 2	Mus musculus	109-114
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 3	Mus musculus	116-121
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 4	Mus musculus	127-132
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	transforming growth factor, beta 1	Mus musculus	134-142
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 2	Mus musculus	220-225
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 3	Mus musculus	227-232
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	SMAD family member 4	Mus musculus	238-243
15711891-8	2005	When MC-26 cells were transiently transfected with dominant-negative carboxyl-terminal truncation mutants of Smad2, Smad3, and Smad4, TGF-beta-induced 3TP-Lux reporter activity was significantly reduced, suggesting that Smad2, Smad3, and Smad4 are attractive novel therapeutic targets for regulating TGF-beta signaling in colorectal cancers.	Methylcholanthrene	5-7	transforming growth factor, beta 1	Mus musculus	300-308
15799453-8	2005	The amounts of MB2, MB4, and MC formed by male and female rat liver microsome preparations were related to the testosterone 6beta-hydroxylase activity and CYP3A1/2 protein content of the preparation.	Methylcholanthrene	29-31	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	111-141
15799453-8	2005	The amounts of MB2, MB4, and MC formed by male and female rat liver microsome preparations were related to the testosterone 6beta-hydroxylase activity and CYP3A1/2 protein content of the preparation.	Methylcholanthrene	29-31	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	155-163
15799453-10	2005	These results suggest that the formation of MB2, MB4, and MC in liver microsomes from 14-wk-old rats of either gender is mediated by CYP3A1 and CYP3A2.	Methylcholanthrene	58-60	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	133-139
15799453-10	2005	These results suggest that the formation of MB2, MB4, and MC in liver microsomes from 14-wk-old rats of either gender is mediated by CYP3A1 and CYP3A2.	Methylcholanthrene	58-60	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	144-150
15754407-4	2005	Patients with a high MC count and patients with a high TAM count were significantly higher showing significantly lower rates of lymph node metastasis, distant metastasis than those with a low MC count and those with a low TAM count.	Methylcholanthrene	192-194	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	55-58
15754407-5	2005	There were significant positive correlation between MC counts and TAM counts (r = 0.852, P&lt;0.01).	Methylcholanthrene	52-54	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	66-69
15805584-8	2005	The only cyclin D1-positive MC was multifocal (both lobes of the gland were affected).	Methylcholanthrene	28-30	cyclin D1	Homo sapiens	9-18
15856279-4	2005	Application of antibodies against ankyrin (ANK), a protein that links integral membrane proteins to the submembrane cytoskeleton, led to intense labeling of the basolateral membranes of numerous cells with characteristic MC morphology.	Methylcholanthrene	221-223	ankyrin 1	Homo sapiens	34-41
15856279-4	2005	Application of antibodies against ankyrin (ANK), a protein that links integral membrane proteins to the submembrane cytoskeleton, led to intense labeling of the basolateral membranes of numerous cells with characteristic MC morphology.	Methylcholanthrene	221-223	ankyrin 1	Homo sapiens	43-46
15770593-15	2005	An important decrease in alfa -SMA expression by MC after rapamycin addition was observed.	Methylcholanthrene	49-51	survival of motor neuron 1, telomeric	Homo sapiens	31-34
15585370-0	2005	Hypoxic inhibition of 3-methylcholanthrene-induced CYP1A1 expression is independent of HIF-1alpha.	Methylcholanthrene	22-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	51-57
15585370-5	2005	Concomitant treatment of cultures with hypoxia (1% O2) and 3-methylcholanthrene (an AhR ligand) did not significantly alter HIF target gene expression.	Methylcholanthrene	59-79	aryl hydrocarbon receptor	Homo sapiens	84-87
15590115-4	2005	This is illustrated by activities of 7-ethoxyresorufin-O-deethylase (EROD) after incubation with 5 microM 3-methylcholanthrene (3-MC), a standard inducer for cytochrome P4501A1 and 1A2.	Methylcholanthrene	128-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	158-184
15620718-3	2005	The effect of dexamethasone on the induction of CYP1A1 by 3-methylcholanthrene is different in rat and human liver cells.	Methylcholanthrene	58-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	48-54
15835536-8	2005	These results suggest that chronic inducible NO-synthase inhibition restores the impaired endothelium-dependent and sGC-dependent relaxation of pulmonary artery in MC-induced PH.	Methylcholanthrene	164-166	nitric oxide synthase 2	Rattus norvegicus	35-56
15835536-8	2005	These results suggest that chronic inducible NO-synthase inhibition restores the impaired endothelium-dependent and sGC-dependent relaxation of pulmonary artery in MC-induced PH.	Methylcholanthrene	164-166	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	116-119
15590115-4	2005	This is illustrated by activities of 7-ethoxyresorufin-O-deethylase (EROD) after incubation with 5 microM 3-methylcholanthrene (3-MC), a standard inducer for cytochrome P4501A1 and 1A2.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	158-184
16421897-9	2005	3-Methylcholanthrene induced CYP1A1, CYP1A2, and CYP1B1.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-35
15915147-0	2005	Estrogen-responsive element (ERE)-like motifs affect the 3-methylcholanthrene induction of eel CYP1A gene.	Methylcholanthrene	57-77	cytochrome P450 1A1	Oryzias latipes	95-100
16421897-9	2005	3-Methylcholanthrene induced CYP1A1, CYP1A2, and CYP1B1.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	37-43
16421897-9	2005	3-Methylcholanthrene induced CYP1A1, CYP1A2, and CYP1B1.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily b, polypeptide 1	Rattus norvegicus	49-55
15637428-4	2005	RESULTS: The uptake of vitamin B12 by MC from renal patients was lower than that by MC from controls (9.3 vs. 12.5 pg/3 x 10(6) cells; p = 0.001).	Methylcholanthrene	38-40	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	31-34
15637428-7	2005	CONCLUSIONS: Our results show that vitamin B12 uptake is impaired in MC from renal patients, with no evidence that the surface receptor is down-regulated.	Methylcholanthrene	69-71	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	43-46
15610895-9	2005	The structure of the N3Ade adduct was established by NMR and MS. We also report here formation of the depurinating 3"-OH-HES-6"-N7Gua and 3"-OH-HES-6"-N3Ade adducts by reaction of HES-3",4"-Q with DNA or by activation of 3"-OH-HES by tyrosinase, lactoperoxidase, prostaglandin H synthase or 3-methylcholanthrene-induced rat liver microsomes in the presence of DNA.	Methylcholanthrene	291-311	tyrosinase	Rattus norvegicus	234-244
15776967-2	2005	Its effect on appetite is mediated by melanocortines (MC) that are derivative of proopiomelanocortin (POMK) and their receptor (MC4-R).	Methylcholanthrene	54-56	protein O-mannose kinase	Homo sapiens	102-106
15610895-9	2005	The structure of the N3Ade adduct was established by NMR and MS. We also report here formation of the depurinating 3"-OH-HES-6"-N7Gua and 3"-OH-HES-6"-N3Ade adducts by reaction of HES-3",4"-Q with DNA or by activation of 3"-OH-HES by tyrosinase, lactoperoxidase, prostaglandin H synthase or 3-methylcholanthrene-induced rat liver microsomes in the presence of DNA.	Methylcholanthrene	291-311	lactoperoxidase	Rattus norvegicus	246-261
15776967-2	2005	Its effect on appetite is mediated by melanocortines (MC) that are derivative of proopiomelanocortin (POMK) and their receptor (MC4-R).	Methylcholanthrene	54-56	melanocortin 4 receptor	Homo sapiens	128-133
15862027-1	2005	OBJECTIVE: To investigate the regulatory effects of micronutrients complex (MC) on the expression of Th1 and Th2 cytokines in diabetic mice for exploring the molecular mechanisms of MC in treating for diabetes.	Methylcholanthrene	76-78	negative elongation factor complex member C/D, Th1l	Mus musculus	101-104
15518646-5	2004	In cerebellar molecular layer, expression of BDNF correlated significantly with time spent in AC and MC over the first 7 days of training and remained elevated after 14 days of AC but not of MC.	Methylcholanthrene	101-103	brain-derived neurotrophic factor	Rattus norvegicus	45-49
15862027-1	2005	OBJECTIVE: To investigate the regulatory effects of micronutrients complex (MC) on the expression of Th1 and Th2 cytokines in diabetic mice for exploring the molecular mechanisms of MC in treating for diabetes.	Methylcholanthrene	76-78	heart and neural crest derivatives expressed 2	Mus musculus	109-112
15862027-6	2005	Combined supplementation of MC markedly decreased blood lymphocytes TNF-alpha expression (P &lt; 0.01) and increased blood lymphocytes IL-10 expression (P &lt; 0.01) and spleen lymphocytes IL-4 expression (P &lt; 0.05) of IDDM mice respectively.	Methylcholanthrene	28-30	tumor necrosis factor	Mus musculus	68-77
15862027-6	2005	Combined supplementation of MC markedly decreased blood lymphocytes TNF-alpha expression (P &lt; 0.01) and increased blood lymphocytes IL-10 expression (P &lt; 0.01) and spleen lymphocytes IL-4 expression (P &lt; 0.05) of IDDM mice respectively.	Methylcholanthrene	28-30	interleukin 10	Mus musculus	135-140
15862027-6	2005	Combined supplementation of MC markedly decreased blood lymphocytes TNF-alpha expression (P &lt; 0.01) and increased blood lymphocytes IL-10 expression (P &lt; 0.01) and spleen lymphocytes IL-4 expression (P &lt; 0.05) of IDDM mice respectively.	Methylcholanthrene	28-30	interleukin 4	Mus musculus	189-193
15862027-7	2005	CONCLUSION: MC may prevent from the onset and development of IDDM by down-regulating Th1 cytokines genes expression and up-regulating Th2 cytokines genes expression of IDDM mice.	Methylcholanthrene	12-14	negative elongation factor complex member C/D, Th1l	Mus musculus	85-88
15862027-7	2005	CONCLUSION: MC may prevent from the onset and development of IDDM by down-regulating Th1 cytokines genes expression and up-regulating Th2 cytokines genes expression of IDDM mice.	Methylcholanthrene	12-14	heart and neural crest derivatives expressed 2	Mus musculus	134-137
15582647-5	2004	In addition, we demonstrate for the first time the induction of Cyp1b1 RNA expression in fetal lung and liver tissues following in utero exposure to 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon.	Methylcholanthrene	149-169	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	64-70
15582647-5	2004	In addition, we demonstrate for the first time the induction of Cyp1b1 RNA expression in fetal lung and liver tissues following in utero exposure to 3-methylcholanthrene (MC), a polycyclic aromatic hydrocarbon.	Methylcholanthrene	171-173	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	64-70
15518646-5	2004	In cerebellar molecular layer, expression of BDNF correlated significantly with time spent in AC and MC over the first 7 days of training and remained elevated after 14 days of AC but not of MC.	Methylcholanthrene	191-193	brain-derived neurotrophic factor	Rattus norvegicus	45-49
15518646-8	2004	Increased expression of BDNF, but not of TrkB, was observed in upper motor cortical layers after 14 days of MC.	Methylcholanthrene	108-110	brain-derived neurotrophic factor	Rattus norvegicus	24-28
15621696-0	2004	Benzo[a]pyrene, 3-methylcholanthrene and beta-naphthoflavone induce oxidative stress in hepatoma hepa 1c1c7 Cells by an AHR-dependent pathway.	Methylcholanthrene	16-36	aryl-hydrocarbon receptor	Mus musculus	120-123
15451302-8	2004	Among the four herbal ingredients of DST, only MC has been shown to significantly inhibit the invasion of Hep3B cells and MMP-2 and -9 activities.	Methylcholanthrene	47-49	matrix metallopeptidase 2	Homo sapiens	122-134
15212418-3	2004	We investigated the physiological role of mGluR1 in regulating MC activity in rat and mouse MOB slices.	Methylcholanthrene	63-65	glutamate metabotropic receptor 1	Rattus norvegicus	42-48
15212418-7	2004	MC excitatory responses to DHPG were absent in mGluR1 knockout mice but persisted in mGluR5 knockout mice.	Methylcholanthrene	0-2	glutamate receptor, metabotropic 1	Mus musculus	47-53
15212418-7	2004	MC excitatory responses to DHPG were absent in mGluR1 knockout mice but persisted in mGluR5 knockout mice.	Methylcholanthrene	0-2	glutamate receptor, ionotropic, kainate 1	Mus musculus	85-91
15212418-11	2004	These findings suggest that endogenous glutamate tonically modulates MC excitability and responsiveness to olfactory nerve input, and hence the operation of the MOB circuitry, via activation of mGluR1.	Methylcholanthrene	69-71	glutamate receptor, metabotropic 1	Mus musculus	194-200
15292452-8	2004	We found endogenous Vg1RBP/Vera and Vg1RBP/Vera-green fluorescent protein to be largely excluded from the MC but subsequently to codistribute with Xcat2 and ER at the vegetal cortex.	Methylcholanthrene	106-108	insulin like growth factor 2 mRNA binding protein 3 L homeolog	Xenopus laevis	20-26
15292452-8	2004	We found endogenous Vg1RBP/Vera and Vg1RBP/Vera-green fluorescent protein to be largely excluded from the MC but subsequently to codistribute with Xcat2 and ER at the vegetal cortex.	Methylcholanthrene	106-108	insulin like growth factor 2 mRNA binding protein 3 L homeolog	Xenopus laevis	36-42
15292452-8	2004	We found endogenous Vg1RBP/Vera and Vg1RBP/Vera-green fluorescent protein to be largely excluded from the MC but subsequently to codistribute with Xcat2 and ER at the vegetal cortex.	Methylcholanthrene	106-108	insulin like growth factor 2 mRNA binding protein 3 L homeolog	Xenopus laevis	43-47
15292452-9	2004	We conclude that germ line RNAs localize into the MC through a diffusion/entrapment mechanism involving Vg1RBP/Vera-independent association with ER.	Methylcholanthrene	50-52	insulin like growth factor 2 mRNA binding protein 3 L homeolog	Xenopus laevis	104-110
15292452-9	2004	We conclude that germ line RNAs localize into the MC through a diffusion/entrapment mechanism involving Vg1RBP/Vera-independent association with ER.	Methylcholanthrene	50-52	insulin like growth factor 2 mRNA binding protein 3 L homeolog	Xenopus laevis	111-115
15325265-2	2004	The effect of a coexposure with 3MC, a AhR ligand, and RA, a RAR ligand, which are, respectively, strong and weak CYP1A1 inducers, is poorly known.	Methylcholanthrene	32-35	aryl hydrocarbon receptor	Homo sapiens	39-42
15325265-2	2004	The effect of a coexposure with 3MC, a AhR ligand, and RA, a RAR ligand, which are, respectively, strong and weak CYP1A1 inducers, is poorly known.	Methylcholanthrene	32-35	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	114-120
15325265-3	2004	We showed in Caco-2 cells that addition of RA significantly decreased 3MC-induced CYP1A1 expression by -55% for mRNA level and -30% for promoter and enzymatic activities.	Methylcholanthrene	70-73	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	82-88
15325265-7	2004	This interaction explains the decrease of 3MC-induced CYP1A1 expression.	Methylcholanthrene	42-45	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	54-60
15245322-3	2004	Application to a light harvesting complex LH2 reveals the important consequences of a MC structure.	Methylcholanthrene	86-88	procollagen-lysine,2-oxoglutarate 5-dioxygenase 2	Homo sapiens	42-45
15363137-3	2004	All patients with stable MC (90% &lt;/= DC &lt; 95%) and bcr/abl negative had a probability of long-term survival with molecular remission, however the result of bcr/abl positivity was not always associated with leukemia relapse, only the patient with decreasing values of donor chimerism as well as bcr/abl positive proved to be in a higher risk of relapse or graft failure.	Methylcholanthrene	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
15144902-1	2004	We have identified an enhancer responsible for induction by 3-methylcholanthrene in the upstream region of the CYP1A2 gene.	Methylcholanthrene	60-80	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-117
15302093-12	2004	The pretreatment with this phenolic of the MC-induced rats however significantly increased the activities of hepatic GST and NQO1 in comparison with MC-treated group.	Methylcholanthrene	43-45	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	125-129
15302093-13	2004	In kidney MC-induced activity of NQO1 was reduced (about 43%) to the control level by tannic acid pretreatment.	Methylcholanthrene	10-12	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	33-37
15331414-9	2004	The mRNAs for hCYP3A4 and hCYP1A1/2 were induced in the liver in a CYP type-specific manner when the mice were treated with rifampicin and 3-methylcholanthrene, respectively.	Methylcholanthrene	139-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-21
15331414-9	2004	The mRNAs for hCYP3A4 and hCYP1A1/2 were induced in the liver in a CYP type-specific manner when the mice were treated with rifampicin and 3-methylcholanthrene, respectively.	Methylcholanthrene	139-159	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	26-35
15197597-7	2004	Furthermore, the NAS1 promoter conferred responsiveness to the polycyclic aromatic hydrocarbon 3-methylcholanthrene (3-MC), but not to thyroid hormone (T(3)) or vitamin D [1,25-(OH)(2)D(3)].	Methylcholanthrene	117-121	solute carrier family 13 member 1	Homo sapiens	17-21
15197597-8	2004	Site-directed mutagenesis of the NAS1 promoter identified a functional xenobiotic response element at -2,052, which conferred 3-MC responsiveness.	Methylcholanthrene	126-130	solute carrier family 13 member 1	Homo sapiens	33-37
15197597-9	2004	The human NAS1 gene promoter is not responsive to Vitamin D or T(3), unlike the mouse Nas1 promoter with which it shares approximately 40% sequence similarity, but is transactivated by 3-MC, suggesting that the control of renal SO(4)(2-) reabsorption via the regulation of NAS1 transcription may be important for maintaining the sulphation potential for kidney polycyclic aromatic hydrocarbon metabolism.	Methylcholanthrene	185-189	solute carrier family 13 member 1	Homo sapiens	10-14
15197597-9	2004	The human NAS1 gene promoter is not responsive to Vitamin D or T(3), unlike the mouse Nas1 promoter with which it shares approximately 40% sequence similarity, but is transactivated by 3-MC, suggesting that the control of renal SO(4)(2-) reabsorption via the regulation of NAS1 transcription may be important for maintaining the sulphation potential for kidney polycyclic aromatic hydrocarbon metabolism.	Methylcholanthrene	185-189	solute carrier family 13 (sodium/sulfate symporters), member 1	Mus musculus	86-90
15232618-5	2004	Moreover, in MC(+/+) but not in Kit(w)/Kit(w-v) mice, a contribution of ACE-independent Ang II generation to blood pressure regulation was evident by a 1.6-fold greater maximal reduction in mean arterial pressure with acute ACE inhibition plus AT(1) receptor blockade than with ACE inhibition alone.	Methylcholanthrene	13-15	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	72-75
15232618-5	2004	Moreover, in MC(+/+) but not in Kit(w)/Kit(w-v) mice, a contribution of ACE-independent Ang II generation to blood pressure regulation was evident by a 1.6-fold greater maximal reduction in mean arterial pressure with acute ACE inhibition plus AT(1) receptor blockade than with ACE inhibition alone.	Methylcholanthrene	13-15	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	88-94
15169886-3	2004	In the HuH7 human hepatoma cell line, PON-1 activity and mRNA levels were increased by dietary polyphenolic compounds such as quercetin but also by toxic ligands of the aryl hydrocarbon receptor (AhR) such as 3-methylcholanthrene (3-MC).	Methylcholanthrene	209-229	paraoxonase 1	Homo sapiens	38-43
15169886-3	2004	In the HuH7 human hepatoma cell line, PON-1 activity and mRNA levels were increased by dietary polyphenolic compounds such as quercetin but also by toxic ligands of the aryl hydrocarbon receptor (AhR) such as 3-methylcholanthrene (3-MC).	Methylcholanthrene	209-229	aryl hydrocarbon receptor	Homo sapiens	169-194
15169886-3	2004	In the HuH7 human hepatoma cell line, PON-1 activity and mRNA levels were increased by dietary polyphenolic compounds such as quercetin but also by toxic ligands of the aryl hydrocarbon receptor (AhR) such as 3-methylcholanthrene (3-MC).	Methylcholanthrene	209-229	aryl hydrocarbon receptor	Homo sapiens	196-199
15169886-3	2004	In the HuH7 human hepatoma cell line, PON-1 activity and mRNA levels were increased by dietary polyphenolic compounds such as quercetin but also by toxic ligands of the aryl hydrocarbon receptor (AhR) such as 3-methylcholanthrene (3-MC).	Methylcholanthrene	231-235	paraoxonase 1	Homo sapiens	38-43
15169886-3	2004	In the HuH7 human hepatoma cell line, PON-1 activity and mRNA levels were increased by dietary polyphenolic compounds such as quercetin but also by toxic ligands of the aryl hydrocarbon receptor (AhR) such as 3-methylcholanthrene (3-MC).	Methylcholanthrene	231-235	aryl hydrocarbon receptor	Homo sapiens	196-199
15169886-6	2004	Deletions and mutations studies showed that a xenobiotic responsive element (XRE)-like sequence within the PON-1 promoter mediated the effect of 3-MC and quercetin.	Methylcholanthrene	145-149	paraoxonase 1	Homo sapiens	107-112
15113961-12	2004	Estrogen-responsive pS2 mRNA expression in tumors did not differ among groups, but expression of the antiapoptotic marker B-cell lymphoma/leukemia-2 (bcl-2) in tumors from the E(2) + MC group was downregulated, compared to that of the E(2) treatment group.	Methylcholanthrene	183-185	BCL2 apoptosis regulator	Homo sapiens	150-155
15148458-6	2004	However, when MC were exposed in in vitro conditions for 24 h to the studied dialysates, we observed that HA containing fluids inhibited the synthesis of MCP-1, s-ICAM, VEGF and fibronectin in these cells.	Methylcholanthrene	14-16	C-C motif chemokine ligand 2	Homo sapiens	154-159
15148458-6	2004	However, when MC were exposed in in vitro conditions for 24 h to the studied dialysates, we observed that HA containing fluids inhibited the synthesis of MCP-1, s-ICAM, VEGF and fibronectin in these cells.	Methylcholanthrene	14-16	vascular endothelial growth factor A	Homo sapiens	169-173
15148458-6	2004	However, when MC were exposed in in vitro conditions for 24 h to the studied dialysates, we observed that HA containing fluids inhibited the synthesis of MCP-1, s-ICAM, VEGF and fibronectin in these cells.	Methylcholanthrene	14-16	fibronectin 1	Homo sapiens	178-189
14991938-7	2004	The expression of Bcl-2, Bax, fas and FasL in colonic epithelial cells in MC was higher than that in NC, and was markedly down- regulated by herbs-partition moxibustion or electro-acupuncture treatment.	Methylcholanthrene	74-76	BCL2, apoptosis regulator	Rattus norvegicus	18-23
15193226-10	2004	CONCLUSION: IC can directly stimulate MCs proliferation through Akt/NF-kappa B signal pathway, suggesting that NF-kappa B probably be a useful molecule for targeted therapy in IC-mediated MC overproliferation.	Methylcholanthrene	38-40	thymoma viral proto-oncogene 1	Mus musculus	64-67
15193226-10	2004	CONCLUSION: IC can directly stimulate MCs proliferation through Akt/NF-kappa B signal pathway, suggesting that NF-kappa B probably be a useful molecule for targeted therapy in IC-mediated MC overproliferation.	Methylcholanthrene	38-40	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-78
15193226-10	2004	CONCLUSION: IC can directly stimulate MCs proliferation through Akt/NF-kappa B signal pathway, suggesting that NF-kappa B probably be a useful molecule for targeted therapy in IC-mediated MC overproliferation.	Methylcholanthrene	38-40	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	111-121
14633661-5	2004	In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice.	Methylcholanthrene	88-91	neuroblastoma ras oncogene	Mus musculus	41-46
14987951-1	2004	Benzimidazoles compounds like omeprazole (OME) and thiabendazole (TBZ) mediate CYP1A1 induction differently from classical aryl hydrocarbon receptor (AhR) ligands, 3-methylcholanthrene (3-MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	186-190	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	79-85
14987951-5	2004	The mechanism of benzimidazole-mediated induction of CYP1A1 was investigated by comparison with 3-MC, a prototypical AhR ligand.	Methylcholanthrene	96-100	aryl hydrocarbon receptor	Rattus norvegicus	117-120
14993811-3	2004	When human fibroblast-like synoviocytes line, MH7A, was treated with 3-methylcholanthrene (3-MC), a polycyclic aromatic hydrocarbon (PAH), mRNA of IL-1beta was up-regulated.	Methylcholanthrene	69-89	interleukin 1 beta	Homo sapiens	147-155
14993811-3	2004	When human fibroblast-like synoviocytes line, MH7A, was treated with 3-methylcholanthrene (3-MC), a polycyclic aromatic hydrocarbon (PAH), mRNA of IL-1beta was up-regulated.	Methylcholanthrene	91-95	interleukin 1 beta	Homo sapiens	147-155
15020204-8	2004	Also, the time taken for the flow of erythrocyte and plasma through the MC-FAN was slower for the high-cholesterol group.	Methylcholanthrene	72-74	neutral sphingomyelinase activation associated factor	Homo sapiens	75-78
14633661-5	2004	In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice.	Methylcholanthrene	66-86	neuroblastoma ras oncogene	Mus musculus	41-46
15031337-7	2004	Pre-incubation of the MC layer for 48 h with 55 mM glucose, a combination of two glucose degradation products, methylglyoxal and 3-deoxyglucosone, or conventional dialysis fluid (1:4 dilution), however, did not change the IL-8-induced migration of neutrophils.	Methylcholanthrene	22-24	C-X-C motif chemokine ligand 8	Homo sapiens	222-226
14993811-4	2004	MH7A cells express functional aryl hydrocarbon receptor (AhR) as shown by 3-MC-inducible CYP1A1 mRNA expression.	Methylcholanthrene	74-78	aryl hydrocarbon receptor	Homo sapiens	30-55
14993811-4	2004	MH7A cells express functional aryl hydrocarbon receptor (AhR) as shown by 3-MC-inducible CYP1A1 mRNA expression.	Methylcholanthrene	74-78	aryl hydrocarbon receptor	Homo sapiens	57-60
14993811-4	2004	MH7A cells express functional aryl hydrocarbon receptor (AhR) as shown by 3-MC-inducible CYP1A1 mRNA expression.	Methylcholanthrene	74-78	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	89-95
15129972-7	2004	MIC Mix was formulated as a combination of insulin powder (MI") and citric acid powder (MC).	Methylcholanthrene	88-90	Mix paired-like homeobox	Homo sapiens	4-7
14991938-7	2004	The expression of Bcl-2, Bax, fas and FasL in colonic epithelial cells in MC was higher than that in NC, and was markedly down- regulated by herbs-partition moxibustion or electro-acupuncture treatment.	Methylcholanthrene	74-76	BCL2 associated X, apoptosis regulator	Rattus norvegicus	25-28
14991938-7	2004	The expression of Bcl-2, Bax, fas and FasL in colonic epithelial cells in MC was higher than that in NC, and was markedly down- regulated by herbs-partition moxibustion or electro-acupuncture treatment.	Methylcholanthrene	74-76	Fas ligand	Rattus norvegicus	38-42
14667934-0	2004	Inhibition of osteoclast formation by 3-methylcholanthrene, a ligand for arylhydrocarbon receptor: suppression of osteoclast differentiation factor in osteogenic cells.	Methylcholanthrene	38-58	aryl-hydrocarbon receptor	Mus musculus	73-97
14672759-7	2004	The induction of AhRR or CYP1A1 expression by 3-methylcholanthrene (3-MC) was observed in MNCs from adults but not from umbilical cord blood.	Methylcholanthrene	46-66	aryl hydrocarbon receptor repressor	Homo sapiens	17-21
14672759-7	2004	The induction of AhRR or CYP1A1 expression by 3-methylcholanthrene (3-MC) was observed in MNCs from adults but not from umbilical cord blood.	Methylcholanthrene	46-66	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	25-31
14672759-7	2004	The induction of AhRR or CYP1A1 expression by 3-methylcholanthrene (3-MC) was observed in MNCs from adults but not from umbilical cord blood.	Methylcholanthrene	68-72	aryl hydrocarbon receptor repressor	Homo sapiens	17-21
14672759-7	2004	The induction of AhRR or CYP1A1 expression by 3-methylcholanthrene (3-MC) was observed in MNCs from adults but not from umbilical cord blood.	Methylcholanthrene	68-72	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	25-31
14759523-1	2004	Differential mRNA display revealed that a cDNA encoding the major urinary protein 2 (MUP2) that belongs to the lipocalin superfamily was absent in livers of mice treated with 3-methylcholanthrene (MC).	Methylcholanthrene	175-195	major urinary protein 2	Mus musculus	60-83
14759523-1	2004	Differential mRNA display revealed that a cDNA encoding the major urinary protein 2 (MUP2) that belongs to the lipocalin superfamily was absent in livers of mice treated with 3-methylcholanthrene (MC).	Methylcholanthrene	175-195	major urinary protein 2	Mus musculus	85-89
14759523-1	2004	Differential mRNA display revealed that a cDNA encoding the major urinary protein 2 (MUP2) that belongs to the lipocalin superfamily was absent in livers of mice treated with 3-methylcholanthrene (MC).	Methylcholanthrene	197-199	major urinary protein 2	Mus musculus	60-83
14759523-1	2004	Differential mRNA display revealed that a cDNA encoding the major urinary protein 2 (MUP2) that belongs to the lipocalin superfamily was absent in livers of mice treated with 3-methylcholanthrene (MC).	Methylcholanthrene	197-199	major urinary protein 2	Mus musculus	85-89
14759523-3	2004	Since MC is an aryl hydrocarbon receptor (AhR) ligand, the effects of MC treatment on the expression of GHR, JAK2 or STAT5 in the livers of wild-type or AhR-null mice were examined.	Methylcholanthrene	70-72	growth hormone receptor	Mus musculus	104-107
14759523-3	2004	Since MC is an aryl hydrocarbon receptor (AhR) ligand, the effects of MC treatment on the expression of GHR, JAK2 or STAT5 in the livers of wild-type or AhR-null mice were examined.	Methylcholanthrene	70-72	signal transducer and activator of transcription 5A	Mus musculus	117-122
14759523-4	2004	The result indicated that the expression of GHR and JAK2 mRNA was greatly decreased by MC in wild-type mice but not in AhR-null mice.	Methylcholanthrene	87-89	growth hormone receptor	Mus musculus	44-47
14759523-4	2004	The result indicated that the expression of GHR and JAK2 mRNA was greatly decreased by MC in wild-type mice but not in AhR-null mice.	Methylcholanthrene	87-89	Janus kinase 2	Mus musculus	52-56
14759523-5	2004	In addition, the binding activity of STAT5 bound to STAT5-binding element was reduced after MC treatment in wild-type mice but not in AhR-null mice.	Methylcholanthrene	92-94	signal transducer and activator of transcription 5A	Mus musculus	37-42
14759523-5	2004	In addition, the binding activity of STAT5 bound to STAT5-binding element was reduced after MC treatment in wild-type mice but not in AhR-null mice.	Methylcholanthrene	92-94	signal transducer and activator of transcription 5A	Mus musculus	52-57
14759523-6	2004	Based on these results, we conclude that the suppression of MUP2 mRNA expression by MC is caused by the AhR-mediated disruption of the GH signaling pathway.	Methylcholanthrene	84-86	major urinary protein 2	Mus musculus	60-64
14759523-6	2004	Based on these results, we conclude that the suppression of MUP2 mRNA expression by MC is caused by the AhR-mediated disruption of the GH signaling pathway.	Methylcholanthrene	84-86	aryl-hydrocarbon receptor	Mus musculus	104-107
14759523-6	2004	Based on these results, we conclude that the suppression of MUP2 mRNA expression by MC is caused by the AhR-mediated disruption of the GH signaling pathway.	Methylcholanthrene	84-86	growth hormone	Mus musculus	135-137
14667934-9	2004	Furthermore, soluble RANKL was able to counteract the inhibitory effect of 3MC on the formation of osteoclast-like cells.	Methylcholanthrene	75-78	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	21-26
14667934-10	2004	Our findings indicate that 3MC inhibits osteoclastogenesis via the inhibition of RANKL expression in osteoblastic cells.	Methylcholanthrene	27-30	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	81-86
14709899-0	2004	Cytochrome P450 1A1 (CYP1A1) inhibitor alpha-naphthoflavone interferes with UDP-glucuronosyltransferase (UGT) activity in intact but not in permeabilized hepatic microsomes from 3-methylcholanthrene-treated rats: possible involvement of UGT-P450 interactions.	Methylcholanthrene	178-198	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-19
14709899-0	2004	Cytochrome P450 1A1 (CYP1A1) inhibitor alpha-naphthoflavone interferes with UDP-glucuronosyltransferase (UGT) activity in intact but not in permeabilized hepatic microsomes from 3-methylcholanthrene-treated rats: possible involvement of UGT-P450 interactions.	Methylcholanthrene	178-198	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	21-27
14667934-1	2004	We investigated the effects of 3-methylcholanthrene (3MC), a ligand for arylhydrocarbon receptor (AhR), on osteoclastogenesis.	Methylcholanthrene	31-51	aryl-hydrocarbon receptor	Mus musculus	72-96
14709899-0	2004	Cytochrome P450 1A1 (CYP1A1) inhibitor alpha-naphthoflavone interferes with UDP-glucuronosyltransferase (UGT) activity in intact but not in permeabilized hepatic microsomes from 3-methylcholanthrene-treated rats: possible involvement of UGT-P450 interactions.	Methylcholanthrene	178-198	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	105-108
14667934-1	2004	We investigated the effects of 3-methylcholanthrene (3MC), a ligand for arylhydrocarbon receptor (AhR), on osteoclastogenesis.	Methylcholanthrene	31-51	aryl-hydrocarbon receptor	Mus musculus	98-101
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	92-112	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	10-37
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	92-112	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	39-42
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	92-112	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	318-321
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	114-116	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	10-37
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	114-116	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	39-42
14709899-2	2004	While the UDP-glucuronosyltransferase (UGT) activity with non-permeabilized microsomes from 3-methylcholanthrene (MC)-treated rats was markedly reduced by alpha-naphthoflavone (NF), this inhibitor had hardly any effect when permeabilized microsomes were used in which the inhibitor was expected to have easy access to UGT.	Methylcholanthrene	114-116	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	318-321
14709899-4	2004	These results suggest that a UGT isoform(s) involved in 3-OH-B(a)P glucuronidation is interfered by a CYP1A inhibitor via a mechanism dependent on the intact nature of microsomal membranes in MC-treated rats.	Methylcholanthrene	192-194	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	29-32
14667934-1	2004	We investigated the effects of 3-methylcholanthrene (3MC), a ligand for arylhydrocarbon receptor (AhR), on osteoclastogenesis.	Methylcholanthrene	53-56	aryl-hydrocarbon receptor	Mus musculus	72-96
14667934-1	2004	We investigated the effects of 3-methylcholanthrene (3MC), a ligand for arylhydrocarbon receptor (AhR), on osteoclastogenesis.	Methylcholanthrene	53-56	aryl-hydrocarbon receptor	Mus musculus	98-101
14667934-7	2004	When we measured the expression levels of RANKL mRNA in ST2 cells, 3MC dose-dependently decreased the level of this mRNA.	Methylcholanthrene	67-70	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	42-47
15746899-3	2004	Complementary DNA of cytochrome CYP1B1 was isolated from carp (Cyprinus carpio) liver 24 h after the injection of 3-methylcholanthrene (3-MC).	Methylcholanthrene	114-134	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	32-38
15746899-3	2004	Complementary DNA of cytochrome CYP1B1 was isolated from carp (Cyprinus carpio) liver 24 h after the injection of 3-methylcholanthrene (3-MC).	Methylcholanthrene	136-140	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	32-38
15746899-10	2004	Carp treated with 3-MC showed expression of CYP1B1 in liver, intestine and gills with distinct induction except for the gills that showed marked constitutive expression.	Methylcholanthrene	18-22	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	44-50
15750580-8	2004	Despite the structural similarity of CYP1B2 with CYP1B1, which showed induced expression in 3-MC-treated liver, intestine, and gills with marked constitutive expression in gills, CYP1B2 revealed induced expression in gills but not in liver or intestine, and no detectable constitutive expression in the tissues studied.	Methylcholanthrene	92-96	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	49-55
15020415-7	2004	While eat-2 appears to be required specifically for MC neurotransmission, eat-18 also appears to be required for the function of other nicotinic receptors in the pharynx.	Methylcholanthrene	52-54	Neuronal acetylcholine receptor subunit eat-2	Caenorhabditis elegans	6-11
14694527-9	2004	Additional comparative analyses of FGF2-mediated effects in two ES cell lines (CADO-ES, RD-ES) and a PNET cell line (SK-N-MC) showed pronounced differentiation in SK-N-MC, but not in CADO-ES or RD-ES cells.	Methylcholanthrene	122-124	fibroblast growth factor 2	Homo sapiens	35-39
15791841-4	2004	Our results showed that expression of ACAT-1 protein and mRNA in MP-group is two times that in MC-group (P&lt;0.05), and the expression of ACAT-1 protein and mRNA increased by up to 4 folds in leptin-MP group-as compared with that of MC group (P&lt;0.01).	Methylcholanthrene	95-97	acetyl-CoA acetyltransferase 1	Homo sapiens	38-44
15791841-4	2004	Our results showed that expression of ACAT-1 protein and mRNA in MP-group is two times that in MC-group (P&lt;0.05), and the expression of ACAT-1 protein and mRNA increased by up to 4 folds in leptin-MP group-as compared with that of MC group (P&lt;0.01).	Methylcholanthrene	234-236	acetyl-CoA acetyltransferase 1	Homo sapiens	38-44
15791841-4	2004	Our results showed that expression of ACAT-1 protein and mRNA in MP-group is two times that in MC-group (P&lt;0.05), and the expression of ACAT-1 protein and mRNA increased by up to 4 folds in leptin-MP group-as compared with that of MC group (P&lt;0.01).	Methylcholanthrene	234-236	acetyl-CoA acetyltransferase 1	Homo sapiens	139-145
14697657-11	2003	Furthermore we show that the inhibitory effect of MC-derived Sema3A on neurite outgrowth is modulated by nerve growth factor.	Methylcholanthrene	50-52	semaphorin 3A	Homo sapiens	61-67
14653967-6	2003	RESULTS: The levels of TNF-alpha, IL-1beta, IL-6, TGF-beta, total and differential WCC in BALF of MC groups were significantly decreased than that of COPD group (P&lt;0.01), and there was no significant difference among MC groups.	Methylcholanthrene	98-100	tumor necrosis factor	Rattus norvegicus	23-32
14653967-6	2003	RESULTS: The levels of TNF-alpha, IL-1beta, IL-6, TGF-beta, total and differential WCC in BALF of MC groups were significantly decreased than that of COPD group (P&lt;0.01), and there was no significant difference among MC groups.	Methylcholanthrene	98-100	interleukin 1 beta	Rattus norvegicus	34-42
14653967-6	2003	RESULTS: The levels of TNF-alpha, IL-1beta, IL-6, TGF-beta, total and differential WCC in BALF of MC groups were significantly decreased than that of COPD group (P&lt;0.01), and there was no significant difference among MC groups.	Methylcholanthrene	98-100	interleukin 6	Rattus norvegicus	44-48
14653967-6	2003	RESULTS: The levels of TNF-alpha, IL-1beta, IL-6, TGF-beta, total and differential WCC in BALF of MC groups were significantly decreased than that of COPD group (P&lt;0.01), and there was no significant difference among MC groups.	Methylcholanthrene	98-100	transforming growth factor, beta 1	Rattus norvegicus	50-58
14688371-4	2004	In contrast, mast cells of the MC(TC) phenotype from skin and lung were resistant to IL-4-mediated apoptosis, even after neutralization of endogenous IL-6.	Methylcholanthrene	31-33	interleukin 4	Homo sapiens	85-89
14688371-4	2004	In contrast, mast cells of the MC(TC) phenotype from skin and lung were resistant to IL-4-mediated apoptosis, even after neutralization of endogenous IL-6.	Methylcholanthrene	31-33	interleukin 6	Homo sapiens	150-154
12941938-0	2003	Oltipraz inhibits 3-methylcholanthrene induction of CYP1A1 by CCAAT/enhancer-binding protein activation.	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-58
12941938-4	2003	3-MC induced CYP1A1 in H4IIE cells in a time- and concentration-dependent manner.	Methylcholanthrene	0-4	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	13-19
12941938-9	2003	Oltipraz (10 microM) significantly inhibited CYP1A1 and CYP1A1-luciferase gene induction by 3-MC with no increase in AhR DNA binding.	Methylcholanthrene	92-96	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	45-51
12941938-9	2003	Oltipraz (10 microM) significantly inhibited CYP1A1 and CYP1A1-luciferase gene induction by 3-MC with no increase in AhR DNA binding.	Methylcholanthrene	92-96	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-62
12941938-11	2003	Overexpression of dominant-negative mutant C/EBP significantly abolished the ability of oltipraz to suppress 3-MC-inducible CYP1A1 and the CYP1A1 reporter gene expression.	Methylcholanthrene	109-113	CCAAT enhancer binding protein alpha	Homo sapiens	43-48
12941938-11	2003	Overexpression of dominant-negative mutant C/EBP significantly abolished the ability of oltipraz to suppress 3-MC-inducible CYP1A1 and the CYP1A1 reporter gene expression.	Methylcholanthrene	109-113	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	124-130
12941938-12	2003	Consistently, C/EBPbeta overexpression blocked CYP1A1 reporter gene induction by 3-MC.	Methylcholanthrene	81-85	CCAAT enhancer binding protein beta	Homo sapiens	14-23
12941938-12	2003	Consistently, C/EBPbeta overexpression blocked CYP1A1 reporter gene induction by 3-MC.	Methylcholanthrene	81-85	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	47-53
14623055-9	2003	We conclude that COX-2 in cancer cells is responsible for PGE(2) and OC production in cocultures with MMT060562, while COX-2 in bone marrow cells, not cancer cells, is responsible for PGE(2) and OC production in cocultures with BALB/c-MC, and EP4 receptors are essential for OC formation in both cocultures.	Methylcholanthrene	235-237	prostaglandin-endoperoxide synthase 2	Mus musculus	17-22
12941938-13	2003	These results provide evidence that oltipraz suppresses 3-MC induction of CYP1A1 gene expression and that activation of C/EBPbeta by oltipraz contributes to suppression of 3-MC-inducible AhR-mediated CYP1A1 expression.	Methylcholanthrene	56-60	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	74-80
12941938-13	2003	These results provide evidence that oltipraz suppresses 3-MC induction of CYP1A1 gene expression and that activation of C/EBPbeta by oltipraz contributes to suppression of 3-MC-inducible AhR-mediated CYP1A1 expression.	Methylcholanthrene	172-176	CCAAT enhancer binding protein beta	Homo sapiens	120-129
12941938-13	2003	These results provide evidence that oltipraz suppresses 3-MC induction of CYP1A1 gene expression and that activation of C/EBPbeta by oltipraz contributes to suppression of 3-MC-inducible AhR-mediated CYP1A1 expression.	Methylcholanthrene	172-176	aryl hydrocarbon receptor	Homo sapiens	187-190
12941938-13	2003	These results provide evidence that oltipraz suppresses 3-MC induction of CYP1A1 gene expression and that activation of C/EBPbeta by oltipraz contributes to suppression of 3-MC-inducible AhR-mediated CYP1A1 expression.	Methylcholanthrene	172-176	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	200-206
14613648-9	2003	(3) In 42 paraffin-embedded GCT specimens, the positive expression rates of NOS1, NOS2, and NOS3 protein were 85.7%, 59.5%, and 31.0% in MGC, 54.8%, 28.6%, and 14.3% in MC, respectively.	Methylcholanthrene	169-171	nitric oxide synthase 1	Homo sapiens	76-80
14613648-9	2003	(3) In 42 paraffin-embedded GCT specimens, the positive expression rates of NOS1, NOS2, and NOS3 protein were 85.7%, 59.5%, and 31.0% in MGC, 54.8%, 28.6%, and 14.3% in MC, respectively.	Methylcholanthrene	169-171	nitric oxide synthase 3	Homo sapiens	92-96
14613648-11	2003	(5)The positive expression rate of NOS1 protein in MC of the recurrent group was significantly higher than that of the non-recurrent group (P=0.018).	Methylcholanthrene	51-53	nitric oxide synthase 1	Homo sapiens	35-39
14569089-8	2003	Infection of MC with the RhoA mutant RhoA-Ala188, which is resistant to NO-dependent phosphorylation, abrogated the effects of NO and cGMP on stretch-induced Erk activation and stress fiber formation.	Methylcholanthrene	13-15	Eph receptor B1	Rattus norvegicus	158-161
12832153-3	2003	32P-postlabeling analysis of DNA incubated with DMBA in the presence of 3-methylcholanthrene (3-MC)-induced microsomes produced three major adducts derived from anti-, syn- and anti-dihydrodiol epoxides through reactions with dGuo and dAdo, respectively.	Methylcholanthrene	72-92	synemin	Homo sapiens	168-171
14569089-3	2003	In an in vitro model of hemodynamically mediated signaling, the authors have reported that subjecting MC to cyclic stretch/relaxation activates the mitogen-activated protein kinase p42/44 (Erk) cascade and that NO and cyclic GMP abrogate stretch-induced Erk activation by inducing actin cytoskeletal disassembly.	Methylcholanthrene	102-104	Eph receptor B1	Rattus norvegicus	189-192
14569089-3	2003	In an in vitro model of hemodynamically mediated signaling, the authors have reported that subjecting MC to cyclic stretch/relaxation activates the mitogen-activated protein kinase p42/44 (Erk) cascade and that NO and cyclic GMP abrogate stretch-induced Erk activation by inducing actin cytoskeletal disassembly.	Methylcholanthrene	102-104	Eph receptor B1	Rattus norvegicus	254-257
14569089-5	2003	In primary rat MC subjected to cyclic mechanical strain, RhoA activity was maximally increased (2.4-fold) after 1 min of stretch, and Erk activation temporally followed.	Methylcholanthrene	15-17	ras homolog family member A	Rattus norvegicus	57-61
14569089-8	2003	Infection of MC with the RhoA mutant RhoA-Ala188, which is resistant to NO-dependent phosphorylation, abrogated the effects of NO and cGMP on stretch-induced Erk activation and stress fiber formation.	Methylcholanthrene	13-15	ras homolog family member A	Rattus norvegicus	25-29
14569089-8	2003	Infection of MC with the RhoA mutant RhoA-Ala188, which is resistant to NO-dependent phosphorylation, abrogated the effects of NO and cGMP on stretch-induced Erk activation and stress fiber formation.	Methylcholanthrene	13-15	ras homolog family member A	Rattus norvegicus	37-41
14569089-9	2003	The authors conclude that the early activation of RhoA is essential for stretch-induced actin stress fiber formation and Erk activation in MC, events which are prevented by NO and cGMP through their action on RhoA.	Methylcholanthrene	139-141	ras homolog family member A	Rattus norvegicus	50-54
14569089-9	2003	The authors conclude that the early activation of RhoA is essential for stretch-induced actin stress fiber formation and Erk activation in MC, events which are prevented by NO and cGMP through their action on RhoA.	Methylcholanthrene	139-141	Eph receptor B1	Rattus norvegicus	121-124
14569089-9	2003	The authors conclude that the early activation of RhoA is essential for stretch-induced actin stress fiber formation and Erk activation in MC, events which are prevented by NO and cGMP through their action on RhoA.	Methylcholanthrene	139-141	ras homolog family member A	Rattus norvegicus	209-213
14566647-3	2003	Double staining was used to distinguish MC(S) as positive for both chymase and tryptase (MC(TC)).	Methylcholanthrene	40-42	chymase 1	Homo sapiens	67-87
12882800-5	2003	RESULTS: AP-1 stimulators, such as beta-naphthoflavone, 3-methylcholanthrene, and tBHQ, significantly upregulated (2-4-fold) TM cell expression of MMP-3.	Methylcholanthrene	56-76	matrix metallopeptidase 3	Homo sapiens	147-152
13677937-4	2003	Our results suggest that blood rheology measured by MC-FAN is related to aging, body weight, body mass index and serum lipid parameters (total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglyceride).	Methylcholanthrene	52-54	neutral sphingomyelinase activation associated factor	Homo sapiens	55-58
13677937-5	2003	These results suggest that MC-FAN is useful to analyze blood rheology in pathophysiological conditions.	Methylcholanthrene	27-29	neutral sphingomyelinase activation associated factor	Homo sapiens	30-33
12832153-3	2003	32P-postlabeling analysis of DNA incubated with DMBA in the presence of 3-methylcholanthrene (3-MC)-induced microsomes produced three major adducts derived from anti-, syn- and anti-dihydrodiol epoxides through reactions with dGuo and dAdo, respectively.	Methylcholanthrene	94-98	synemin	Homo sapiens	168-171
12823241-2	2003	METHODS: Based on material from the Diabetes Control and Complications Trial study (n=1441), patients were considered as under good or poor MC if their HbA1c mean level up to last visit fell in the lowest (&lt; or =6.9%) or highest (&gt;or =9.5%) quintile of the overall HbA1c distribution, respectively.	Methylcholanthrene	140-142	hemoglobin subunit alpha 1	Homo sapiens	152-156
12845369-0	2003	Expression of CYP2A3 mRNA and its regulation by 3-methylcholanthrene, pyrazole, and beta-ionone in rat tissues.	Methylcholanthrene	48-68	cytochrome P450, family 2, subfamily a, polypeptide 3	Rattus norvegicus	14-20
12845369-9	2003	CYP2A3 mRNA levels were increased in the esophagus by treatment with 3-methylcholanthrene and pyrazole (17- and 7-fold, respectively), in lung by pyrazole and  -ionone (3- and 4-fold, respectively, although not statistically significant), in the distal part of the intestine and kidney by 3-methylcholanthrene and pyrazole, and in the proximal part of the intestine by pyrazole.	Methylcholanthrene	69-89	cytochrome P450, family 2, subfamily a, polypeptide 3	Rattus norvegicus	0-6
12845369-9	2003	CYP2A3 mRNA levels were increased in the esophagus by treatment with 3-methylcholanthrene and pyrazole (17- and 7-fold, respectively), in lung by pyrazole and  -ionone (3- and 4-fold, respectively, although not statistically significant), in the distal part of the intestine and kidney by 3-methylcholanthrene and pyrazole, and in the proximal part of the intestine by pyrazole.	Methylcholanthrene	289-309	cytochrome P450, family 2, subfamily a, polypeptide 3	Rattus norvegicus	0-6
12730689-5	2003	Treatment of methylcholanthrene-induced (Meth A) ascites tumors with IL-2 and &gt; or =3 mg per kg body weight M40403 induced 50% complete remissions lasting for more than 200 d, which was longer than those of untreated mice (15-d median survival) or mice treated with IL-2 alone (22-d median).	Methylcholanthrene	13-31	interleukin 2	Mus musculus	69-73
12730689-5	2003	Treatment of methylcholanthrene-induced (Meth A) ascites tumors with IL-2 and &gt; or =3 mg per kg body weight M40403 induced 50% complete remissions lasting for more than 200 d, which was longer than those of untreated mice (15-d median survival) or mice treated with IL-2 alone (22-d median).	Methylcholanthrene	13-31	interleukin 2	Mus musculus	269-273
12934447-6	2003	Thus, for MC patient, the DRB 1 * 0301/DQB*0201 haplotype might be associated with less occurrence of fistulas or severe forms requiring immunosuppressive therapy.	Methylcholanthrene	10-12	major histocompatibility complex, class II, DR beta 1	Homo sapiens	26-31
12672449-4	2003	REGgamma is highly expressed in brain, located in the nucleus and actually suppresses the proteasome active sites principally responsible for cleaving glutamine-MCA bonds.	Methylcholanthrene	161-164	proteasome activator subunit 3	Homo sapiens	0-8
12938821-8	2003	However, incubation of MC with higher concentrations of HA (30-1000 mg/dL) resulted in a concentration- and time- (8- 48 hours) dependent decrease in t-PA antigen release and mRNA expression.	Methylcholanthrene	23-25	plasminogen activator, tissue type	Homo sapiens	150-154
12938821-10	2003	CONCLUSION: The expression of t-PA and PAI-1 in MC was not affected by low concentrations of HA.	Methylcholanthrene	48-50	plasminogen activator, tissue type	Homo sapiens	30-34
12938821-10	2003	CONCLUSION: The expression of t-PA and PAI-1 in MC was not affected by low concentrations of HA.	Methylcholanthrene	48-50	serpin family E member 1	Homo sapiens	39-44
12700417-5	2003	Treatment of mice with MC or OAT caused CYP1A1 accumulation in the liver of C57BL and A/Sn mice, but not in AKR, SWR, and DBA mice.	Methylcholanthrene	23-25	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	40-46
12700417-8	2003	After treatment with MC and OAT the CYP1A1 mRNA level dramatically increased in all strains examined while the increase in the CYP1A2 mRNA level was not striking.	Methylcholanthrene	21-23	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	36-42
12851037-6	2003	In 3-methylcholanthrene-treated mouse liver microsomes, tanshinone IIA and two minor tanshinones, tanshinone I and cryptotanshinone, inhibited liver microsomal MROD activity without affecting EROD and benzo(a)pyrene hydroxylation activities at the concentrations up to 1 microM.	Methylcholanthrene	3-23	ATPase, class II, type 9A	Mus musculus	67-70
12872719-6	2003	In hamsters, the concentration of M-4 was increased to 1.8-fold of untreated animals by PB treatment and 2.6-fold by MC treatment.	Methylcholanthrene	117-119	cholinergic receptor, muscarinic 4	Rattus norvegicus	34-37
12700417-0	2003	Cytochrome P4501A1 and 1A2 gene expression in the liver of 3-methylcholanthrene- and o-aminoazotoluene-treated mice: a comparison between PAH-responsive and PAH-nonresponsive strains.	Methylcholanthrene	59-79	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-26
12700417-1	2003	The objective of this study was to investigate cytochrome P4501A1 and 1A2 mRNA, protein, and enzyme activity in the liver of male mice differing in the aryl hydrocarbon receptor (AhR) genotype during treatment with the carcinogenic compounds 3-methylcholanthrene (MC) and o-aminoazotoluene (OAT).	Methylcholanthrene	242-262	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	47-73
12700417-1	2003	The objective of this study was to investigate cytochrome P4501A1 and 1A2 mRNA, protein, and enzyme activity in the liver of male mice differing in the aryl hydrocarbon receptor (AhR) genotype during treatment with the carcinogenic compounds 3-methylcholanthrene (MC) and o-aminoazotoluene (OAT).	Methylcholanthrene	242-262	aryl-hydrocarbon receptor	Mus musculus	152-177
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	150-170	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	75-80
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	150-170	phosphoglycolate phosphatase	Homo sapiens	85-88
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	150-170	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	110-115
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	172-175	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	75-80
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	172-175	phosphoglycolate phosphatase	Homo sapiens	85-88
12657491-5	2003	For this reason, in this work, the time dependent responses of the hepatic CYP1A and Pgp, to the prototypical CYP1A inducers, benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in X. laevis have been assessed at the protein level and compared.	Methylcholanthrene	172-175	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	110-115
12657491-8	2003	Western blot evidenced that a single injection of B(a)P (100 mg/kg), 3MC (20 mg/kg), and TCDD (3 microg/kg) elicited a statistically significant induction of hepatic CYP1A at all time points considered (72, 120 and 168 h) which decreased in time.	Methylcholanthrene	69-72	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	166-171
12657491-13	2003	For the first time the modulation of CYP1A and Pgp levels by B(a)P, 3MC and in particular by TCDD and T(3) in Xenopus has been demonstrated and the results herewith indicate that the two target defence mechanisms respond to AHR agonists in a dissimilar way in terms of proteins induction in Xenopus.	Methylcholanthrene	68-71	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	37-42
12657491-13	2003	For the first time the modulation of CYP1A and Pgp levels by B(a)P, 3MC and in particular by TCDD and T(3) in Xenopus has been demonstrated and the results herewith indicate that the two target defence mechanisms respond to AHR agonists in a dissimilar way in terms of proteins induction in Xenopus.	Methylcholanthrene	68-71	phosphoglycolate phosphatase	Homo sapiens	47-50
12657491-13	2003	For the first time the modulation of CYP1A and Pgp levels by B(a)P, 3MC and in particular by TCDD and T(3) in Xenopus has been demonstrated and the results herewith indicate that the two target defence mechanisms respond to AHR agonists in a dissimilar way in terms of proteins induction in Xenopus.	Methylcholanthrene	68-71	aryl hydrocarbon receptor L homeolog	Xenopus laevis	224-227
12633663-1	2003	IFN-gamma contributes to the rejection of transplantable tumors and the inhibition of methylcholanthrene (MCA)-induced carcinogenesis by different mechanisms.	Methylcholanthrene	86-104	interferon gamma	Homo sapiens	0-9
12633663-1	2003	IFN-gamma contributes to the rejection of transplantable tumors and the inhibition of methylcholanthrene (MCA)-induced carcinogenesis by different mechanisms.	Methylcholanthrene	106-109	interferon gamma	Homo sapiens	0-9
12642474-7	2003	In addition, CYP1A1 protein was detected in microsomes from HepG2 cells pretreated with 3-methylcholanthrene but not with the vehicle.	Methylcholanthrene	88-108	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	13-19
12719028-5	2003	Blood samples were taken over the next 24 h. RESULTS: Subcutaneous injection of Semitard MC caused a greater fall in plasma glucose concentration and lower mean plasma glucose levels throughout the study compared to NPH, reflecting the higher insulin concentrations observed during the 24-h study period.	Methylcholanthrene	89-91	insulin	Homo sapiens	243-250
12655030-7	2003	The expression of AhRR mRNA was induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylchoranthrene (3-MC) in HepG2, MCF-7, LS-180, and OMC-3 cells, but not in ACHN, A549, HT-1197, HeLa, and NEC14 cells.	Methylcholanthrene	111-115	aryl hydrocarbon receptor repressor	Homo sapiens	18-22
12655030-7	2003	The expression of AhRR mRNA was induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3-methylchoranthrene (3-MC) in HepG2, MCF-7, LS-180, and OMC-3 cells, but not in ACHN, A549, HT-1197, HeLa, and NEC14 cells.	Methylcholanthrene	111-115	La ribonucleoprotein 6, translational regulator	Homo sapiens	170-174
12505372-5	2003	A highly relevant function of the Ah receptor, the induction of CYP 1A1 in hepatocytes of C57BL/6 mice by the established inducers 3-methylcholanthrene (MC) and PCB77 was compared to the effect of PBF by measurement of ethoxyresorufin-o-deethylase (EROD) activity.	Methylcholanthrene	153-155	aryl-hydrocarbon receptor	Mus musculus	34-45
12594260-6	2003	Moreover, formation of adherent macrophagic cells was decreased in response to PAHs distinct from BP such as dimethylbenz(a)anthracene and 3-methylcholanthrene, which interact, like BP, with the arylhydrocarbon receptor (AhR) known to mediate many PAH effects.	Methylcholanthrene	139-159	aryl hydrocarbon receptor	Homo sapiens	195-219
12594260-6	2003	Moreover, formation of adherent macrophagic cells was decreased in response to PAHs distinct from BP such as dimethylbenz(a)anthracene and 3-methylcholanthrene, which interact, like BP, with the arylhydrocarbon receptor (AhR) known to mediate many PAH effects.	Methylcholanthrene	139-159	aryl hydrocarbon receptor	Homo sapiens	221-224
12592386-5	2003	We describe here that 2-5-fold overexpression of both Cdk6 and D3 enhances by 5x10(3)-10(6)-fold the susceptibility of the BALB/c3T3 and C3H10T1/2 mouse fibroblast lines to ultraviolet irradiation- as well as 3-methylcholanthrene-induced transformation.	Methylcholanthrene	209-229	cyclin-dependent kinase 6	Mus musculus	54-58
12446702-6	2003	Enzymatic studies performed with autophagin-3, the most widely expressed human autophagin, revealed that the recombinant protein hydrolyzed the synthetic substrate Mca-Thr-Phe-Gly-Met-Dpa-NH(2) whose sequence derives from that present around the Apg4 cleavage site in yeast Apg8/Aut7.	Methylcholanthrene	164-167	cysteine protease ATG4	Saccharomyces cerevisiae S288C	246-250
12446702-6	2003	Enzymatic studies performed with autophagin-3, the most widely expressed human autophagin, revealed that the recombinant protein hydrolyzed the synthetic substrate Mca-Thr-Phe-Gly-Met-Dpa-NH(2) whose sequence derives from that present around the Apg4 cleavage site in yeast Apg8/Aut7.	Methylcholanthrene	164-167	ubiquitin-like protein ATG8	Saccharomyces cerevisiae S288C	274-278
12604190-5	2003	Somewhat at odds with the foregoing, transient exposure to 3-methylcholanthrene also induced increased levels of ALDH3A1 and CYP1A1 in cultured, essentially ER(-), human breast epithelial MCF-10A cells.	Methylcholanthrene	59-79	aldehyde dehydrogenase 3 family member A1	Homo sapiens	113-120
12604190-5	2003	Somewhat at odds with the foregoing, transient exposure to 3-methylcholanthrene also induced increased levels of ALDH3A1 and CYP1A1 in cultured, essentially ER(-), human breast epithelial MCF-10A cells.	Methylcholanthrene	59-79	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	125-131
12604190-4	2003	Thus, transient exposure to 3-methylcholanthrene induced increased levels of ALDH3A1 in five cultured human breast (adeno)carcinoma cell lines that were documented as being ER(+), viz., MCF-7/0, MCF-7/OAP, T-47D, ZR-75-1 and MDA-MB-468, but failed to induce increased levels of this enzyme in four cultured human breast (adeno)carcinoma cell lines that have been historically viewed as being ER(-), viz., MDA-MB-231, SK-BR-3, HS-578-T and MDA-MB-435.	Methylcholanthrene	28-48	aldehyde dehydrogenase 3 family member A1	Homo sapiens	77-84
12604190-5	2003	Somewhat at odds with the foregoing, transient exposure to 3-methylcholanthrene also induced increased levels of ALDH3A1 and CYP1A1 in cultured, essentially ER(-), human breast epithelial MCF-10A cells.	Methylcholanthrene	59-79	estrogen receptor 1	Homo sapiens	157-159
12604190-4	2003	Thus, transient exposure to 3-methylcholanthrene induced increased levels of ALDH3A1 in five cultured human breast (adeno)carcinoma cell lines that were documented as being ER(+), viz., MCF-7/0, MCF-7/OAP, T-47D, ZR-75-1 and MDA-MB-468, but failed to induce increased levels of this enzyme in four cultured human breast (adeno)carcinoma cell lines that have been historically viewed as being ER(-), viz., MDA-MB-231, SK-BR-3, HS-578-T and MDA-MB-435.	Methylcholanthrene	28-48	estrogen receptor 1	Homo sapiens	173-175
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	145-165	aryl-hydrocarbon receptor	Mus musculus	4-15
12604190-4	2003	Thus, transient exposure to 3-methylcholanthrene induced increased levels of ALDH3A1 in five cultured human breast (adeno)carcinoma cell lines that were documented as being ER(+), viz., MCF-7/0, MCF-7/OAP, T-47D, ZR-75-1 and MDA-MB-468, but failed to induce increased levels of this enzyme in four cultured human breast (adeno)carcinoma cell lines that have been historically viewed as being ER(-), viz., MDA-MB-231, SK-BR-3, HS-578-T and MDA-MB-435.	Methylcholanthrene	28-48	estrogen receptor 1	Homo sapiens	392-394
12665258-2	2003	Most responses to aromatic hydrocarbons such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin are mediated by the aromatic hydrocarbon receptor (AHR).	Methylcholanthrene	48-68	aryl hydrocarbon receptor	Rattus norvegicus	134-163
12665258-2	2003	Most responses to aromatic hydrocarbons such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin are mediated by the aromatic hydrocarbon receptor (AHR).	Methylcholanthrene	48-68	aryl hydrocarbon receptor	Rattus norvegicus	165-168
12665258-2	2003	Most responses to aromatic hydrocarbons such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin are mediated by the aromatic hydrocarbon receptor (AHR).	Methylcholanthrene	70-72	aryl hydrocarbon receptor	Rattus norvegicus	134-163
12665258-2	2003	Most responses to aromatic hydrocarbons such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin are mediated by the aromatic hydrocarbon receptor (AHR).	Methylcholanthrene	70-72	aryl hydrocarbon receptor	Rattus norvegicus	165-168
12665258-7	2003	MC attenuates the ability of GH to stimulate hepatic CYP2C11 expression in hypophysectomized (hypx) male rats, and this prompted studies of effects of aromatic hydrocarbons on hepatic GH signaling pathways as a novel aspect of endocrine disruption.	Methylcholanthrene	0-2	gonadotropin releasing hormone receptor	Rattus norvegicus	29-31
12665258-7	2003	MC attenuates the ability of GH to stimulate hepatic CYP2C11 expression in hypophysectomized (hypx) male rats, and this prompted studies of effects of aromatic hydrocarbons on hepatic GH signaling pathways as a novel aspect of endocrine disruption.	Methylcholanthrene	0-2	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	53-60
12665258-7	2003	MC attenuates the ability of GH to stimulate hepatic CYP2C11 expression in hypophysectomized (hypx) male rats, and this prompted studies of effects of aromatic hydrocarbons on hepatic GH signaling pathways as a novel aspect of endocrine disruption.	Methylcholanthrene	0-2	gonadotropin releasing hormone receptor	Rattus norvegicus	184-186
14710951-1	2003	Interferon-gamma-receptor (IFN-gammaR)-deficient mice are more susceptible to tumor induction by methylcholanthrene (MCA) in comparison to control littermates.	Methylcholanthrene	97-115	interferon gamma receptor 1	Mus musculus	0-25
14710951-1	2003	Interferon-gamma-receptor (IFN-gammaR)-deficient mice are more susceptible to tumor induction by methylcholanthrene (MCA) in comparison to control littermates.	Methylcholanthrene	97-115	interferon gamma receptor 1	Mus musculus	27-37
14710951-1	2003	Interferon-gamma-receptor (IFN-gammaR)-deficient mice are more susceptible to tumor induction by methylcholanthrene (MCA) in comparison to control littermates.	Methylcholanthrene	117-120	interferon gamma receptor 1	Mus musculus	0-25
14710951-1	2003	Interferon-gamma-receptor (IFN-gammaR)-deficient mice are more susceptible to tumor induction by methylcholanthrene (MCA) in comparison to control littermates.	Methylcholanthrene	117-120	interferon gamma receptor 1	Mus musculus	27-37
12589119-6	2003	Using multivariate logistic regression, the following score was identified to have excellent prognostic significance for MC: CRP (mg/l) - 10 x Lyc (%).	Methylcholanthrene	121-123	C-reactive protein	Homo sapiens	125-128
12589119-8	2003	Combined use of CRP levels and relative lymphocyte counts may be helpful in accurately predicting an MC after AMI and should therefore be routinely assessed.	Methylcholanthrene	101-103	C-reactive protein	Homo sapiens	16-19
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	145-165	aryl-hydrocarbon receptor	Mus musculus	17-20
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	145-165	cytochrome P450, family 27, subfamily b, polypeptide 1	Mus musculus	64-68
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	145-165	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	84-90
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	167-169	aryl-hydrocarbon receptor	Mus musculus	4-15
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	167-169	aryl-hydrocarbon receptor	Mus musculus	17-20
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	167-169	cytochrome P450, family 27, subfamily b, polypeptide 1	Mus musculus	64-68
12455047-3	2003	The Ah receptor (AHR) plays a critical role in the induction of CYP1 enzymes (i.e., CYP1A1, 1A2 and 1B1) by PAHs such as benzo[a]pyrene (BP) and 3-methylcholanthrene (MC).	Methylcholanthrene	167-169	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	84-90
12455047-7	2003	On the other hand, DNA adduct formation was markedly suppressed in AHR-null animals exposed to MC, although the major MC-DNA adduct was produced in these animals.	Methylcholanthrene	95-97	aryl-hydrocarbon receptor	Mus musculus	67-70
12455047-7	2003	On the other hand, DNA adduct formation was markedly suppressed in AHR-null animals exposed to MC, although the major MC-DNA adduct was produced in these animals.	Methylcholanthrene	118-120	aryl-hydrocarbon receptor	Mus musculus	67-70
12455047-9	2003	CYP1B1 expression was also induced, albeit to a lesser extent by the PAH MC, but not BP, in the wild-type animals.	Methylcholanthrene	73-75	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	0-6
12891939-7	2003	RESULTS: Insulin shows a dose-dependent effect on MC growth, with a limit that is stimulated by the addition of fetal bovine serum (FBS).	Methylcholanthrene	50-52	insulin	Homo sapiens	9-16
12490585-4	2003	As2O3 (2.5-5 microM) was demonstrated to markedly reduce induction of CYP1A1 mRNA and apoprotein levels and gene promotor activity in 3MC-treated Hep3B cells, whereas lower concentrations (0.25-1 microM) were ineffective.	Methylcholanthrene	134-137	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	70-76
12558906-18	2003	In patients with a chronic active HCV infection, the presence of a lymphoproliferative disease, either MC or B-NHL, is associated with lower expression of CD81 and higher expression of CD19 receptor on peripheral B cells.	Methylcholanthrene	103-105	CD81 molecule	Homo sapiens	155-159
12558906-18	2003	In patients with a chronic active HCV infection, the presence of a lymphoproliferative disease, either MC or B-NHL, is associated with lower expression of CD81 and higher expression of CD19 receptor on peripheral B cells.	Methylcholanthrene	103-105	CD19 molecule	Homo sapiens	185-189
16233383-11	2003	The cytochrome P-450 activity per culture of 3-methyl-cholanthrene-treated HepG2-Bcl2 was double that of treated HepG2-mock.	Methylcholanthrene	45-66	BCL2 apoptosis regulator	Homo sapiens	81-85
12498806-3	2002	VLA-1(+) MC formed 13 +/- 5.3% of MC eluting from columns loaded with PBMC of patients with seropositive rheumatoid arthritis (n = 6) and 2.3 +/- 1.6% of patients (n = 4) with other arthritides (P &lt; 0.022).	Methylcholanthrene	9-11	integrin subunit alpha 1	Homo sapiens	0-8
12740648-0	2003	Immunocytochemical detection of p21ras, Raf-1, ERK1/MAP kinase and PKC isoforms in a 20-methylcholanthrene-induced transformed murine embryonal fibroblast cells in culture.	Methylcholanthrene	85-106	Harvey rat sarcoma virus oncogene	Mus musculus	32-38
12740648-0	2003	Immunocytochemical detection of p21ras, Raf-1, ERK1/MAP kinase and PKC isoforms in a 20-methylcholanthrene-induced transformed murine embryonal fibroblast cells in culture.	Methylcholanthrene	85-106	v-raf-leukemia viral oncogene 1	Mus musculus	40-45
12740648-0	2003	Immunocytochemical detection of p21ras, Raf-1, ERK1/MAP kinase and PKC isoforms in a 20-methylcholanthrene-induced transformed murine embryonal fibroblast cells in culture.	Methylcholanthrene	85-106	mitogen-activated protein kinase 3	Mus musculus	47-51
12740648-0	2003	Immunocytochemical detection of p21ras, Raf-1, ERK1/MAP kinase and PKC isoforms in a 20-methylcholanthrene-induced transformed murine embryonal fibroblast cells in culture.	Methylcholanthrene	85-106	protein kinase C, alpha	Mus musculus	67-70
12505364-7	2002	Agglomerative hierarchical cluster analysis showed A-277249 to have a profile most similar to the aromatic hydrocarbons Aroclor 1254 and 3-methylcholanthrene (3MC), two known activators of the aryl hydrocarbon nuclear receptor (AhR).	Methylcholanthrene	137-157	aryl hydrocarbon receptor	Rattus norvegicus	193-226
12505364-7	2002	Agglomerative hierarchical cluster analysis showed A-277249 to have a profile most similar to the aromatic hydrocarbons Aroclor 1254 and 3-methylcholanthrene (3MC), two known activators of the aryl hydrocarbon nuclear receptor (AhR).	Methylcholanthrene	137-157	aryl hydrocarbon receptor	Rattus norvegicus	228-231
12505364-7	2002	Agglomerative hierarchical cluster analysis showed A-277249 to have a profile most similar to the aromatic hydrocarbons Aroclor 1254 and 3-methylcholanthrene (3MC), two known activators of the aryl hydrocarbon nuclear receptor (AhR).	Methylcholanthrene	159-162	aryl hydrocarbon receptor	Rattus norvegicus	193-226
12505364-7	2002	Agglomerative hierarchical cluster analysis showed A-277249 to have a profile most similar to the aromatic hydrocarbons Aroclor 1254 and 3-methylcholanthrene (3MC), two known activators of the aryl hydrocarbon nuclear receptor (AhR).	Methylcholanthrene	159-162	aryl hydrocarbon receptor	Rattus norvegicus	228-231
12498806-3	2002	VLA-1(+) MC formed 13 +/- 5.3% of MC eluting from columns loaded with PBMC of patients with seropositive rheumatoid arthritis (n = 6) and 2.3 +/- 1.6% of patients (n = 4) with other arthritides (P &lt; 0.022).	Methylcholanthrene	34-36	integrin subunit alpha 1	Homo sapiens	0-8
12498806-4	2002	Importantly, only the VLA-1(+) MC from PB and SF adhered to collagen IV upon triggering with phorbol 12-myristate 13-acetate.	Methylcholanthrene	31-33	integrin subunit alpha 1	Homo sapiens	22-27
12409613-1	2002	The aryl hydrocarbon receptor (AHR) is a ligand-inducible transcription factor that is best known because it mediates the actions of polycyclic and halogenated aromatic hydrocarbon environmental toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	213-233	aryl hydrocarbon receptor	Homo sapiens	4-29
12464667-4	2002	Here we report that injection of an antagonistic mAb against PDGFR-beta into murine neonates provides such an experimental system in the retina by completely blocking MC recruitment to developing vessels.	Methylcholanthrene	167-169	platelet derived growth factor receptor, beta polypeptide	Mus musculus	61-71
12464667-6	2002	Using this vascular system ideal for direct assessment of the activities of MC-derived molecules, we show that addition of recombinant modified angiopoietin-1 restored a hierarchical vasculature, and also rescued retinal edema and hemorrhage in the complete absence of MCs.	Methylcholanthrene	76-78	angiopoietin 1	Mus musculus	144-158
12464667-7	2002	These observations demonstrate the potential of Ang1 as a new therapeutic modality for MC dropout in diseases such as diabetic retinopathies.	Methylcholanthrene	87-89	angiopoietin 1	Mus musculus	48-52
12438513-0	2002	Differential regulation of expression of hepatic and pulmonary cytochrome P4501A enzymes by 3-methylcholanthrene in mice lacking the CYP1A2 gene.	Methylcholanthrene	92-112	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	133-139
12438513-3	2002	In this study, we tested the hypothesis that CYP1A2, a liver-specific P450 isozyme, plays an important role in the mechanisms governing persistent CYP1A1 induction by MC in liver but not in extra-hepatic tissues such as lung, which is devoid of endogenous CYP1A2.	Methylcholanthrene	167-169	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	45-51
12438513-3	2002	In this study, we tested the hypothesis that CYP1A2, a liver-specific P450 isozyme, plays an important role in the mechanisms governing persistent CYP1A1 induction by MC in liver but not in extra-hepatic tissues such as lung, which is devoid of endogenous CYP1A2.	Methylcholanthrene	167-169	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	147-153
12438513-4	2002	Administration of wild-type (WT) or CYP1A2-null mice with MC (100 micromol/kg i.p.)	Methylcholanthrene	58-60	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	36-42
12438513-7	2002	In the lung, MC caused persistent CYP1A1 induction for 15 days in both the genotypes.	Methylcholanthrene	13-15	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	34-40
12438513-8	2002	Since MC is almost completely eliminated by day 15, we hypothesize that CYP1A2 contributes to the up-regulation of CYP1A1 in liver, but not lung, by a novel mechanism, presumably involving a CYP1A2-dependent persistent metabolite.	Methylcholanthrene	6-8	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	72-78
12438513-8	2002	Since MC is almost completely eliminated by day 15, we hypothesize that CYP1A2 contributes to the up-regulation of CYP1A1 in liver, but not lung, by a novel mechanism, presumably involving a CYP1A2-dependent persistent metabolite.	Methylcholanthrene	6-8	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	115-121
12438513-8	2002	Since MC is almost completely eliminated by day 15, we hypothesize that CYP1A2 contributes to the up-regulation of CYP1A1 in liver, but not lung, by a novel mechanism, presumably involving a CYP1A2-dependent persistent metabolite.	Methylcholanthrene	6-8	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	191-197
12409613-1	2002	The aryl hydrocarbon receptor (AHR) is a ligand-inducible transcription factor that is best known because it mediates the actions of polycyclic and halogenated aromatic hydrocarbon environmental toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	213-233	aryl hydrocarbon receptor	Homo sapiens	31-34
12490138-1	2002	The aromatic hydrocarbon receptor (AHR) acts as a ligand-activated transcription factor that mediates many of the biological responses to aromatic hydrocarbons, such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	169-189	aryl hydrocarbon receptor	Rattus norvegicus	35-38
12206817-6	2002	Pretreatment with PB increased the activity of NADPH cytochrome c reductase, and 3-MC increased DT-diaphorase activity in hepatocytes.	Methylcholanthrene	81-85	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	96-109
12490138-1	2002	The aromatic hydrocarbon receptor (AHR) acts as a ligand-activated transcription factor that mediates many of the biological responses to aromatic hydrocarbons, such as 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	191-193	aryl hydrocarbon receptor	Rattus norvegicus	35-38
12415424-9	2002	In agreement with this hypothesis, in vitro experiments conducted on liver microsomes overexpressing Cyp1a1 after treatment of mice with 3-methylcholanthrene showed that TDI markedly inhibited in a concentration-dependent manner Cyp1a1 activity.	Methylcholanthrene	137-157	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	101-107
12641979-9	2002	The highest induction of MC to GST activity was at a dose of 25 mg/L, 2, 5 times as that in controls.	Methylcholanthrene	25-27	glutathione S-transferase kappa 1	Homo sapiens	31-34
12641979-11	2002	MC at a dose of 200 mg/L could lower the activity of GST by 18.7%.	Methylcholanthrene	0-2	glutathione S-transferase kappa 1	Homo sapiens	53-56
12641979-14	2002	However, UC at a dose of 200 mg/L and MC at 100 mg/L could increase the activity of GST induced by benzo(a)pyrene.	Methylcholanthrene	38-40	glutathione S-transferase kappa 1	Homo sapiens	84-87
12237923-9	2002	A significant difference in MC also was observed between regions of squamous metaplasia or dysplasia with projections of capillary loops into the bronchial mucosa and similar lesions without capillary loops (P &lt; 0.005); however, there was no difference in either the PI or the incidence of p53 overexpression between these groups.	Methylcholanthrene	28-30	tumor protein p53	Homo sapiens	293-296
12351158-7	2002	Unlike human hepatocytes, rat cell preparations, even following pretreatment with the potent CYP1A1/CYP1A2 inducer 3-methylcholanthrene (3-MC) did not produce IQx-8-COOH but did catalyze the formation of 2-amino-3,8-dimethyl-5-hydroxyimidazo[4,5-f]quinoxaline (5-HO-MeIQx) as a major CYP-mediated detoxication product.	Methylcholanthrene	115-135	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	93-99
12351158-7	2002	Unlike human hepatocytes, rat cell preparations, even following pretreatment with the potent CYP1A1/CYP1A2 inducer 3-methylcholanthrene (3-MC) did not produce IQx-8-COOH but did catalyze the formation of 2-amino-3,8-dimethyl-5-hydroxyimidazo[4,5-f]quinoxaline (5-HO-MeIQx) as a major CYP-mediated detoxication product.	Methylcholanthrene	115-135	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	100-106
12237110-0	2002	Serum increases CYP1A1 induction by 3-methylcholanthrene.	Methylcholanthrene	36-56	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	16-22
12237110-4	2002	In this work, we show evidence that the serum does not contain an AhR ligand and we evaluated the effect of a 3-methylcholanthrene (3-MC) and FBS cotreatment on CYP1A1 expression.	Methylcholanthrene	110-130	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	161-167
12237110-4	2002	In this work, we show evidence that the serum does not contain an AhR ligand and we evaluated the effect of a 3-methylcholanthrene (3-MC) and FBS cotreatment on CYP1A1 expression.	Methylcholanthrene	132-136	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	161-167
12237110-7	2002	FBS potentiation of CYP1A1 PAH-mediated induction was related to a significant increase of single strand breaks of DNA as compared to a single 3-MC treatment.	Methylcholanthrene	143-147	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	20-26
12358349-6	2002	Beta2-agonist use was associated with 5-day mean NC(0.01-0.1) and MC(0.01-2.5).	Methylcholanthrene	66-68	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	0-5
12193573-0	2002	3-Methylcholanthrene, which binds to the arylhydrocarbon receptor, inhibits proliferation and differentiation of osteoblasts in vitro and ossification in vivo.	Methylcholanthrene	0-20	aryl-hydrocarbon receptor	Mus musculus	41-65
12193573-1	2002	3-Methylcholanthrene (3MC) is a ligand for arylhydrocarbon receptor (AhR), which binds dioxin.	Methylcholanthrene	0-20	aryl-hydrocarbon receptor	Mus musculus	43-67
12193573-1	2002	3-Methylcholanthrene (3MC) is a ligand for arylhydrocarbon receptor (AhR), which binds dioxin.	Methylcholanthrene	0-20	aryl-hydrocarbon receptor	Mus musculus	69-72
12193573-1	2002	3-Methylcholanthrene (3MC) is a ligand for arylhydrocarbon receptor (AhR), which binds dioxin.	Methylcholanthrene	22-25	aryl-hydrocarbon receptor	Mus musculus	43-67
12193573-1	2002	3-Methylcholanthrene (3MC) is a ligand for arylhydrocarbon receptor (AhR), which binds dioxin.	Methylcholanthrene	22-25	aryl-hydrocarbon receptor	Mus musculus	69-72
12193573-6	2002	The level of expression of mRNA for osteocalcin, which is a marker of osteoblastic differentiation, was also depressed by 3MC.	Methylcholanthrene	122-125	bone gamma-carboxyglutamate protein 2	Mus musculus	36-47
12193540-1	2002	We are investigating the mechanisms by which aromatic hydrocarbons, such as 3-methylcholanthrene (MC), suppress hepatic cytochrome P450 2C11 (CYP2C11) gene expression.	Methylcholanthrene	76-96	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	120-140
12193540-1	2002	We are investigating the mechanisms by which aromatic hydrocarbons, such as 3-methylcholanthrene (MC), suppress hepatic cytochrome P450 2C11 (CYP2C11) gene expression.	Methylcholanthrene	76-96	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	142-149
12193540-1	2002	We are investigating the mechanisms by which aromatic hydrocarbons, such as 3-methylcholanthrene (MC), suppress hepatic cytochrome P450 2C11 (CYP2C11) gene expression.	Methylcholanthrene	98-100	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	120-140
12193540-1	2002	We are investigating the mechanisms by which aromatic hydrocarbons, such as 3-methylcholanthrene (MC), suppress hepatic cytochrome P450 2C11 (CYP2C11) gene expression.	Methylcholanthrene	98-100	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	142-149
12193540-3	2002	We have previously shown that MC attenuates the stimulatory effect of GH on CYP2C11 expression in hypophysectomized male rats.	Methylcholanthrene	30-32	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	76-83
12193540-4	2002	In follow-up studies we evaluated the effect of MC on GH-stimulated signal transducer and activator of transcription 5b (STAT5b) phosphorylation, nuclear translocation, and DNA-binding activity.	Methylcholanthrene	48-50	signal transducer and activator of transcription 5B	Rattus norvegicus	68-119
12149199-5	2002	Furthermore, with use of 2-color FCM-WASP, the MC status could be characterized by cell lineage.	Methylcholanthrene	47-49	WASP actin nucleation promoting factor	Homo sapiens	37-41
12373001-9	2002	In addition, the PC of IgE was increased with the increase in the MC-derived vascular endothelial growth factor/permeability factor (VEGF).	Methylcholanthrene	66-68	vascular endothelial growth factor A	Rattus norvegicus	77-131
12373001-9	2002	In addition, the PC of IgE was increased with the increase in the MC-derived vascular endothelial growth factor/permeability factor (VEGF).	Methylcholanthrene	66-68	vascular endothelial growth factor A	Rattus norvegicus	133-137
12373001-12	2002	Release of VEGF from the activated MC increases, and the VEGF enhances the permeability of IgE.	Methylcholanthrene	35-37	vascular endothelial growth factor A	Rattus norvegicus	11-15
12214666-13	2002	The CYP1A2-induced hepatocytes isolated from 3-methylcholanthrene administered rats were much more susceptible to some arylamines and were protected by CYP1A2 inhibitors.	Methylcholanthrene	45-65	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	4-10
12214666-13	2002	The CYP1A2-induced hepatocytes isolated from 3-methylcholanthrene administered rats were much more susceptible to some arylamines and were protected by CYP1A2 inhibitors.	Methylcholanthrene	45-65	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	152-158
12296987-11	2002	DEX is a permissive factor for induction of CYP2A1 activity by 3-methylcholanthrene (3MC), as evidenced by the formation of 7alpha-OHT.	Methylcholanthrene	63-83	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	44-50
12169827-4	2002	The results showed a lower ability of MC from preterm newborns to produce IL-1ra as compared with adult cells, supporting the assumption of neonatal immune cell immaturity.	Methylcholanthrene	38-40	interleukin 1 receptor antagonist	Homo sapiens	74-80
12716469-0	2002	Sequential involvement of two distinct CD4+ regulatory T cells during the course of transplantable tumor growth and protection from 3-methylcholanthrene-induced tumorigenesis by CD25-depletion.	Methylcholanthrene	132-152	interleukin 2 receptor, alpha chain	Mus musculus	178-182
12716469-7	2002	The present study also demonstrated that the treatment of BALB/c mice with anti-CD25 mAb (PC61) at 4 or 6 weeks after 3-methylcholanthrene (3-MC) inoculation retarded tumor occurrence and prolonged survival.	Methylcholanthrene	118-138	interleukin 2 receptor, alpha chain	Mus musculus	80-84
12716469-7	2002	The present study also demonstrated that the treatment of BALB/c mice with anti-CD25 mAb (PC61) at 4 or 6 weeks after 3-methylcholanthrene (3-MC) inoculation retarded tumor occurrence and prolonged survival.	Methylcholanthrene	140-144	interleukin 2 receptor, alpha chain	Mus musculus	80-84
12417091-1	2002	OBJECTIVE: To investigate the roles of p53 and K-ras gene in carcinogenesis and development of the lung carcinoma induced by 3-methylcholanthrene (MCA) and diethylinitrosamine (DEN) in Wistar rats, and to elucidate the relationships between the protein expression and gene mutation of p53 and K-ras.	Methylcholanthrene	125-145	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	39-42
12417091-1	2002	OBJECTIVE: To investigate the roles of p53 and K-ras gene in carcinogenesis and development of the lung carcinoma induced by 3-methylcholanthrene (MCA) and diethylinitrosamine (DEN) in Wistar rats, and to elucidate the relationships between the protein expression and gene mutation of p53 and K-ras.	Methylcholanthrene	125-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-52
12296987-11	2002	DEX is a permissive factor for induction of CYP2A1 activity by 3-methylcholanthrene (3MC), as evidenced by the formation of 7alpha-OHT.	Methylcholanthrene	85-88	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	44-50
12408358-6	2002	It was observed differences in morphology and molecular distribution (alpha5 and beta1 integrins, actin filaments and Fc receptors) between the groups control and treated with MC.	Methylcholanthrene	176-178	hemoglobin, beta adult major chain	Mus musculus	81-86
12408358-8	2002	In addition, macrophages culture with two doses of MC showed that TNF-alpha production decreased when compared with control group.	Methylcholanthrene	51-53	tumor necrosis factor	Mus musculus	66-75
12628305-7	2002	RESULTS: CYP1A1 reporter gene system can be used to identify strong inducers, such as 3-MC, beta-NF and alpha-NF, and weak inducers, such as 3-indocarbinol.	Methylcholanthrene	86-90	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	9-15
11941455-0	2002	Immunization with heat shock protein 70 from methylcholanthrene-induced sarcomas induces tumor protection correlating with in vitro T cell responses.	Methylcholanthrene	45-63	heat shock protein 1B	Mus musculus	18-39
11941455-2	2002	In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells.	Methylcholanthrene	31-49	tumor necrosis factor	Mus musculus	179-206
11941455-2	2002	In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells.	Methylcholanthrene	31-49	tumor necrosis factor	Mus musculus	208-217
11941455-2	2002	In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells.	Methylcholanthrene	51-53	tumor necrosis factor	Mus musculus	179-206
11941455-2	2002	In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells.	Methylcholanthrene	51-53	tumor necrosis factor	Mus musculus	208-217
12110372-0	2002	Coordinate regulation of UDP-glucuronosyltransferase UGT1A6 induction by 3-methylcholanthrene and multidrug resistance protein MRP2 expression by dexamethasone in primary rat hepatocytes.	Methylcholanthrene	73-93	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	53-59
12110372-1	2002	Concentration-dependent regulation of 3-methylcholanthrene (MC) inducibility of UDP-glucuronosyltransferase UGT1A6 by the synthetic glucocorticoid, dexamethasone (DEX) was studied.	Methylcholanthrene	38-58	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	108-114
12110372-1	2002	Concentration-dependent regulation of 3-methylcholanthrene (MC) inducibility of UDP-glucuronosyltransferase UGT1A6 by the synthetic glucocorticoid, dexamethasone (DEX) was studied.	Methylcholanthrene	60-62	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	108-114
11975423-3	2002	MC-derived TNF alpha and leukotrienes are shown to be important for bacterial clearance and early recruitment of phagocytic help at the site of infection.	Methylcholanthrene	0-2	tumor necrosis factor	Mus musculus	11-20
11967242-5	2002	The inhibitory effects of estradiol on VSMCs were enhanced by cytochrome-P450 (CYP450) inducers 3-methylcholanthrene and phenobarbital.	Methylcholanthrene	96-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-77
11967242-5	2002	The inhibitory effects of estradiol on VSMCs were enhanced by cytochrome-P450 (CYP450) inducers 3-methylcholanthrene and phenobarbital.	Methylcholanthrene	96-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-85
11975423-7	2002	Although the exact mechanism(s) of how MC-dependent inflammatory responses are regulated is currently not known, recent studies have shown that complement, CD11 beta/CD18 (Mac-1) and protein tyrosine kinase JAK3, and TLR4 are important for the full expression of MC-dependent innate immunity in mice.	Methylcholanthrene	39-41	integrin beta 2	Mus musculus	166-170
11975423-7	2002	Although the exact mechanism(s) of how MC-dependent inflammatory responses are regulated is currently not known, recent studies have shown that complement, CD11 beta/CD18 (Mac-1) and protein tyrosine kinase JAK3, and TLR4 are important for the full expression of MC-dependent innate immunity in mice.	Methylcholanthrene	39-41	toll-like receptor 4	Mus musculus	217-221
11805143-3	2002	Administration of neutralizing monoclonal antibody against TRAIL promoted tumor development in mice subcutaneously inoculated with a chemical carcinogen methylcholanthrene (MCA).	Methylcholanthrene	153-171	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	59-64
11933075-1	2002	The PCPH proto-oncogene was identified by its frequent activation in Syrian hamster fetal cells exposed to 3-methylcholanthrene.	Methylcholanthrene	107-127	ectonucleoside triphosphate diphosphohydrolase 5 (inactive)	Homo sapiens	4-8
11922910-0	2002	The atherogen 3-methylcholanthrene induces multiple DNA adducts in mouse aortic smooth muscle cells: role of cytochrome P4501B1.	Methylcholanthrene	14-34	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	109-127
11922910-9	2002	MC treatment caused induction of CYP1B1, but not CYP1A1.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	33-39
11922910-11	2002	The significant inhibition by EP of MC-induced DNA adduct formation indicated that CYP1B1 was the primary CYP enzyme responsible for formation of genotoxic metabolites that may play a role in the induction of atherosclerosis by MC.	Methylcholanthrene	36-38	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	83-89
11922910-11	2002	The significant inhibition by EP of MC-induced DNA adduct formation indicated that CYP1B1 was the primary CYP enzyme responsible for formation of genotoxic metabolites that may play a role in the induction of atherosclerosis by MC.	Methylcholanthrene	228-230	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	83-89
11854140-9	2002	3-MC and PCB increased UGT1A6 mRNA 6- and 4-fold, respectively.	Methylcholanthrene	0-4	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	23-29
11854140-10	2002	3-MC and PCB each increased UGT1A7 mRNA 4-fold but did not significantly increase any other UGT mRNAs.	Methylcholanthrene	0-4	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	28-34
11854140-11	2002	These findings suggest that PCN enhances T(4) UGT activity by increased expression of UGT1A1 and that 3-MC and PCB enhance T(4) UGT activity by increased expression of UGT1A6.	Methylcholanthrene	102-106	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	168-174
11742002-3	2002	A mouse bHLH-PAS protein closely related to AHR and designated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional activity of the AHR.	Methylcholanthrene	98-118	aryl-hydrocarbon receptor	Mus musculus	44-47
11742002-3	2002	A mouse bHLH-PAS protein closely related to AHR and designated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional activity of the AHR.	Methylcholanthrene	98-118	aryl-hydrocarbon receptor repressor	Mus musculus	63-76
11742002-3	2002	A mouse bHLH-PAS protein closely related to AHR and designated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional activity of the AHR.	Methylcholanthrene	98-118	aryl-hydrocarbon receptor repressor	Mus musculus	78-82
11742002-3	2002	A mouse bHLH-PAS protein closely related to AHR and designated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional activity of the AHR.	Methylcholanthrene	98-118	aryl-hydrocarbon receptor	Mus musculus	63-66
11992647-10	2002	Transcriptional activation of the UGT1A8 by 3-MC does not appear to require de novo protein synthesis.	Methylcholanthrene	44-48	UDP glucuronosyltransferase family 1 member A8	Rattus norvegicus	34-40
11812922-5	2002	Whereas PCN, 3MC, and PCB all increase microsomal UGT activity toward T(4), only PCN causes an increase in T(3)-UGT activity in vitro.	Methylcholanthrene	13-16	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	50-53
11706017-8	2002	MC induced p38 MAPK activation in p53 expressing cells but not in p53-deficient cells, indicating that the p38 MAPK activation was dependent on early p53 activation.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	11-14
11706017-8	2002	MC induced p38 MAPK activation in p53 expressing cells but not in p53-deficient cells, indicating that the p38 MAPK activation was dependent on early p53 activation.	Methylcholanthrene	0-2	tumor protein p53	Homo sapiens	34-37
11706017-8	2002	MC induced p38 MAPK activation in p53 expressing cells but not in p53-deficient cells, indicating that the p38 MAPK activation was dependent on early p53 activation.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	107-110
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	tumor protein p53	Homo sapiens	34-37
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	mitogen-activated protein kinase 14	Homo sapiens	42-45
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	tumor protein p53	Homo sapiens	162-165
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	mitogen-activated protein kinase 14	Homo sapiens	170-173
11992647-3	2002	This study demonstrates that the expression of the UGT1 gene UGT1A6, 1A7 and 1A8 is regulated at the transcriptional level by 3-methylcholanthene (3-MC) in rat hepatoma H-4-II-E cells.	Methylcholanthrene	147-151	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	51-55
11992647-3	2002	This study demonstrates that the expression of the UGT1 gene UGT1A6, 1A7 and 1A8 is regulated at the transcriptional level by 3-methylcholanthene (3-MC) in rat hepatoma H-4-II-E cells.	Methylcholanthrene	147-151	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	61-67
11992647-4	2002	Following 3-MC treatment, there is a gradual increase in the amount of UGT1A6 and UGT1A7 mRNA to the maximum levels after 16hr of treatment.	Methylcholanthrene	10-14	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	71-77
11992647-4	2002	Following 3-MC treatment, there is a gradual increase in the amount of UGT1A6 and UGT1A7 mRNA to the maximum levels after 16hr of treatment.	Methylcholanthrene	10-14	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	82-88
11992647-5	2002	The induction effect of 3-MC led to the expression of UGT1A8 which has not been reported before.	Methylcholanthrene	24-28	UDP glucuronosyltransferase family 1 member A8	Rattus norvegicus	54-60
11992647-7	2002	Northern blot analysis showed a 4-fold increase in UGT1A8 transcription after treatment with 3-MC.	Methylcholanthrene	93-97	UDP glucuronosyltransferase family 1 member A8	Rattus norvegicus	51-57
11706017-0	2002	Mechanism of p53-dependent apoptosis induced by 3-methylcholanthrene: involvement of p53 phosphorylation and p38 MAPK.	Methylcholanthrene	48-68	tumor protein p53	Homo sapiens	13-16
11706017-0	2002	Mechanism of p53-dependent apoptosis induced by 3-methylcholanthrene: involvement of p53 phosphorylation and p38 MAPK.	Methylcholanthrene	48-68	tumor protein p53	Homo sapiens	85-88
11805143-3	2002	Administration of neutralizing monoclonal antibody against TRAIL promoted tumor development in mice subcutaneously inoculated with a chemical carcinogen methylcholanthrene (MCA).	Methylcholanthrene	173-176	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	59-64
12200961-5	2002	Adhesion assays of MC to fibronectin and laminin were performed.	Methylcholanthrene	19-21	fibronectin 1	Homo sapiens	25-36
11706017-0	2002	Mechanism of p53-dependent apoptosis induced by 3-methylcholanthrene: involvement of p53 phosphorylation and p38 MAPK.	Methylcholanthrene	48-68	mitogen-activated protein kinase 14	Homo sapiens	109-112
11706017-3	2002	MC induced apoptosis, preceded by serine 15 phosphorylation and accumulation of p53.	Methylcholanthrene	0-2	tumor protein p53	Homo sapiens	80-83
11706017-4	2002	MC failed to cause apoptosis in p53-deficient MG63 cells, whereas ectopic expression of p53 in MG63 cells restored the response to MC.	Methylcholanthrene	131-133	tumor protein p53	Homo sapiens	88-91
11706017-5	2002	Therefore, MC-induced apoptosis was dependent on p53.	Methylcholanthrene	11-13	tumor protein p53	Homo sapiens	49-52
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	18-54
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	18-21
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	183-186
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	183-186
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Methylcholanthrene	0-2	mitogen-activated protein kinase 14	Homo sapiens	183-186
12200961-13	2002	Floating MC freshly isolated from effusions carried fibronectin and laminin on their surface and showed specific binding to these ECM proteins.	Methylcholanthrene	9-11	fibronectin 1	Homo sapiens	52-63
12200961-17	2002	By capturing soluble fibronectin and laminin and by matrix-mediated bridging, readhering MC may contribute to pleural obstruction.	Methylcholanthrene	89-91	fibronectin 1	Homo sapiens	21-32
12200961-18	2002	Further, soluble fibronectin bound to alpha 5 beta 1 might be life-sustaining for floating MC by driving cells into cell cycle.	Methylcholanthrene	91-93	fibronectin 1	Homo sapiens	17-28
12200961-18	2002	Further, soluble fibronectin bound to alpha 5 beta 1 might be life-sustaining for floating MC by driving cells into cell cycle.	Methylcholanthrene	91-93	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	46-52
11756232-14	2002	Some human hepatocyte populations are more active at transforming PhIP to a genotoxic species than rat hepatocytes pretreated with the potent CYP1A2 inducer 3-MC.	Methylcholanthrene	157-161	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	142-148
12200961-6	2002	In situ, resting MC expressed beta 1-, beta 3-, and beta 4-, and alpha v-subunits.	Methylcholanthrene	17-19	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	30-36
12200961-6	2002	In situ, resting MC expressed beta 1-, beta 3-, and beta 4-, and alpha v-subunits.	Methylcholanthrene	17-19	tubulin beta 3 class III	Homo sapiens	52-58
12200961-7	2002	Activated MC were beta 1- and alpha v-positive and also expressed alpha 3 and alpha 6; beta 4 was confined to the basal surface of MC; beta 3 was absent.	Methylcholanthrene	10-12	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	18-24
12200961-7	2002	Activated MC were beta 1- and alpha v-positive and also expressed alpha 3 and alpha 6; beta 4 was confined to the basal surface of MC; beta 3 was absent.	Methylcholanthrene	10-12	tubulin beta 3 class III	Homo sapiens	66-93
12200961-7	2002	Activated MC were beta 1- and alpha v-positive and also expressed alpha 3 and alpha 6; beta 4 was confined to the basal surface of MC; beta 3 was absent.	Methylcholanthrene	131-133	tubulin beta 3 class III	Homo sapiens	66-93
12200961-9	2002	In vitro, MC surface expressed beta 1, beta 3, alpha 3, alpha 5, alpha 6, alpha v, and also alpha 1 and alpha 2.	Methylcholanthrene	10-12	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	31-37
12201000-7	2002	A correlation was also encountered between the PCNA, Ki67 and MC values (p = 0.02).	Methylcholanthrene	62-64	proliferating cell nuclear antigen	Homo sapiens	47-51
11840258-13	2002	In five patients mixed chimerism simultaneously detected by RCP and CYT was associated with MC in all subsets.	Methylcholanthrene	92-94	CGRP receptor component	Homo sapiens	60-63
15244038-1	2002	It was reported that the total body clearance (CL) of 2-(allylthio)pyrazine (2-AP) was significantly faster after intravenous administration of 2-AP to rats pretreated with 3-methylcholanthrene (an inducer of CYP1A1/2 and 2E1 in rats) than that in control rats.	Methylcholanthrene	173-193	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	209-215
12688506-7	2002	Furthermore, we provide evidence, by using L-band ESR non-invasively, that the decay rate of MC-PROXYL in the head region is faster in live SHRSPs than in live WKYs.	Methylcholanthrene	93-95	esterase 5 regulator	Mus musculus	50-53
12575594-4	2001	The expression of CD40 on MC was detected by reverse transcript polymerase chain reaction (RT-PCR) and flow cytometry analysis.	Methylcholanthrene	26-28	CD40 molecule	Rattus norvegicus	18-22
11595750-2	2001	When murine MC38 (methylcholanthrene-induced adenocarcinoma 38) cells were transfected with human CEACAM1-L and stimulated with sodium pervanadate, actin was found to co-localize with CEACAM1-L at cell-cell boundaries but not in untreated cells.	Methylcholanthrene	18-36	CEA cell adhesion molecule 1	Homo sapiens	98-105
11595750-2	2001	When murine MC38 (methylcholanthrene-induced adenocarcinoma 38) cells were transfected with human CEACAM1-L and stimulated with sodium pervanadate, actin was found to co-localize with CEACAM1-L at cell-cell boundaries but not in untreated cells.	Methylcholanthrene	18-36	CEA cell adhesion molecule 1	Homo sapiens	184-191
11713596-1	2001	PCPH was initially defined as a proto-oncogene on the basis of its frequent detection as an activated oncogene in tumorigenic Syrian hamster embryo fibroblast cell lines converted to the neoplastic state by a single treatment with the carcinogen 3-methylcholanthrene (MC).	Methylcholanthrene	246-266	ectonucleoside triphosphate diphosphohydrolase 5 (inactive)	Homo sapiens	0-4
11713596-1	2001	PCPH was initially defined as a proto-oncogene on the basis of its frequent detection as an activated oncogene in tumorigenic Syrian hamster embryo fibroblast cell lines converted to the neoplastic state by a single treatment with the carcinogen 3-methylcholanthrene (MC).	Methylcholanthrene	268-270	ectonucleoside triphosphate diphosphohydrolase 5 (inactive)	Homo sapiens	0-4
11714839-7	2001	Advanced 10-day 3-methylcholanthrene 205 intracranial tumors could be cured by the transfer of 15 x 10(6) L-selectin(low) T cells derived from draining lymph nodes.	Methylcholanthrene	16-36	selectin, lymphocyte	Mus musculus	106-116
12575594-5	2001	RESULTS: MC cultured in vitro expressed CD40 markedly, the expression of CD40 mRNA and its protein was markedly up-regulated following stimulation with 4.25% PDS or IFN-gamma and 4.25% PDS.	Methylcholanthrene	9-11	CD40 molecule	Rattus norvegicus	40-44
12575594-5	2001	RESULTS: MC cultured in vitro expressed CD40 markedly, the expression of CD40 mRNA and its protein was markedly up-regulated following stimulation with 4.25% PDS or IFN-gamma and 4.25% PDS.	Methylcholanthrene	9-11	CD40 molecule	Rattus norvegicus	73-77
12575594-5	2001	RESULTS: MC cultured in vitro expressed CD40 markedly, the expression of CD40 mRNA and its protein was markedly up-regulated following stimulation with 4.25% PDS or IFN-gamma and 4.25% PDS.	Methylcholanthrene	9-11	interferon gamma	Rattus norvegicus	165-180
11682644-8	2001	When tested in the Ames test, Aroclor S9 and PB/NF S9 were the most effective in the activation of benzo[a]pyrene and 3-methylcholanthrene which are metabolized mainly by CYP1A1; additionally, the highest mutagenic potency of 2-aminofluorene and N-nitrosodipropylamine, which are activated by CYP1A2 and CYP2B, respectively, were obtained with PB/NF S9.	Methylcholanthrene	118-138	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	171-177
11698172-5	2001	The MC-induced ECOD and EROD activities were also dose-dependently inhibited by alpha-naphothflavone, which was given to the cells during the incubation with CYP 1A1 inducers.	Methylcholanthrene	4-6	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	158-165
11698172-8	2001	The phase II enzymes glutathione S-transferase, aldehyde dehydrogenase and quinone reductase were all highly expressed and inducible by MC.	Methylcholanthrene	136-138	glutathione S-transferase kappa 1	Homo sapiens	21-46
11691505-5	2001	In study 2, optical analysis of MC membrane fluidity was correlated with soluble CD14 (sCD14), a cellular activation marker.	Methylcholanthrene	32-34	CD14 molecule	Homo sapiens	81-85
11673526-3	2001	We subjected a heterozygous 3-methylcholanthrene-induced murine sarcoma cell line to CTL immunoselection, selecting for the loss of a tumor-specific Ag, recognized antigen from MCA-induced tumor 1 (Ram1).	Methylcholanthrene	28-48	recognized antigen from MCA-induced tumor 1	Mus musculus	153-196
11673526-3	2001	We subjected a heterozygous 3-methylcholanthrene-induced murine sarcoma cell line to CTL immunoselection, selecting for the loss of a tumor-specific Ag, recognized antigen from MCA-induced tumor 1 (Ram1).	Methylcholanthrene	28-48	recognized antigen from MCA-induced tumor 1	Mus musculus	198-202
11682644-8	2001	When tested in the Ames test, Aroclor S9 and PB/NF S9 were the most effective in the activation of benzo[a]pyrene and 3-methylcholanthrene which are metabolized mainly by CYP1A1; additionally, the highest mutagenic potency of 2-aminofluorene and N-nitrosodipropylamine, which are activated by CYP1A2 and CYP2B, respectively, were obtained with PB/NF S9.	Methylcholanthrene	118-138	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	293-299
11768231-1	2001	Aryl hydrocarbon receptor (AhR) belongs to the bHLH/PAS transcription factor family and is activated by various polycyclic or halogenated aromatic hydrocarbons, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3MC).	Methylcholanthrene	210-230	aryl hydrocarbon receptor	Homo sapiens	0-25
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	96-98	melanocortin 5 receptor	Homo sapiens	149-152
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	96-98	melanocortin 3 receptor	Homo sapiens	255-258
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	96-98	melanocortin 5 receptor	Homo sapiens	307-310
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	96-98	melanocortin 3 receptor	Homo sapiens	315-318
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	149-151	melanocortin 3 receptor	Homo sapiens	255-258
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	149-151	melanocortin 5 receptor	Homo sapiens	307-310
11765789-2	2001	Absorption, fluorescence excitation and fluorescence spectra have revealed that the monocation (MC) of DMAPPI, protonated at the imidazole nitrogen (MC2) (Scheme 2) is present in the S0 state at w0 = 0, along with the MC, protonated at pyridine nitrogen (MC3) and only normal emission is observed from both MC2 and MC3.	Methylcholanthrene	149-151	melanocortin 3 receptor	Homo sapiens	315-318
11595130-5	2001	Using the transplacental carcinogenesis model, which results in the induction of both lung and liver tumors following in utero exposure to MC, the results of this and our previous studies show that alterations in the Ink4a locus occur in only 15 and 27% of the lung and liver tumors, respectively.	Methylcholanthrene	139-141	cyclin dependent kinase inhibitor 2A	Mus musculus	217-222
11595130-6	2001	Preliminary data also suggests that the type of mutation induced in the Ki-ras gene following the initial exposure to MC may influence lung tumor progression.	Methylcholanthrene	118-120	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	72-78
11768231-1	2001	Aryl hydrocarbon receptor (AhR) belongs to the bHLH/PAS transcription factor family and is activated by various polycyclic or halogenated aromatic hydrocarbons, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3MC).	Methylcholanthrene	210-230	aryl hydrocarbon receptor	Homo sapiens	27-30
11768231-1	2001	Aryl hydrocarbon receptor (AhR) belongs to the bHLH/PAS transcription factor family and is activated by various polycyclic or halogenated aromatic hydrocarbons, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3MC).	Methylcholanthrene	232-235	aryl hydrocarbon receptor	Homo sapiens	0-25
11768231-1	2001	Aryl hydrocarbon receptor (AhR) belongs to the bHLH/PAS transcription factor family and is activated by various polycyclic or halogenated aromatic hydrocarbons, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3MC).	Methylcholanthrene	232-235	aryl hydrocarbon receptor	Homo sapiens	27-30
11502733-8	2001	Treatment of CL5 cells with 10 microM 3-methylcholanthrene for 24 h induced monooxygenase activity and P450s 1A1 and 1B1 proteins and mRNA levels.	Methylcholanthrene	38-58	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	103-120
11814149-5	2001	Moreover, the muscle content of facilitative glucose transporter isoform 4 (GLUT4) protein content in the plasma membrane fraction from muscle significantly increased in the orally MC-treated mice when compared with that of the controls (p&lt;0.01).	Methylcholanthrene	181-183	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	76-81
11814149-6	2001	These results suggest that the antidiabetic effect of MC is derived, at least in part, from a decrease in insulin resistance because of the increase of GLUT4 protein content in the plasma membrane of the muscle.	Methylcholanthrene	54-56	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	152-157
11549291-3	2001	MC is generally known to bind to aryl hydrocarbon receptor (AhR) as an initial event to cause effects in vivo.	Methylcholanthrene	0-2	aryl-hydrocarbon receptor	Mus musculus	33-58
11549291-3	2001	MC is generally known to bind to aryl hydrocarbon receptor (AhR) as an initial event to cause effects in vivo.	Methylcholanthrene	0-2	aryl-hydrocarbon receptor	Mus musculus	60-63
11549291-4	2001	In accordance with the results, Northern blot analysis for LMW prekininogen mRNA using total RNAs from wild-type and AhR-null mice indicated that the suppression of the mRNA expression by MC was seen in wild-type mice but not in AhR-null mice.	Methylcholanthrene	188-190	aryl-hydrocarbon receptor	Mus musculus	117-120
11313419-3	2001	Stimulation of MC with TNF-alpha up-regulated mRNA and protein of CC and CXC chemokines but not constitutive expression of the CX(3)C chemokine fractalkine.	Methylcholanthrene	15-17	tumor necrosis factor	Rattus norvegicus	23-32
11497333-9	2001	Cells pretreated with 50 degrees M 3-methylcholanthrene (3MC), a CYP 1A inducer, for 72 h prior to 0.15 microM AFB1, produced the activated AFB1 8,9-epoxide (AFBO).	Methylcholanthrene	35-55	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-68
11497333-9	2001	Cells pretreated with 50 degrees M 3-methylcholanthrene (3MC), a CYP 1A inducer, for 72 h prior to 0.15 microM AFB1, produced the activated AFB1 8,9-epoxide (AFBO).	Methylcholanthrene	57-60	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-68
11497333-13	2001	Expression of CYP 1A was significantly increased in 3MC-pretreated cells, while CYP 3A4 expression increased slightly, but not to the extent of the 1A isoforms.	Methylcholanthrene	52-55	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	14-17
11497333-14	2001	The principal AFBO detoxifying enzyme, glutathione S-transferase (GST), was constitutively expressed in NHBE cells, and was increased approximately twofold by 3MC pretreatment.	Methylcholanthrene	159-162	glutathione S-transferase kappa 1	Homo sapiens	39-64
11497333-14	2001	The principal AFBO detoxifying enzyme, glutathione S-transferase (GST), was constitutively expressed in NHBE cells, and was increased approximately twofold by 3MC pretreatment.	Methylcholanthrene	159-162	glutathione S-transferase kappa 1	Homo sapiens	66-69
11497333-17	2001	These data support earlier findings showing modest CYP-mediated AFB1 activation in human airways, but indicate that exposure to polycyclic aromatic hydrocarbons (PAHs), such as 3MC, which induce CYP(s) that specifically activate AFB1 may increase the harmful effects of AFB1 exposures in human airways.	Methylcholanthrene	177-180	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	195-198
11459429-4	2001	That this increase in the activity of EROD could be primarily due to the increase in the expression of CYP1A1 isoenzymes was demonstrated by RT-PCR and western immunoblotting studies indicating an increase in the expression of CYP1A1 in blood lymphocytes after MC pretreatment.	Methylcholanthrene	261-263	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	103-109
11459429-4	2001	That this increase in the activity of EROD could be primarily due to the increase in the expression of CYP1A1 isoenzymes was demonstrated by RT-PCR and western immunoblotting studies indicating an increase in the expression of CYP1A1 in blood lymphocytes after MC pretreatment.	Methylcholanthrene	261-263	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	227-233
11459429-5	2001	Significant inhibition in the EROD activity of MC induced lymphocyte by anti-CYP1A1/1A2 and alpha-naphthoflavone further provided evidence that the CYP1A1/1A2 isoenzymes are involved in the activity of EROD in blood lymphocytes.	Methylcholanthrene	47-49	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	77-83
11459429-5	2001	Significant inhibition in the EROD activity of MC induced lymphocyte by anti-CYP1A1/1A2 and alpha-naphthoflavone further provided evidence that the CYP1A1/1A2 isoenzymes are involved in the activity of EROD in blood lymphocytes.	Methylcholanthrene	47-49	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	148-154
11391536-8	2001	Oatp2 expression was suppressed in response to 3-MC.	Methylcholanthrene	47-51	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	0-5
11441047-9	2001	During metamorphosis, X-dll3 is also expressed throughout the developing MC epithelium and becomes restricted to neurons and basal cells at metamorphic climax.	Methylcholanthrene	73-75	distal-less homeobox 5 L homeolog	Xenopus laevis	22-28
11441047-11	2001	In contrast, Pax-6 expression is restricted to the olfactory placode, larval PC and metamorphic MC, suggesting that Pax-6 is specifically involved in the formation of water-sensing epithelium.	Methylcholanthrene	96-98	paired box 6 L homeolog	Xenopus laevis	13-18
11484331-3	2001	Our results suggest that TSL-1 antigens induce the release from MC of regulatory molecules, such as IL-4 by an IgE independent mechanism.	Methylcholanthrene	64-66	interleukin 4	Rattus norvegicus	100-104
11301045-4	2001	In the present work, we evaluated whether MAT1A expression could be targeted by the polycyclic arylhydrocarbon (PAH) 3-methylcholanthrene (3-MC) in rat liver and cultured hepatocytes.	Methylcholanthrene	139-143	methionine adenosyltransferase 1A	Rattus norvegicus	42-47
11301045-5	2001	MAT1A mRNA levels were reduced by 50% following in vivo administration of 3-MC to adult male rats (100 mg/kg, p.o., 4 days" treatment).	Methylcholanthrene	74-78	methionine adenosyltransferase 1A	Rattus norvegicus	0-5
11301045-8	2001	3-MC inhibited transcription driven by a MAT1A promoter-reporter construct transfected into rat hepatocytes, but MAT1A mRNA stability was not affected.	Methylcholanthrene	0-4	methionine adenosyltransferase 1A	Rattus norvegicus	41-46
11301045-10	2001	Here, we observed that exogenously added AdoMet prevented the negative effects of 3-MC on MAT1A expression.	Methylcholanthrene	82-86	methionine adenosyltransferase 1A	Rattus norvegicus	90-95
11513080-6	2001	Expression of CYP 1A1 and 1A2 messenger ribonucleic acid by the cells was induced by treatment with benz[a]pyrene, 3-methylcholanthrene, and benz[a]anthracene.	Methylcholanthrene	115-135	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	14-21
11423533-6	2001	Transient transfection analyses of HeLa cells with reporter genes that contain deletions and point mutations in the AhRR promoter revealed that all three XREs mediated the inducible expression of the AhRR gene by 3-methylcholanthrene treatment, and furthermore, GC box sequences were indispensable for a high level of inducible expression and for constitutive expression.	Methylcholanthrene	213-233	aryl hydrocarbon receptor repressor	Homo sapiens	116-120
11423533-6	2001	Transient transfection analyses of HeLa cells with reporter genes that contain deletions and point mutations in the AhRR promoter revealed that all three XREs mediated the inducible expression of the AhRR gene by 3-methylcholanthrene treatment, and furthermore, GC box sequences were indispensable for a high level of inducible expression and for constitutive expression.	Methylcholanthrene	213-233	aryl hydrocarbon receptor repressor	Homo sapiens	200-204
11423533-9	2001	Finally, both transient transfection analysis and gel mobility shift assay revealed that the AhRR gene is up-regulated by a p65/p50 heterodimer that binds to the NF-kappaB site when the cells has been exposed to 12-O-tetradecanoylphorbol-13-acetate, and this inducible expression was further enhanced by cotreatment of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene.	Methylcholanthrene	360-380	aryl hydrocarbon receptor repressor	Homo sapiens	93-97
11423533-9	2001	Finally, both transient transfection analysis and gel mobility shift assay revealed that the AhRR gene is up-regulated by a p65/p50 heterodimer that binds to the NF-kappaB site when the cells has been exposed to 12-O-tetradecanoylphorbol-13-acetate, and this inducible expression was further enhanced by cotreatment of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene.	Methylcholanthrene	360-380	RELA proto-oncogene, NF-kB subunit	Homo sapiens	124-127
11423533-9	2001	Finally, both transient transfection analysis and gel mobility shift assay revealed that the AhRR gene is up-regulated by a p65/p50 heterodimer that binds to the NF-kappaB site when the cells has been exposed to 12-O-tetradecanoylphorbol-13-acetate, and this inducible expression was further enhanced by cotreatment of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene.	Methylcholanthrene	360-380	nuclear factor kappa B subunit 1	Homo sapiens	128-131
11474290-18	2001	We suggest p63 as a reliable, highly specific, and sensitive MC marker in both histologic and cytologic preparations.	Methylcholanthrene	61-63	tumor protein p63	Homo sapiens	11-14
11713574-3	2001	Preliminary induction of cytochrome P-450 with 3-methylcholanthrene modified the cytotoxic effect of Nd-YAG laser.	Methylcholanthrene	47-67	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	25-41
11511786-7	2001	MC was significantly higher in K-ras(+) tumors than in K-ras(-) tumors, although it did not differ according to the level of mutant p53 protein expression.	Methylcholanthrene	0-2	KRAS proto-oncogene, GTPase	Homo sapiens	31-36
11511786-7	2001	MC was significantly higher in K-ras(+) tumors than in K-ras(-) tumors, although it did not differ according to the level of mutant p53 protein expression.	Methylcholanthrene	0-2	KRAS proto-oncogene, GTPase	Homo sapiens	55-60
11453662-6	2001	Tg, but not triiodothyronine (T(3)) significantly increased MC proliferation above control as determined by DNA content of MC cultures.	Methylcholanthrene	60-62	thyroglobulin	Mus musculus	0-2
11453662-6	2001	Tg, but not triiodothyronine (T(3)) significantly increased MC proliferation above control as determined by DNA content of MC cultures.	Methylcholanthrene	123-125	thyroglobulin	Mus musculus	0-2
11389885-10	2001	In addition to the CYP4A enzymes, immunoblot analysis revealed that CYP2B4 is constitutively present, and that CYP1A1 is induced in these glands by treatment with 3-methylcholanthrene.	Methylcholanthrene	163-183	cytochrome P450 1A1	Oryctolagus cuniculus	111-117
11437649-3	2001	Exposure to certain chemicals, such as 3-methylcholanthrene, benzo[a]pyrene, beta-naphthoflavone, and oltipraz elevates UGT1A6 mRNA in liver and to a lesser extent gastrointestinal tract and kidney, but not in other tissues.	Methylcholanthrene	39-59	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	120-126
11313419-5	2001	Firm adhesion and sequestration of monocytes on activated MC was supported by the GRO-alpha receptor CXCR2 and to a lesser extent by CX(3)CR, whereas the MCP-1 receptor CCR2 contributed to their transendothelial chemotaxis toward activated MC.	Methylcholanthrene	154-156	C-C motif chemokine receptor 2	Rattus norvegicus	169-173
12747768-1	2001	Immunotherapy with gp96 was highly effective in mice bearing methylcholanthrene-induced fibrosarcomas (Meth A tumors) when treatment began 7 days or less after tumor challenge, but significantly less effective if the treatment began 9 days after challenge.	Methylcholanthrene	61-79	heat shock protein 90, beta (Grp94), member 1	Mus musculus	19-23
11249854-2	2001	Addition of the ET(A) receptor antagonists or neutralizing anti-endothelin antibody into MC cultures markedly augmented the secretion and activation of MMP-2.	Methylcholanthrene	89-91	matrix metallopeptidase 2	Rattus norvegicus	152-157
11249854-3	2001	On the contrary, addition of the exogenous ET-1 into MC culture significantly inhibited the synthesis of MMP-2 in both basal and cytokines (tumor necrosis factor-alpha and interferon-gamma) plus lipopolysaccharide-stimulated conditions.	Methylcholanthrene	53-55	endothelin 1	Rattus norvegicus	43-47
11249854-3	2001	On the contrary, addition of the exogenous ET-1 into MC culture significantly inhibited the synthesis of MMP-2 in both basal and cytokines (tumor necrosis factor-alpha and interferon-gamma) plus lipopolysaccharide-stimulated conditions.	Methylcholanthrene	53-55	matrix metallopeptidase 2	Rattus norvegicus	105-110
11249854-3	2001	On the contrary, addition of the exogenous ET-1 into MC culture significantly inhibited the synthesis of MMP-2 in both basal and cytokines (tumor necrosis factor-alpha and interferon-gamma) plus lipopolysaccharide-stimulated conditions.	Methylcholanthrene	53-55	tumor necrosis factor	Rattus norvegicus	140-167
11249854-3	2001	On the contrary, addition of the exogenous ET-1 into MC culture significantly inhibited the synthesis of MMP-2 in both basal and cytokines (tumor necrosis factor-alpha and interferon-gamma) plus lipopolysaccharide-stimulated conditions.	Methylcholanthrene	53-55	interferon gamma	Rattus norvegicus	172-188
11285323-8	2001	Expression of the Ah receptor correlated with 3-MC-inducibility of CYP1A1 mRNA in rats fed the three diets.	Methylcholanthrene	46-50	aryl hydrocarbon receptor	Rattus norvegicus	18-29
11274077-5	2001	IL-4 preferentially colocalized to the tryptase+-chymase+ mast cell phenotype (MC(TC)) with MC(TC) cells comprising 93.3% of cytokine+ mast cells in symptomatic SAC (P = 0.0017), 89.2% in asymptomatic SAC (P = 0.0008), and 77.8% in normal subjects (P = 0.0472).	Methylcholanthrene	79-81	interleukin 4	Homo sapiens	0-4
11274077-6	2001	IL-13 appeared to colocalize preferentially to the MC(TC) phenotype and IL-5 and IL-6 to the MC(T) phenotype.	Methylcholanthrene	51-53	interleukin 13	Homo sapiens	0-5
11285323-8	2001	Expression of the Ah receptor correlated with 3-MC-inducibility of CYP1A1 mRNA in rats fed the three diets.	Methylcholanthrene	46-50	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	67-73
11301348-7	2001	Coexpression of cathepsin B and cystatin C occurred only in a few MC.	Methylcholanthrene	66-68	cathepsin B	Homo sapiens	16-27
11274859-13	2001	In addition, the method could determine the non-inducible, and 3-methylcholanthrene- and phenobarbital-inducible activities of UGT1A6 in rat liver microsomes under the same assay conditions.	Methylcholanthrene	63-83	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	127-133
11370625-7	2001	A negative association was found between total IGFBP-1 concentrations and birthweight of both MC (r = 0.47; P &lt; 0.05) and DC (r = 0.58; P &lt; 0.01) twins.	Methylcholanthrene	94-96	insulin like growth factor binding protein 1	Homo sapiens	47-54
12747766-3	2001	This study reports on the ability of the methylcholanthrene-induced fibrosarcoma, Meth A, as well as other tumors of varied histological origins to downregulate the lytic activity of CD8+ T cells.	Methylcholanthrene	41-59	CD8a molecule	Homo sapiens	183-186
11274422-1	2001	CD4(+) T lymphocyte clones, generated from mice immunized with the methylcholanthrene-induced fibrosarcoma Meth A (H-2(d)), are restricted by I-E(d) and recognize a unique antigen on Meth A.	Methylcholanthrene	67-85	CD4 antigen	Mus musculus	0-3
11324719-4	2001	CYP1A1 mRNA level is induced 1) in HepG2 and HT29-D4 cells by 3-methylcholanthrene 2) only in HepG2 after treatment by serum.	Methylcholanthrene	62-82	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
11262762-5	2001	Exposure of the cells to either 5microM 3-MC or 25 microM beta-NF, added to the culture medium, resulted in strong increases of CYP1A1/2 activity in both culture models.	Methylcholanthrene	40-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	128-134
11243847-3	2001	The treatment of mice with 3-methylcholanthrene also induced XO/XDH activities, but phenobarbital and dexamethasone had no effect.	Methylcholanthrene	27-47	xanthine dehydrogenase	Mus musculus	61-67
11243847-5	2001	The inducing effect of TCDD and 3-methylcholanthrene was not observed in null mice (AhR(-/-)), which lack the AhR gene.	Methylcholanthrene	32-52	aryl-hydrocarbon receptor	Mus musculus	110-113
11231298-5	2001	Methylcholanthrene induced an increase in CYP1A1/2 enzyme activity (eightfold), phenobarbital induced CYP2B6 activity (1.7-fold), and dexamethasone induced CYP3A4 activity (fivefold).	Methylcholanthrene	0-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	42-48
11231298-5	2001	Methylcholanthrene induced an increase in CYP1A1/2 enzyme activity (eightfold), phenobarbital induced CYP2B6 activity (1.7-fold), and dexamethasone induced CYP3A4 activity (fivefold).	Methylcholanthrene	0-18	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	156-162
11301348-7	2001	Coexpression of cathepsin B and cystatin C occurred only in a few MC.	Methylcholanthrene	66-68	cystatin C	Homo sapiens	32-42
11096091-0	2001	Aromatic hydrocarbon receptor (AhR).AhR nuclear translocator- and p53-mediated induction of the murine multidrug resistance mdr1 gene by 3-methylcholanthrene and benzo(a)pyrene in hepatoma cells.	Methylcholanthrene	137-157	aryl-hydrocarbon receptor	Mus musculus	31-34
11279838-4	2001	By 3-MC- and PB-pretreatment, a significant increase was noticed in PL elimination and also in the formation of PL metabolites, NDP, NLA and NAA.	Methylcholanthrene	3-7	norrin cystine knot growth factor NDP	Rattus norvegicus	128-131
11096091-0	2001	Aromatic hydrocarbon receptor (AhR).AhR nuclear translocator- and p53-mediated induction of the murine multidrug resistance mdr1 gene by 3-methylcholanthrene and benzo(a)pyrene in hepatoma cells.	Methylcholanthrene	137-157	transformation related protein 53, pseudogene	Mus musculus	66-69
11096091-0	2001	Aromatic hydrocarbon receptor (AhR).AhR nuclear translocator- and p53-mediated induction of the murine multidrug resistance mdr1 gene by 3-methylcholanthrene and benzo(a)pyrene in hepatoma cells.	Methylcholanthrene	137-157	malic enzyme complex, mitochondrial	Mus musculus	124-128
11096091-2	2001	We show that the expression of mdr1 is increased at the transcriptional level upon treatment of the hepatoma cell line Hepa-1c1c7 with the polycyclic aromatic hydrocarbon 3-methylcholanthrene (3-MC).	Methylcholanthrene	171-191	malic enzyme complex, mitochondrial	Mus musculus	31-35
11096091-2	2001	We show that the expression of mdr1 is increased at the transcriptional level upon treatment of the hepatoma cell line Hepa-1c1c7 with the polycyclic aromatic hydrocarbon 3-methylcholanthrene (3-MC).	Methylcholanthrene	193-197	malic enzyme complex, mitochondrial	Mus musculus	31-35
11096091-4	2001	We show that the mdr1 promoter (-1165 to +84) is able to activate the expression of a reporter gene in response to 3-MC in Hepa-1c1c7 but not in BP(r)c1 cells.	Methylcholanthrene	115-119	malic enzyme complex, mitochondrial	Mus musculus	17-21
11096091-6	2001	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the mdr1 promoter in an AhR.Arnt-dependent manner.	Methylcholanthrene	0-4	transformation related protein 53, pseudogene	Mus musculus	52-55
11096091-6	2001	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the mdr1 promoter in an AhR.Arnt-dependent manner.	Methylcholanthrene	0-4	transformation related protein 53, pseudogene	Mus musculus	68-71
11096091-6	2001	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the mdr1 promoter in an AhR.Arnt-dependent manner.	Methylcholanthrene	0-4	malic enzyme complex, mitochondrial	Mus musculus	87-91
11096091-0	2001	Aromatic hydrocarbon receptor (AhR).AhR nuclear translocator- and p53-mediated induction of the murine multidrug resistance mdr1 gene by 3-methylcholanthrene and benzo(a)pyrene in hepatoma cells.	Methylcholanthrene	137-157	aryl-hydrocarbon receptor	Mus musculus	36-39
11270661-1	2001	The induction of CYP1A1 by 3-methylcholanthrene occurs in neonatal but not in adult rabbits.	Methylcholanthrene	27-47	cytochrome P450 1A1	Oryctolagus cuniculus	17-23
11096091-6	2001	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the mdr1 promoter in an AhR.Arnt-dependent manner.	Methylcholanthrene	0-4	aryl-hydrocarbon receptor	Mus musculus	107-110
11096091-6	2001	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the mdr1 promoter in an AhR.Arnt-dependent manner.	Methylcholanthrene	0-4	aryl hydrocarbon receptor nuclear translocator	Mus musculus	111-115
11096091-8	2001	Benzo(a)pyrene, a polycyclic aromatic hydrocarbon and AhR ligand, which, like 3-MC, is oxidized by metabolizing enzymes regulated by AhR.Arnt, also activated p53 and induced mdr1 transcription.	Methylcholanthrene	78-82	aryl-hydrocarbon receptor	Mus musculus	54-57
11096091-8	2001	Benzo(a)pyrene, a polycyclic aromatic hydrocarbon and AhR ligand, which, like 3-MC, is oxidized by metabolizing enzymes regulated by AhR.Arnt, also activated p53 and induced mdr1 transcription.	Methylcholanthrene	78-82	aryl-hydrocarbon receptor	Mus musculus	133-136
11096091-8	2001	Benzo(a)pyrene, a polycyclic aromatic hydrocarbon and AhR ligand, which, like 3-MC, is oxidized by metabolizing enzymes regulated by AhR.Arnt, also activated p53 and induced mdr1 transcription.	Methylcholanthrene	78-82	aryl hydrocarbon receptor nuclear translocator	Mus musculus	137-141
11096091-8	2001	Benzo(a)pyrene, a polycyclic aromatic hydrocarbon and AhR ligand, which, like 3-MC, is oxidized by metabolizing enzymes regulated by AhR.Arnt, also activated p53 and induced mdr1 transcription.	Methylcholanthrene	78-82	transformation related protein 53, pseudogene	Mus musculus	158-161
11096091-8	2001	Benzo(a)pyrene, a polycyclic aromatic hydrocarbon and AhR ligand, which, like 3-MC, is oxidized by metabolizing enzymes regulated by AhR.Arnt, also activated p53 and induced mdr1 transcription.	Methylcholanthrene	78-82	malic enzyme complex, mitochondrial	Mus musculus	174-178
11096091-10	2001	These results indicate that the transcriptional induction of mdr1 by 3-MC and benzo(a)pyrene is directly mediated by p53 but that the metabolic activation of these compounds into reactive species is necessary to trigger p53 activation.	Methylcholanthrene	69-73	malic enzyme complex, mitochondrial	Mus musculus	61-65
11096091-10	2001	These results indicate that the transcriptional induction of mdr1 by 3-MC and benzo(a)pyrene is directly mediated by p53 but that the metabolic activation of these compounds into reactive species is necessary to trigger p53 activation.	Methylcholanthrene	69-73	transformation related protein 53, pseudogene	Mus musculus	117-120
11096091-10	2001	These results indicate that the transcriptional induction of mdr1 by 3-MC and benzo(a)pyrene is directly mediated by p53 but that the metabolic activation of these compounds into reactive species is necessary to trigger p53 activation.	Methylcholanthrene	69-73	transformation related protein 53, pseudogene	Mus musculus	220-223
11306048-0	2001	Effects of 3-methylcholanthrene and aspirin co-administration on ALDH3A1 in HepG2 cells.	Methylcholanthrene	11-31	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	65-72
11306048-2	2001	During this work, we have performed toxicity tests for cell viability/cell proliferation as well as studies on the expression of ALDH3A1 after exposure of HepG2 cells to 3MC or/and aspirin.	Methylcholanthrene	170-173	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	129-136
11306048-6	2001	The expression of ALDH3A1 in HepG2 cells showed typical time- and dose-response curves of induction after application of 3MC (1-5 days, 1.5-5.0 microM, respectively).	Methylcholanthrene	121-124	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	18-25
11306048-7	2001	When cells were firstly exposed to 3MC (2.5 and 5.0 microM) and then to aspirin (0.25 mM), the induced ALDH3A1 activity was further enhanced in a statistically significant way (P&lt;0.05).	Methylcholanthrene	35-38	aldehyde dehydrogenase 3 family member A1	Homo sapiens	103-110
11306048-8	2001	On the contrary, when aspirin application was preceded 3MC exposuring a statistically significant decrease in ALDH3A1 inducibility was observed, as compared with the application of 3MC alone.	Methylcholanthrene	55-58	aldehyde dehydrogenase 3 family member A1	Homo sapiens	110-117
11306048-8	2001	On the contrary, when aspirin application was preceded 3MC exposuring a statistically significant decrease in ALDH3A1 inducibility was observed, as compared with the application of 3MC alone.	Methylcholanthrene	181-184	aldehyde dehydrogenase 3 family member A1	Homo sapiens	110-117
11123328-4	2001	First, it is shown that prior vaccination with hsp110 or grp170 purified from methylcholanthrene-induced fibrosarcoma caused complete regression of the tumor.	Methylcholanthrene	78-96	heat shock 105kDa/110kDa protein 1	Mus musculus	47-53
11510297-11	2001	The MC apoptosis: PCNA ratio was significantly higher for 3.86% and 2.27% PDS than for the control, but no significant difference was seen between 1.36% PDS and control.	Methylcholanthrene	4-6	proliferating cell nuclear antigen	Rattus norvegicus	18-22
11133760-4	2001	Previous experiments in a model of fibrosarcoma induced by the chemical carcinogen methylcholanthrene indicated an important role for NK1.1(+) T cells.	Methylcholanthrene	83-101	tachykinin receptor 1	Homo sapiens	134-137
11531013-4	2001	Lipid peroxide accumulation, decreased glutathione (GSH) content, and decreased activities of glutathione S-transferase (GST) and quinone reductase (QR) were observed in the liver of MC-induced tumor-bearing mice.	Methylcholanthrene	183-185	hematopoietic prostaglandin D synthase	Mus musculus	94-119
11531013-4	2001	Lipid peroxide accumulation, decreased glutathione (GSH) content, and decreased activities of glutathione S-transferase (GST) and quinone reductase (QR) were observed in the liver of MC-induced tumor-bearing mice.	Methylcholanthrene	183-185	hematopoietic prostaglandin D synthase	Mus musculus	121-124
11531013-4	2001	Lipid peroxide accumulation, decreased glutathione (GSH) content, and decreased activities of glutathione S-transferase (GST) and quinone reductase (QR) were observed in the liver of MC-induced tumor-bearing mice.	Methylcholanthrene	183-185	crystallin, zeta	Mus musculus	130-147
11531013-6	2001	Mice treated with TQ along with MC showed reduction in hepatic lipid peroxides and increased GSH content and increased enzyme activities of GST and QR as compared to results of the control group.	Methylcholanthrene	32-34	hematopoietic prostaglandin D synthase	Mus musculus	140-143
11123328-4	2001	First, it is shown that prior vaccination with hsp110 or grp170 purified from methylcholanthrene-induced fibrosarcoma caused complete regression of the tumor.	Methylcholanthrene	78-96	hypoxia up-regulated 1	Mus musculus	57-63
11588892-1	2001	Monoclonal antibody (MAb) 1-7-1 against 3-methylcholanthrene (MC)-induced forms of cytochrome P-450 (CYP) was used to characterize benzo[a]pyrene (B[a]P) metabolism in rat liver and extrahepatic tissues and its modulation by phenolic antioxidants, propyl and octyl gallates.	Methylcholanthrene	40-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
11588892-1	2001	Monoclonal antibody (MAb) 1-7-1 against 3-methylcholanthrene (MC)-induced forms of cytochrome P-450 (CYP) was used to characterize benzo[a]pyrene (B[a]P) metabolism in rat liver and extrahepatic tissues and its modulation by phenolic antioxidants, propyl and octyl gallates.	Methylcholanthrene	40-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-104
11588892-1	2001	Monoclonal antibody (MAb) 1-7-1 against 3-methylcholanthrene (MC)-induced forms of cytochrome P-450 (CYP) was used to characterize benzo[a]pyrene (B[a]P) metabolism in rat liver and extrahepatic tissues and its modulation by phenolic antioxidants, propyl and octyl gallates.	Methylcholanthrene	62-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
11588892-1	2001	Monoclonal antibody (MAb) 1-7-1 against 3-methylcholanthrene (MC)-induced forms of cytochrome P-450 (CYP) was used to characterize benzo[a]pyrene (B[a]P) metabolism in rat liver and extrahepatic tissues and its modulation by phenolic antioxidants, propyl and octyl gallates.	Methylcholanthrene	62-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-104
11588892-7	2001	In MC-treated rats, MAb reduced AHH activity by 43% in liver.	Methylcholanthrene	3-5	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	32-35
11588892-12	2001	Combined treatment with MC and propyl or octyl gallate slightly reduced the effect of MAb on AHH activity in liver and significantly reduced the level of inhibition in kidney but did not affect AHH activity in lung.	Methylcholanthrene	24-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	93-96
11120842-2	2000	In the present study we confirmed that rejection of established methylcholanthrene-205 (MCA-205) pulmonary metastases displayed a requirement for T cell IFN-gamma expression.	Methylcholanthrene	64-82	interferon gamma	Mus musculus	153-162
11072249-4	2000	MC were produced by using GM-CSF and SCF.	Methylcholanthrene	0-2	colony stimulating factor 2	Homo sapiens	26-32
11141177-9	2000	Priming in polyethylene glycol (PEG, -1.0 MPa) for 5 d or 13 d also improved the longevity of low vigour seeds stored at their initial and 12% mc at 10 degrees C for 8 months, as reflected in their laboratory and CD germination.	Methylcholanthrene	143-145	progestagen associated endometrial protein	Homo sapiens	32-45
11072249-4	2000	MC were produced by using GM-CSF and SCF.	Methylcholanthrene	0-2	KIT ligand	Homo sapiens	37-40
11072249-7	2000	MC were CD14+, CD1a-, CD33+ and HLA-DR+.	Methylcholanthrene	0-2	CD14 molecule	Homo sapiens	8-12
11072249-7	2000	MC were CD14+, CD1a-, CD33+ and HLA-DR+.	Methylcholanthrene	0-2	CD1a molecule	Homo sapiens	15-19
11072249-7	2000	MC were CD14+, CD1a-, CD33+ and HLA-DR+.	Methylcholanthrene	0-2	CD33 molecule	Homo sapiens	22-26
11069840-5	2000	IL-8 mRNA expression was significantly greater in tumor tissue; high expression was highly associated with tumor in advanced stages (p = 0.03), distant lymph node metastasis (p = 0.02), high tumor MC (&gt; 123) (p = 0.00003), short survival (&lt; 26 mo) (p &lt; 0.00001), and early relapse (&lt; 16 mo) (p &lt; 0.00001).	Methylcholanthrene	197-199	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
30754781-7	2000	The transferase-to-semibiosynthetic activity ratio for the MC isoforms, which was higher than the ratio for the BSC isoforms, and the differences shown by the isoforms in susceptibility to PPT predict important differences in the biochemical properties and regulation of GS isoenzymes.	Methylcholanthrene	59-61	Omega-hydroxypalmitate O-feruloyl transferase	Zea mays	4-15
11326640-7	2000	MC and mesenchymal cells were positive for vimentin AB.	Methylcholanthrene	0-2	vimentin	Rattus norvegicus	43-51
11137894-7	2000	Although acute administration (16 hr) of PCB, 3-methylcholanthrene, and phenobarbital induced cytochrome P-450 gene expression in the liver, hepatic apo A-I gene expression was not increased by these xenobiotics.	Methylcholanthrene	46-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
10873607-4	2000	Model inducers like rifampicin, phenobarbital, or 3-methylcholanthrene and beta-naphtoflavone were able to induce CYP1A or CYP3A4 as well as EROD or T6H activities for up to 30 days.	Methylcholanthrene	50-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	123-129
10925362-1	2000	Elimination of CD4(+) T cells by anti-CD4 antibody caused regression of a methylcholanthrene-induced S713a sarcoma growing in syngeneic A/J mice, and the tumor regression was essentially required for CD8(+) T cells.	Methylcholanthrene	74-92	CD4 antigen	Mus musculus	15-18
10925362-1	2000	Elimination of CD4(+) T cells by anti-CD4 antibody caused regression of a methylcholanthrene-induced S713a sarcoma growing in syngeneic A/J mice, and the tumor regression was essentially required for CD8(+) T cells.	Methylcholanthrene	74-92	CD4 antigen	Mus musculus	38-41
10908299-3	2000	Previously, we reported the absence of 3-methylcholanthrene- or oltipraz-responsive elements in the 1.6-kbp region flanking the UGT1A7 promoter.	Methylcholanthrene	39-59	UDP glucuronosyltransferase 1 family, polypeptide A7C	Rattus norvegicus	128-134
10908299-10	2000	Mutation of PR-1 inhibited binding in the gel shift assay, prevented activation by overexpressed HNF1 in human embryonic kidney cells, and reduced by &gt;80% the maximal luciferase activities expressed from basal and 3-methylcholanthrene-responsive UGT1A7 gene reporter constructs in primary rat hepatocytes.	Methylcholanthrene	217-237	transmembrane protein 37	Homo sapiens	12-16
11180198-1	2000	In order to find what form of hepatic cytochrome P450 (CYP) is involved in the metabolism of parathion to form paraoxon, rats were pretreated with the enzyme inhibitors, such as SKF 525-A and ketoconazole or enzyme inducers, such as dexamethasone, isoniazid, phenobarbital, and 3-methylcholanthrene.	Methylcholanthrene	278-298	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-53
11180198-1	2000	In order to find what form of hepatic cytochrome P450 (CYP) is involved in the metabolism of parathion to form paraoxon, rats were pretreated with the enzyme inhibitors, such as SKF 525-A and ketoconazole or enzyme inducers, such as dexamethasone, isoniazid, phenobarbital, and 3-methylcholanthrene.	Methylcholanthrene	278-298	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-58
11048673-11	2000	On the other hand, anti-mullet CYP1A1 antibodies showed very weak cross-reactivity with two proteins (presumably CYP1A1 and CYP1A2) in 3MC-treated rat liver microsomes.	Methylcholanthrene	135-138	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	31-37
11048673-11	2000	On the other hand, anti-mullet CYP1A1 antibodies showed very weak cross-reactivity with two proteins (presumably CYP1A1 and CYP1A2) in 3MC-treated rat liver microsomes.	Methylcholanthrene	135-138	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	113-119
11048673-11	2000	On the other hand, anti-mullet CYP1A1 antibodies showed very weak cross-reactivity with two proteins (presumably CYP1A1 and CYP1A2) in 3MC-treated rat liver microsomes.	Methylcholanthrene	135-138	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	124-130
11048673-12	2000	Moreover, 3MC-treated rat liver microsomal EROD activity was weakly inhibited by the anti-L. saliens liver CYP1A1.	Methylcholanthrene	10-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	107-113
11106163-4	2000	In the present study, small-angle X-ray scattering was used to investigate structural changes of Ca2+/CaM induced by its binding to mC/N9 in solution.	Methylcholanthrene	132-134	calmodulin 1	Homo sapiens	102-105
11106163-5	2000	The binding of one mC/N9 molecule induced an insignificant structural change in Ca2+/CaM.	Methylcholanthrene	19-21	calmodulin 1	Homo sapiens	85-88
10992045-5	2000	Using methylcholanthrene, CYP1A2 can be induced dramatically, and it is inhibited by furafylline, a mechanism-based inhibitor of this enzyme.	Methylcholanthrene	6-24	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	26-32
10859152-7	2000	In three independent experiments, a 48-h exposure to 3-methylcholanthrene, omeprazole, and lansoprazole significantly induced CYP1A1 expression in comparison to untreated cultures (P &lt;.05).	Methylcholanthrene	53-73	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	126-132
10871328-1	2000	We reported earlier that 3-methylcholanthrene (MC) persistently induces hepatic ethoxyresorufin O-deethylase activities (CYP1A1) in rats for up to 45 days.	Methylcholanthrene	25-45	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	121-127
10871328-1	2000	We reported earlier that 3-methylcholanthrene (MC) persistently induces hepatic ethoxyresorufin O-deethylase activities (CYP1A1) in rats for up to 45 days.	Methylcholanthrene	47-49	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	121-127
10871328-4	2000	MC-elicited increases in CYP1A1/1A2 activities, apoprotein contents, and mRNA levels were sustained for several weeks after the last dose of MC treatment.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	25-31
10871328-5	2000	MC also caused long-term induction of CYP1A1 in lungs and mammary glands.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-44
10871328-9	2000	Dose-response studies showed that administration of MC (2 micromol/kg), which produced an intrahepatic concentration of 271 pmol/g after 24 h, did not induce CYP1A1/1A2 activities, strongly suggesting that the sustained induction of CYP1A1/1A2 was not due to retention of the parent MC in the body.	Methylcholanthrene	52-54	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	233-239
10871328-11	2000	In conclusion, our results support the hypothesis that persistent expression of CYP1A1/1A2 by MC is mediated by mechanisms independent of the retention of the parent carcinogen.	Methylcholanthrene	94-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	80-86
10901160-4	2000	Based on these findings, in vivo experiments with MC were conducted to determine its ability to downregulate the NFkappaB activation in mouse liver.	Methylcholanthrene	50-52	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-121
10901160-5	2000	Results clearly showed that MC is a potent suppressor of BHP-induced NFkappaB activation.	Methylcholanthrene	28-30	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	69-77
10901160-6	2000	We observed a significant reduction by MC on BHP-induced translocation of p65 subunit of NFkappaB.	Methylcholanthrene	39-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	89-97
10901160-10	2000	The present results suggest that MC may inhibit NFkappaB activation, exhibiting its ability to downregulate the NFkappaB-dependent gene expression.	Methylcholanthrene	33-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	48-56
10901160-10	2000	The present results suggest that MC may inhibit NFkappaB activation, exhibiting its ability to downregulate the NFkappaB-dependent gene expression.	Methylcholanthrene	33-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-120
10901160-11	2000	Thus, it can be expected that MC may have potential for therapeutic intervention on various NFkappaB-dependent pathological conditions such as inflammatory or possibly mutagenic processes.	Methylcholanthrene	30-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	92-100
10751551-0	2000	Transcriptional suppression of cytochrome P450 2C11 gene expression by 3-methylcholanthrene.	Methylcholanthrene	71-91	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	31-51
10751551-1	2000	Aromatic hydrocarbon receptor-mediated transcriptional up-regulation of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (MC) is accompanied by down-regulation of rat hepatic CYP2C11 expression at the catalytic activity, protein, and mRNA levels.	Methylcholanthrene	176-196	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-87
10751551-1	2000	Aromatic hydrocarbon receptor-mediated transcriptional up-regulation of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (MC) is accompanied by down-regulation of rat hepatic CYP2C11 expression at the catalytic activity, protein, and mRNA levels.	Methylcholanthrene	176-196	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-92
10751551-1	2000	Aromatic hydrocarbon receptor-mediated transcriptional up-regulation of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (MC) is accompanied by down-regulation of rat hepatic CYP2C11 expression at the catalytic activity, protein, and mRNA levels.	Methylcholanthrene	176-196	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	251-258
10751551-1	2000	Aromatic hydrocarbon receptor-mediated transcriptional up-regulation of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (MC) is accompanied by down-regulation of rat hepatic CYP2C11 expression at the catalytic activity, protein, and mRNA levels.	Methylcholanthrene	198-200	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-87
10751551-1	2000	Aromatic hydrocarbon receptor-mediated transcriptional up-regulation of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by polycyclic aromatic hydrocarbons (PAHs) such as 3-methylcholanthrene (MC) is accompanied by down-regulation of rat hepatic CYP2C11 expression at the catalytic activity, protein, and mRNA levels.	Methylcholanthrene	198-200	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-92
10751551-2	2000	To gain insight into the molecular mechanism of this CYP2C11 suppression response, we have used a nuclear run-on assay to assess directly the effect of MC on the hepatic transcription rate of the CYP2C11 gene following in vivo administration of MC to adult male rats.	Methylcholanthrene	152-154	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	53-60
10751551-2	2000	To gain insight into the molecular mechanism of this CYP2C11 suppression response, we have used a nuclear run-on assay to assess directly the effect of MC on the hepatic transcription rate of the CYP2C11 gene following in vivo administration of MC to adult male rats.	Methylcholanthrene	152-154	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	196-203
10751551-2	2000	To gain insight into the molecular mechanism of this CYP2C11 suppression response, we have used a nuclear run-on assay to assess directly the effect of MC on the hepatic transcription rate of the CYP2C11 gene following in vivo administration of MC to adult male rats.	Methylcholanthrene	245-247	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	196-203
10751551-3	2000	A single intraperitoneal dose of MC (40 mg/kg) caused a 179-fold increase in the rate of CYP1A gene transcription at 6 hr, and the rate of CYP2C11 gene transcription was reduced by 51% at this time point, compared with vehicle controls.	Methylcholanthrene	33-35	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	139-146
10751551-4	2000	By 48 hr after MC treatment, the rates of CYP1A and CYP2C11 gene transcription were no longer significantly different from the corresponding vehicle controls.	Methylcholanthrene	15-17	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	52-59
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Methylcholanthrene	151-171	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	32-39
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Methylcholanthrene	151-171	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	41-48
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Methylcholanthrene	151-171	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	54-60
10867521-3	2000	Comparison of resting MC and activated MC during peritonitis in vivo by means of immunohistochemistry revealed an increased expression of HSP 72/73.	Methylcholanthrene	22-24	heat shock protein family A (Hsp70) member 1A	Homo sapiens	138-144
10867521-3	2000	Comparison of resting MC and activated MC during peritonitis in vivo by means of immunohistochemistry revealed an increased expression of HSP 72/73.	Methylcholanthrene	39-41	heat shock protein family A (Hsp70) member 1A	Homo sapiens	138-144
10867521-4	2000	As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation.	Methylcholanthrene	53-55	tumor necrosis factor	Homo sapiens	70-97
10867521-4	2000	As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation.	Methylcholanthrene	53-55	tumor necrosis factor	Homo sapiens	99-108
10867521-4	2000	As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation.	Methylcholanthrene	53-55	interleukin 1 beta	Homo sapiens	114-131
10867521-4	2000	As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation.	Methylcholanthrene	53-55	interleukin 1 beta	Homo sapiens	133-141
10867521-4	2000	As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation.	Methylcholanthrene	53-55	heat shock protein family A (Hsp70) member 1A	Homo sapiens	180-186
10867521-5	2000	We suggest that the increased HSP 72/73 expression of MC during peritonitis is in part induced by TNF-alpha and IL-1beta and may exert a cell-protective function, lessening MC damage during peritonitis.	Methylcholanthrene	54-56	heat shock protein family A (Hsp70) member 1A	Homo sapiens	30-36
10867521-5	2000	We suggest that the increased HSP 72/73 expression of MC during peritonitis is in part induced by TNF-alpha and IL-1beta and may exert a cell-protective function, lessening MC damage during peritonitis.	Methylcholanthrene	54-56	tumor necrosis factor	Homo sapiens	98-107
10867521-5	2000	We suggest that the increased HSP 72/73 expression of MC during peritonitis is in part induced by TNF-alpha and IL-1beta and may exert a cell-protective function, lessening MC damage during peritonitis.	Methylcholanthrene	54-56	interleukin 1 beta	Homo sapiens	112-120
10867521-5	2000	We suggest that the increased HSP 72/73 expression of MC during peritonitis is in part induced by TNF-alpha and IL-1beta and may exert a cell-protective function, lessening MC damage during peritonitis.	Methylcholanthrene	173-175	heat shock protein family A (Hsp70) member 1A	Homo sapiens	30-36
10769184-8	2000	Thus, the patterns of sedimentation, distribution and elimination of radioactivity from the 8 S fraction of the liver cytosols from beta-NF-, 3-MC-, TCDD- or alpha-NF-treated rats were characteristic for the AhR, whereas those from the 4 S fraction appeared specific for [(3)H]beta-NF binding.	Methylcholanthrene	142-146	aryl hydrocarbon receptor	Rattus norvegicus	208-211
11180194-1	2000	In order to find what types of hepatic cytochrome P450 (CYP) isozymes are involved in the metabolism of 2-(allylthio)pyrazine (2-AP) in rats, enzyme inducers, such as phenobarbital, 3-methylcholanthrene, dexamethasone, or isoniazid, and an enzyme inhibitor, such as SKF 525-A were pretreated.	Methylcholanthrene	182-202	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-54
11180194-1	2000	In order to find what types of hepatic cytochrome P450 (CYP) isozymes are involved in the metabolism of 2-(allylthio)pyrazine (2-AP) in rats, enzyme inducers, such as phenobarbital, 3-methylcholanthrene, dexamethasone, or isoniazid, and an enzyme inhibitor, such as SKF 525-A were pretreated.	Methylcholanthrene	182-202	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-59
10845702-0	2000	Distribution and inducibility by 3-methylcholanthrene of family 1 UDP-glucuronosyltransferases in the rat gastrointestinal tract.	Methylcholanthrene	33-53	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	66-94
10845702-13	2000	Rats treated with 3-methylcholanthrene (3-MC) displayed a 10-fold induction of hepatic UGT1A6 and UGT1A7 mRNAs.	Methylcholanthrene	18-38	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	87-93
10845702-13	2000	Rats treated with 3-methylcholanthrene (3-MC) displayed a 10-fold induction of hepatic UGT1A6 and UGT1A7 mRNAs.	Methylcholanthrene	18-38	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	98-104
10845702-13	2000	Rats treated with 3-methylcholanthrene (3-MC) displayed a 10-fold induction of hepatic UGT1A6 and UGT1A7 mRNAs.	Methylcholanthrene	40-44	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	87-93
10845702-13	2000	Rats treated with 3-methylcholanthrene (3-MC) displayed a 10-fold induction of hepatic UGT1A6 and UGT1A7 mRNAs.	Methylcholanthrene	40-44	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	98-104
10845702-16	2000	Effects of 3-MC on UGT1A1 expression revealed downregulation in the liver and highly variable effects in duodenum and stomach.	Methylcholanthrene	11-15	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	19-25
10769184-9	2000	The data indicate that potent AhR agonists, TCDD, 3-MC and beta-NF, and to a lesser extent alpha-NF, a weak AhR agonist, induce a 4 S [(3)H]beta-NF-binding protein in liver cytosol of female rats.	Methylcholanthrene	50-54	aryl hydrocarbon receptor	Rattus norvegicus	30-33
10772642-8	2000	Male Sprague-Dawley rats were administered 3-methylcholanthrene, PB, isoniazid, pregnenolone-16alpha-carbonitrile, or clofibric acid to induce transcription of CYP1A1, CYP1A2, CYP2B1/2, CYP2E1, CYP3A1/23, and CYP4A2/3 mRNA, respectively.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	160-166
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Methylcholanthrene	104-124	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	133-139
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Methylcholanthrene	104-124	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	144-150
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Methylcholanthrene	104-124	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	277-283
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Methylcholanthrene	104-124	cytochrome P450, family 4, subfamily a, polypeptide 2	Rattus norvegicus	334-340
10772642-8	2000	Male Sprague-Dawley rats were administered 3-methylcholanthrene, PB, isoniazid, pregnenolone-16alpha-carbonitrile, or clofibric acid to induce transcription of CYP1A1, CYP1A2, CYP2B1/2, CYP2E1, CYP3A1/23, and CYP4A2/3 mRNA, respectively.	Methylcholanthrene	43-63	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	168-174
10788562-8	2000	T(4) UDP-GT activity was increased in rats treated with PB (120%), PCN (250 to 400%), 3MC (400 to 600%), or PCB (300 to 430%).	Methylcholanthrene	86-89	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	5-11
10799337-7	2000	Surprisingly, in corresponding experiments using 3-methylcholanthrene (3-MC) as a CYP1A1 inducer, DFB was less effective.	Methylcholanthrene	49-69	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	82-88
10799337-7	2000	Surprisingly, in corresponding experiments using 3-methylcholanthrene (3-MC) as a CYP1A1 inducer, DFB was less effective.	Methylcholanthrene	71-75	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	82-88
12501620-2	2000	The results showed that there were basic production of interleukin-6(IL-6) and tumor necrosis factor-alpha (TNF-alpha) on MC in the control group without LPS, that high-concentration heparin(500 U/ml) increased the effects of LPS on MC, and that low-concentration heparin (5 U/ml) conversely inhibited the effects of LPS on MC.	Methylcholanthrene	122-124	interleukin 6	Homo sapiens	55-68
10729196-11	2000	Cells exposed to 3-methylcholanthrene showed a characteristic increased expression of CYP1A2 and 1A1 mRNAs.	Methylcholanthrene	17-37	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	86-100
10702363-4	2000	We hypothesized that increased conversion of T(4) to T(3), catalyzed by outer-ring deiodinases (ORD) type-I and -II, is the reason serum T(3) is maintained in rats treated with 3MC or PCB.	Methylcholanthrene	177-180	pyruvate carboxylase	Rattus norvegicus	184-187
10772282-6	2000	The in vitro production of IL-6 by MC in the two groups was not affected by the addition of IM.	Methylcholanthrene	35-37	interleukin 6	Homo sapiens	27-31
10808205-9	2000	In samples from all five patients having MC in the B cell lineage, the patient-specific IgH or TcR rearrangement was also detected.	Methylcholanthrene	41-43	immunoglobulin heavy constant delta	Homo sapiens	88-91
10808205-9	2000	In samples from all five patients having MC in the B cell lineage, the patient-specific IgH or TcR rearrangement was also detected.	Methylcholanthrene	41-43	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	95-98
12539348-9	2000	Is1 connected Mc by a straight line extended to V to form the reference lines.	Methylcholanthrene	14-16	IS1	Homo sapiens	0-3
10772282-4	2000	MC isolated from preterm newborns were less sensitive to the in vitro effect of IM on IL-1beta and TNFalpha secretion than adult cells.	Methylcholanthrene	0-2	interleukin 1 beta	Homo sapiens	86-94
10772282-4	2000	MC isolated from preterm newborns were less sensitive to the in vitro effect of IM on IL-1beta and TNFalpha secretion than adult cells.	Methylcholanthrene	0-2	tumor necrosis factor	Homo sapiens	99-107
12501620-2	2000	The results showed that there were basic production of interleukin-6(IL-6) and tumor necrosis factor-alpha (TNF-alpha) on MC in the control group without LPS, that high-concentration heparin(500 U/ml) increased the effects of LPS on MC, and that low-concentration heparin (5 U/ml) conversely inhibited the effects of LPS on MC.	Methylcholanthrene	122-124	interleukin 6	Homo sapiens	69-73
12501620-2	2000	The results showed that there were basic production of interleukin-6(IL-6) and tumor necrosis factor-alpha (TNF-alpha) on MC in the control group without LPS, that high-concentration heparin(500 U/ml) increased the effects of LPS on MC, and that low-concentration heparin (5 U/ml) conversely inhibited the effects of LPS on MC.	Methylcholanthrene	122-124	tumor necrosis factor	Homo sapiens	79-106
12501620-2	2000	The results showed that there were basic production of interleukin-6(IL-6) and tumor necrosis factor-alpha (TNF-alpha) on MC in the control group without LPS, that high-concentration heparin(500 U/ml) increased the effects of LPS on MC, and that low-concentration heparin (5 U/ml) conversely inhibited the effects of LPS on MC.	Methylcholanthrene	122-124	tumor necrosis factor	Homo sapiens	108-117
10698668-0	2000	Interference with growth hormone stimulation of hepatic cytochrome P4502C11 expression in hypophysectomized male rats by 3-methylcholanthrene.	Methylcholanthrene	121-141	gonadotropin releasing hormone receptor	Rattus norvegicus	18-32
10698668-2	2000	Hepatic CYP2C11 expression is down-regulated by polycyclic aromatic hydrocarbons such as 3-methylcholanthrene (MC).	Methylcholanthrene	89-109	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	8-15
10698668-2	2000	Hepatic CYP2C11 expression is down-regulated by polycyclic aromatic hydrocarbons such as 3-methylcholanthrene (MC).	Methylcholanthrene	111-113	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	8-15
10698668-7	2000	As a positive control response, pronounced induction of hepatic CYP1A1 apoprotein was observed in all MC-treated rats.	Methylcholanthrene	102-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-70
10698668-10	2000	CYP2C11 expression in hypx rats receiving both GH and MC was significantly lower at the mRNA, apoprotein, and catalytic activity levels than that observed in hypx rats treated with GH alone, but significantly higher at the mRNA, apoprotein, and catalytic activity levels than that observed in vehicle-treated hypx rats and in hypx rats treated with MC alone.	Methylcholanthrene	54-56	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	0-7
10698668-10	2000	CYP2C11 expression in hypx rats receiving both GH and MC was significantly lower at the mRNA, apoprotein, and catalytic activity levels than that observed in hypx rats treated with GH alone, but significantly higher at the mRNA, apoprotein, and catalytic activity levels than that observed in vehicle-treated hypx rats and in hypx rats treated with MC alone.	Methylcholanthrene	54-56	gonadotropin releasing hormone receptor	Rattus norvegicus	181-183
10698668-10	2000	CYP2C11 expression in hypx rats receiving both GH and MC was significantly lower at the mRNA, apoprotein, and catalytic activity levels than that observed in hypx rats treated with GH alone, but significantly higher at the mRNA, apoprotein, and catalytic activity levels than that observed in vehicle-treated hypx rats and in hypx rats treated with MC alone.	Methylcholanthrene	349-351	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	0-7
10698668-10	2000	CYP2C11 expression in hypx rats receiving both GH and MC was significantly lower at the mRNA, apoprotein, and catalytic activity levels than that observed in hypx rats treated with GH alone, but significantly higher at the mRNA, apoprotein, and catalytic activity levels than that observed in vehicle-treated hypx rats and in hypx rats treated with MC alone.	Methylcholanthrene	349-351	gonadotropin releasing hormone receptor	Rattus norvegicus	47-49
10698668-11	2000	These data suggest that MC interferes with the ability of GH to stimulate CYP2C11 expression.	Methylcholanthrene	24-26	gonadotropin releasing hormone receptor	Rattus norvegicus	58-60
10698668-11	2000	These data suggest that MC interferes with the ability of GH to stimulate CYP2C11 expression.	Methylcholanthrene	24-26	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	74-81
10685026-10	2000	The difference in glycosylation pattern of rLCAT from Mc-7777 and BHK cells underlines the importance of appropriate expression system, both in vivo and in vitro.	Methylcholanthrene	54-56	lecithin cholesterol acyltransferase	Rattus norvegicus	43-48
10674571-8	2000	(4) Monoclonal antibody immunoblotting using a murine monoclonal antibody with strong affinity for the gp40 major allergen of MC.	Methylcholanthrene	126-128	podoplanin	Homo sapiens	103-107
10728918-1	2000	Differences in expression of CYP1A isoforms (CYP1A1 and CYP1A2) in liver and small intestine of male Wistar rats and their inducibility by 3-methylcholanthrene as well as the effect of different CYP1A1/1A2 expression on caffeine metabolism were investigated.	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	45-51
10728918-1	2000	Differences in expression of CYP1A isoforms (CYP1A1 and CYP1A2) in liver and small intestine of male Wistar rats and their inducibility by 3-methylcholanthrene as well as the effect of different CYP1A1/1A2 expression on caffeine metabolism were investigated.	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	56-62
10728918-2	2000	In rat liver, CYP1A2 is the predominant isoform and CYP1A1 protein expression in liver is significantly increased after treatment by 3-methylcholanthrene.	Methylcholanthrene	133-153	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	14-20
10728918-2	2000	In rat liver, CYP1A2 is the predominant isoform and CYP1A1 protein expression in liver is significantly increased after treatment by 3-methylcholanthrene.	Methylcholanthrene	133-153	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	52-58
10728918-3	2000	In contrast, only CYP1A1 was detected in control and 3-methylcholanthrene induced small intestine microsomes.	Methylcholanthrene	53-73	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	18-24
10728918-4	2000	Treatment with 3-methylcholanthrene (40 mg/kg intraperitoneally daily during 1, 2, 3 or 4 days) demonstrated that liver CYP1A1 is more sensitive for the induction effects than CYP1A2 and also that significant induction of CYP1A1 in rat small intestine only occurred after 3 to 4 days pretreatment.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	120-126
10728918-4	2000	Treatment with 3-methylcholanthrene (40 mg/kg intraperitoneally daily during 1, 2, 3 or 4 days) demonstrated that liver CYP1A1 is more sensitive for the induction effects than CYP1A2 and also that significant induction of CYP1A1 in rat small intestine only occurred after 3 to 4 days pretreatment.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	222-228
10728918-8	2000	Overall, this study shows different expression and inducibility of CYP1A1/1A2 by 3-methylcholanthrene in rat liver and small intestine.	Methylcholanthrene	81-101	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	67-73
10631103-4	2000	After treatment of CaCo-2 cells with fetal bovine serum, CYP1A1 mRNA level increased to the same extent as that observed after 3-methylcholanthrene induction.	Methylcholanthrene	127-147	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	57-63
10611137-10	2000	In contrast, concentration of UGT1A6 was increased by MC.	Methylcholanthrene	54-56	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	30-36
10611137-14	2000	In our study, MC increased the rate of T4 glucuronidation, and DEX had no additional effect on this reaction, suggesting that UGT1A6 is not the only enzyme inducible by MC that can catalyze T4 conjugation.	Methylcholanthrene	169-171	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	126-132
10912627-7	2000	However, after 72 h of incubation with IL-1 the GSH level increased in MC in the presence of 10% FCS, p&lt;0.05.	Methylcholanthrene	71-73	interleukin 1 beta	Homo sapiens	39-43
10912627-11	2000	We conclude that the activity of antioxidant mechanisms in MC is decreased by IL-1beta in ways that might increase their vulnerability to the cytotoxic effect of free radicals.	Methylcholanthrene	59-61	interleukin 1 beta	Homo sapiens	78-86
10757128-3	2000	Moreover, we found that TNF-alpha stimulated transformation of BALB/3T3 cells initiated with 3-methylcholanthrene 1,000 times stronger than did TPA (Cancer Res.	Methylcholanthrene	93-113	tumor necrosis factor	Mus musculus	24-33
10594572-10	1999	The fourth group of related MoAbs consisted of MC-PR3-2, 4A3 and WGM3.	Methylcholanthrene	47-49	proteinase 3	Homo sapiens	50-53
10936788-1	2000	Eleven cases with mucinous noncystic carcinoma (MC) of the pancreas were studied by histology and mucin immunohistochemistry, to elucidate the mechanism, or route of development, and pre-existing histological type of MC of the pancreas.	Methylcholanthrene	48-50	LOC100508689	Homo sapiens	18-23
10936788-4	2000	The mechanism and routes to MC were divided into four types as follows: IPMC directly invaded the stroma (4 cases), over-production of mucin in IPMC expanded the branches of the pancreatic duct possibly resulting in rupture (3 cases), DA underwent extreme mucinous degeneration (3 cases), and a recurrent form, as MC, at the surgical stump of IPMC (one case).	Methylcholanthrene	28-30	LOC100508689	Homo sapiens	135-140
10936788-8	2000	These two pre-existing types of MC involved mucin overproduction and mucinous degeneration.	Methylcholanthrene	32-34	LOC100508689	Homo sapiens	44-49
10528797-0	1999	Regression and prevention of autochthonous tumors induced by 3-methylcholanthrene after injection of a T-cell receptor alpha /beta positive and CD4/CD8 double negative T-cells.	Methylcholanthrene	61-81	CD4 molecule	Homo sapiens	144-147
10637450-2	1999	Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth.	Methylcholanthrene	176-194	interferon alpha	Mus musculus	40-49
10637450-2	1999	Here, we report that the combination of IFN-alpha and CD80 cancer gene therapy in poorly immunogenic murine tumor models, the colorectal adenocarcinoma cell line MC38, and the methylcholanthrene-induced fibrosarcoma cell line MCA205 reduces tumor growth more efficiently without affecting in vitro growth.	Methylcholanthrene	176-194	CD80 antigen	Mus musculus	54-58
10545214-7	1999	The expression of CYP2A15 mRNA was slightly induced by treatment with either rifampicin or 3-methylcholanthrene.	Methylcholanthrene	91-111	cytochrome P450 2A15	Cricetulus griseus	18-25
10525285-4	1999	In order to obtain structural information about this CYP1A-like protein, a liver cDNA library of 3MC-treated frog was constructed and screened using a fragment of rat CYP1A2 cDNA under low stringency conditions.	Methylcholanthrene	97-100	cytochrome P450 family 1 subfamily A member 1 S homeolog	Xenopus laevis	53-58
10525285-4	1999	In order to obtain structural information about this CYP1A-like protein, a liver cDNA library of 3MC-treated frog was constructed and screened using a fragment of rat CYP1A2 cDNA under low stringency conditions.	Methylcholanthrene	97-100	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	167-173
10545420-8	1999	Similar incidences of Ki-ras mutations were previously found following transplacental exposure of [D2xB6D2F(1)]F(2) mice to MC and treatment of adult A/J mice with urethane.	Methylcholanthrene	124-126	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	22-28
10528997-2	1999	The dihydrodiol is metabolized at a rate of 2.4 nmol/nmol of cytochrome P450 1A1/min with microsomes from 3-methylcholanthrene-treated rats, a rate more than 10-fold higher than that observed with microsomes from control or phenobarbital-treated rats.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	61-80
10528997-4	1999	A highly purified monooxygenase system reconstituted with cytochrome P450 1A1 and epoxide hydrolase (17 nmol of metabolites/nmol of cytochrome P450 1A1/min) gave a metabolite profile very similar to that observed with liver microsomes from 3-methylcholanthrene-treated rats.	Methylcholanthrene	240-260	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	58-77
10776840-6	1999	MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2 in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3+ CD4+ and CD8 + splenic cells.	Methylcholanthrene	0-2	interleukin 2	Mus musculus	103-116
10776840-6	1999	MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2 in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3+ CD4+ and CD8 + splenic cells.	Methylcholanthrene	0-2	CD3 antigen, epsilon polypeptide	Mus musculus	205-208
10776840-6	1999	MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2 in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3+ CD4+ and CD8 + splenic cells.	Methylcholanthrene	0-2	CD4 antigen	Mus musculus	210-213
10493908-4	1999	Among the various peptidyl-[4-methylcoumarin 7-amide (MCA)] substrates tested, the one that was preferred the most by rPC4A was acetyl (Ac)-Arg-Lys-Lys-Arg-MCA, which is cleaved 9 times faster (as judged from V(max)/K(m) measurements) than the best furin and PC1 substrate, pGlu-Arg-Thr-Lys-Arg-MCA.	Methylcholanthrene	54-57	furin, paired basic amino acid cleaving enzyme	Homo sapiens	249-254
10493908-4	1999	Among the various peptidyl-[4-methylcoumarin 7-amide (MCA)] substrates tested, the one that was preferred the most by rPC4A was acetyl (Ac)-Arg-Lys-Lys-Arg-MCA, which is cleaved 9 times faster (as judged from V(max)/K(m) measurements) than the best furin and PC1 substrate, pGlu-Arg-Thr-Lys-Arg-MCA.	Methylcholanthrene	54-57	proprotein convertase subtilisin/kexin type 1	Homo sapiens	259-262
10510446-9	1999	3MC treatment increased the amount of CYP1A1 and 1A2 proteins.	Methylcholanthrene	0-3	cytochrome P450 1A1	Oryctolagus cuniculus	38-52
10424773-1	1999	We used in situ hybridization to examine organ- and cell type-specific constitutive and 3-methylcholanthrene (3MC)-inducible cytochrome P450 (CYP)1A1 and CYP1A2 mRNA expression in various tissues of the C57BL/6N mouse.	Methylcholanthrene	88-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	125-149
10424773-1	1999	We used in situ hybridization to examine organ- and cell type-specific constitutive and 3-methylcholanthrene (3MC)-inducible cytochrome P450 (CYP)1A1 and CYP1A2 mRNA expression in various tissues of the C57BL/6N mouse.	Methylcholanthrene	88-108	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	154-160
10424773-1	1999	We used in situ hybridization to examine organ- and cell type-specific constitutive and 3-methylcholanthrene (3MC)-inducible cytochrome P450 (CYP)1A1 and CYP1A2 mRNA expression in various tissues of the C57BL/6N mouse.	Methylcholanthrene	110-113	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	125-149
10424773-5	1999	In contrast, constitutive CYP1A2 mRNA was measurable in liver, and 3MC-inducible CYP1A2 mRNA was observed only in liver, lung, and duodenum (having cell-type locations similar to those of CYP1A1); the other above-mentioned tissues were negative for CYP1A2 mRNA.	Methylcholanthrene	67-70	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	81-87
10424773-5	1999	In contrast, constitutive CYP1A2 mRNA was measurable in liver, and 3MC-inducible CYP1A2 mRNA was observed only in liver, lung, and duodenum (having cell-type locations similar to those of CYP1A1); the other above-mentioned tissues were negative for CYP1A2 mRNA.	Methylcholanthrene	67-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	188-194
10424773-5	1999	In contrast, constitutive CYP1A2 mRNA was measurable in liver, and 3MC-inducible CYP1A2 mRNA was observed only in liver, lung, and duodenum (having cell-type locations similar to those of CYP1A1); the other above-mentioned tissues were negative for CYP1A2 mRNA.	Methylcholanthrene	67-70	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	81-87
10424773-7	1999	Because of the ubiquitous nature of 3MC-inducible CYP1A1 throughout the animal rather than just "portals of entry," these results support our hypothesis that CYP1A1, induced by particular endogenous signals in various tissues and cell types, might participate in one or more critical life processes--in addition to its well-established role of metabolism of polycyclic hydrocarbons, certain drugs, and other environmental pollutants.	Methylcholanthrene	36-39	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	50-56
10424773-7	1999	Because of the ubiquitous nature of 3MC-inducible CYP1A1 throughout the animal rather than just "portals of entry," these results support our hypothesis that CYP1A1, induced by particular endogenous signals in various tissues and cell types, might participate in one or more critical life processes--in addition to its well-established role of metabolism of polycyclic hydrocarbons, certain drugs, and other environmental pollutants.	Methylcholanthrene	36-39	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	158-164
10810558-9	1999	The concurrent treatment of dams with 3-MC and RA led to an increased inducibility of cytochrome P-450 and subsequently, CYP1A1 dependent enzyme activity higher than those observed after the injection of 3-MC alone.	Methylcholanthrene	38-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	121-127
10421657-9	1999	Induction studies using hepatocytes treated for 48 hours with phenobarbital (2 mmol/L), oltipraz (50 micromol/L), or 3-methylcholanthrene (2.5 micromol/L) revealed UGT1A1-inducing effects of phenobarbital, oltipraz, and, in particular, 3-methylcholanthrene.	Methylcholanthrene	117-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
10373399-2	1999	Pretreatment with phenobarbital (PB), 3-methylcholanthrene (3MC), and PB plus 3MC elicited significant induction of multiple CYP enzymes in alligator, as detected by antibodies to CYP1A, CYP2B, CYP2C, CYP2E, CYP2K, and CYP3A.	Methylcholanthrene	78-81	cytochrome P450 3A21	Alligator mississippiensis	219-224
10409630-4	1999	OCT-treated early passage mesangial cells (MC-E cells) had increased expression levels of type IV collagen and smooth muscle alpha actin mRNA, but 1, 25(OH)(2)D(3)-treated MC-E cells did not.	Methylcholanthrene	43-45	plexin A2	Homo sapiens	0-3
10445394-1	1999	Benzimidazole compounds, such as omeprazole and thiabendazole, are a different type of CYP1A1-inducer from Ah receptor-ligands, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene.	Methylcholanthrene	183-203	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	87-93
10404433-1	1999	Previously we described that the adoptive transfer of tumor-infiltrating lymphocytes (TIL) + interleukin-2 (IL-2) leads to eradication of established methylcholanthrene (MCA)-105 fibrosarcoma pulmonary metastases in a congenic murine model.	Methylcholanthrene	150-168	interleukin 2	Mus musculus	93-106
10404433-1	1999	Previously we described that the adoptive transfer of tumor-infiltrating lymphocytes (TIL) + interleukin-2 (IL-2) leads to eradication of established methylcholanthrene (MCA)-105 fibrosarcoma pulmonary metastases in a congenic murine model.	Methylcholanthrene	150-168	interleukin 2	Mus musculus	108-112
10404433-1	1999	Previously we described that the adoptive transfer of tumor-infiltrating lymphocytes (TIL) + interleukin-2 (IL-2) leads to eradication of established methylcholanthrene (MCA)-105 fibrosarcoma pulmonary metastases in a congenic murine model.	Methylcholanthrene	170-173	interleukin 2	Mus musculus	93-106
10404433-1	1999	Previously we described that the adoptive transfer of tumor-infiltrating lymphocytes (TIL) + interleukin-2 (IL-2) leads to eradication of established methylcholanthrene (MCA)-105 fibrosarcoma pulmonary metastases in a congenic murine model.	Methylcholanthrene	170-173	interleukin 2	Mus musculus	108-112
10383160-5	1999	The results demonstrate that mice bearing primary MC tumors had significantly diminished T-cell and NK-cell functions, impaired capacity to produce Th1 cytokines, and markedly reduced levels of the signal-transducing zeta chain in T cells and NK cells, similar to that described in cancer patients.	Methylcholanthrene	50-52	negative elongation factor complex member C/D, Th1l	Mus musculus	148-151
10383160-6	1999	Moreover, a substantial number of CD8+ T cells in mice with large primary MC tumors were undergoing apoptosis, correlating with alterations in CD4/CD8 ratios.	Methylcholanthrene	74-76	CD4 antigen	Mus musculus	143-146
10396878-3	1999	This result suggests that a MC-inducible cytochrome P450 isoform, probably CYP1A1, is more important in the in vitro metabolism of 3,5,3",4"-TCB in rat liver and that the isoform attacks the 3,5-dichloro-substituted phenyl ring more predominantly than 3,4-dichloro-substituted one.	Methylcholanthrene	28-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	75-81
20654500-4	1999	CYP 1A1/1A2 protein was not detected, neither in G nor in C HepG2 cells but was strongly induced by 3-methylcholanthrene (3-MC) treatment.	Methylcholanthrene	100-120	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-7
20654500-4	1999	CYP 1A1/1A2 protein was not detected, neither in G nor in C HepG2 cells but was strongly induced by 3-methylcholanthrene (3-MC) treatment.	Methylcholanthrene	122-126	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-7
10381141-0	1999	Inhibition by retinoids of benzo(A)pyrene metabolism catalyzed by 3-methylcholanthrene-induced rat cytochrome P-450 1A1.	Methylcholanthrene	66-86	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	99-119
10381141-2	1999	We recently reported that rat CYP 1A1 induced by 3-methylcholanthrene (3-MC) catalyzed the conversion of retinal to retinoic acid.	Methylcholanthrene	49-69	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-37
10381141-2	1999	We recently reported that rat CYP 1A1 induced by 3-methylcholanthrene (3-MC) catalyzed the conversion of retinal to retinoic acid.	Methylcholanthrene	71-75	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-37
10220487-5	1999	Phenobarbital, 3-methylcholanthrene, and clofibrate enhanced the glucuronidation of LF 4.0212 on positions 2, 3, and 4 of the thioxyloside ring, thus indicating that several UGT isoforms were involved in this process.	Methylcholanthrene	15-35	beta-1,3-glucuronyltransferase 2	Homo sapiens	174-177
10329919-11	1999	Mc lymphoma showed an homogeneous pattern, characterized by similar expression of CD5 than CLL but significantly stronger expression of CD79b whilst PLL and SLVL had weak CD5 and moderate CD79b expression.	Methylcholanthrene	0-2	CD5 molecule	Homo sapiens	82-85
10329919-11	1999	Mc lymphoma showed an homogeneous pattern, characterized by similar expression of CD5 than CLL but significantly stronger expression of CD79b whilst PLL and SLVL had weak CD5 and moderate CD79b expression.	Methylcholanthrene	0-2	CD79b molecule	Homo sapiens	136-141
10329919-11	1999	Mc lymphoma showed an homogeneous pattern, characterized by similar expression of CD5 than CLL but significantly stronger expression of CD79b whilst PLL and SLVL had weak CD5 and moderate CD79b expression.	Methylcholanthrene	0-2	CD79b molecule	Homo sapiens	188-193
10206093-17	1999	In conclusion, MC effectively converted VF or VT. MCs increased post-ischaemic myocardial cell damage, as judged from increased cTnT release.	Methylcholanthrene	15-17	troponin T2, cardiac type	Rattus norvegicus	128-132
10203613-1	1999	Interleukin-2 and CD80 transfectants of a methylcholanthrene-induced murine sarcoma Mc12 (Mc12-IL-2 and Mc12-CD80 cells) with similar tumorigenicity in euthymic mice were utilized for experiments designed to investigate a co-stimulatory role of the CD80 molecule in allogeneic, congenitally athymic (nu/nu) mice.	Methylcholanthrene	42-60	interleukin 2	Mus musculus	0-13
10203613-1	1999	Interleukin-2 and CD80 transfectants of a methylcholanthrene-induced murine sarcoma Mc12 (Mc12-IL-2 and Mc12-CD80 cells) with similar tumorigenicity in euthymic mice were utilized for experiments designed to investigate a co-stimulatory role of the CD80 molecule in allogeneic, congenitally athymic (nu/nu) mice.	Methylcholanthrene	42-60	CD80 antigen	Mus musculus	18-22
10203613-1	1999	Interleukin-2 and CD80 transfectants of a methylcholanthrene-induced murine sarcoma Mc12 (Mc12-IL-2 and Mc12-CD80 cells) with similar tumorigenicity in euthymic mice were utilized for experiments designed to investigate a co-stimulatory role of the CD80 molecule in allogeneic, congenitally athymic (nu/nu) mice.	Methylcholanthrene	42-60	interleukin 2	Mus musculus	95-99
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Methylcholanthrene	86-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	198-213
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Methylcholanthrene	86-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	215-218
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Methylcholanthrene	86-106	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	228-234
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Methylcholanthrene	86-106	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	303-309
10391116-14	1999	In the RT-PCR assay, expression of NK-1 receptor mRNA was evident in Slc:Wistar PMCs, but not in the non-MC fraction from Slc:Wistar or Slc: SD PMCs.	Methylcholanthrene	81-83	tachykinin receptor 1	Rattus norvegicus	35-48
10188639-5	1999	Similarly, quantitative autoradiography using the radiolabeled 5-HT(1A) receptor agonist 8-hydroxy-2-(di-N-propylamino) tetralin demonstrated a significant decline in receptor density in 3- and 13-month MC and HC groups as compared to age-matched LC groups in the hippocampus.	Methylcholanthrene	203-205	5-hydroxytryptamine receptor 1A	Homo sapiens	63-80
10080958-1	1999	Cellular and molecular mechanisms of insulin resistance in isolated adipocytes from methylcholanthrene-induced sarcoma-bearing rats were investigated by measuring 3-O-[14C]methyl glucose transport activity, glucose transporter-4 (GLUT4) protein in both plasma membrane and low-density microsomes, and insulin-stimulated tyrosine phosphorylation of the insulin receptor (IR) and insulin receptor substrate-1 (IRS-1).	Methylcholanthrene	84-102	solute carrier family 2 member 4	Rattus norvegicus	230-235
10095131-1	1999	We report the ability of beta-carotene (betaC) to affect the cell transforming activity of 3-methylcholanthrene (3-MCA), benzo(a)pyrene (B(a)P) and cigarette-smoke condensate (TAR) in an in vitro medium-term (approximately 8 weeks) experimental model utilizing BALB/c 3T3 cells.	Methylcholanthrene	91-111	colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)	Mus musculus	25-46
10095131-1	1999	We report the ability of beta-carotene (betaC) to affect the cell transforming activity of 3-methylcholanthrene (3-MCA), benzo(a)pyrene (B(a)P) and cigarette-smoke condensate (TAR) in an in vitro medium-term (approximately 8 weeks) experimental model utilizing BALB/c 3T3 cells.	Methylcholanthrene	114-118	colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)	Mus musculus	25-46
9885234-7	1999	Characterization of the alloantibodies showed that the low levels of MC significantly influenced the isotype of the antidonor IgG; the presence of 1 MC/microL was associated with induction of noncomplement fixing IgG1 antidonor antibodies, whereas platelet transfusions, devoid of MC (&lt;0.	Methylcholanthrene	149-151	LOC105243590	Mus musculus	213-217
11601021-9	1999	ET-1 is one of the important inflammatory mediators which can stimulate MC proliferation and mesangial matrix expansion in vivo.	Methylcholanthrene	72-74	endothelin 1	Rattus norvegicus	0-4
9927619-1	1999	CYP2A8 is a major form of cytochrome P-450 inducible by 3-methylcholanthrene in Syrian hamster liver.	Methylcholanthrene	56-76	cytochrome P450 2A8	Mesocricetus auratus	0-6
9989819-1	1999	Cph was isolated from neoplastic Syrian hamster embryo fibroblasts initiated by 3-methylcholanthrene (MCA), and was shown to be a single copy gene in the hamster genome, conserved from yeast to human cells, expressed in fetal cells and most adult tissues, and acting synergistically with H-ras in the transformation of murine NIH3T3 fibroblasts.	Methylcholanthrene	80-100	ectonucleoside triphosphate diphosphohydrolase 5	Mesocricetus auratus	0-3
9989819-1	1999	Cph was isolated from neoplastic Syrian hamster embryo fibroblasts initiated by 3-methylcholanthrene (MCA), and was shown to be a single copy gene in the hamster genome, conserved from yeast to human cells, expressed in fetal cells and most adult tissues, and acting synergistically with H-ras in the transformation of murine NIH3T3 fibroblasts.	Methylcholanthrene	102-105	ectonucleoside triphosphate diphosphohydrolase 5	Mesocricetus auratus	0-3
10478593-6	1999	The results show that cultured MC can form large domes and express the most characteristic IsK protein, indicating that they maintain their vectorial electrolyte transport function and, possibly, the ability to secrete K+ in this condition.	Methylcholanthrene	31-33	potassium voltage-gated channel subfamily E regulatory subunit 1	Rattus norvegicus	91-94
9858665-2	1999	CYP1A1 but not CYP1A2 was detected by Western blot analysis of lymphocytes from untreated rats and was induced in lymphocytes from rats treated with the known CYP1A inducers beta-naphthoflavone [CAS #6051-87-2] or 3-methylcholanthrene [CAS #56-49-5] (7.3-fold), cigarette smoke (2.	Methylcholanthrene	214-234	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
10682113-7	1999	Incubation of MC with anti-CD59 mAb abrogated the protective effect of CD59 (100% cytotoxicity).	Methylcholanthrene	14-16	CD59 molecule (CD59 blood group)	Homo sapiens	27-31
9882450-10	1999	Western analysis confirms the presence of AhR and ARNT proteins in 3-methylcholanthrene-treated rat liver, as well as ARNT protein in rat corneal epithelium.	Methylcholanthrene	67-87	aryl hydrocarbon receptor	Rattus norvegicus	42-45
9882450-10	1999	Western analysis confirms the presence of AhR and ARNT proteins in 3-methylcholanthrene-treated rat liver, as well as ARNT protein in rat corneal epithelium.	Methylcholanthrene	67-87	aryl hydrocarbon receptor nuclear translocator	Rattus norvegicus	50-54
10682113-5	1999	MC lines were positive for staining with anti-CD59 mAb.	Methylcholanthrene	0-2	CD59 molecule (CD59 blood group)	Homo sapiens	46-50
10682113-6	1999	Western blotting analysis of MC membrane demonstrated a band with the same molecular weight as CD59.	Methylcholanthrene	29-31	CD59 molecule (CD59 blood group)	Homo sapiens	95-99
10026370-5	1999	Spontaneous secretion of IL-1beta or IL-6 by MC of preterm neonates was less inhibited by dexamethasone as compared with cells from adults.	Methylcholanthrene	45-47	interleukin 1 beta	Homo sapiens	25-33
10682113-7	1999	Incubation of MC with anti-CD59 mAb abrogated the protective effect of CD59 (100% cytotoxicity).	Methylcholanthrene	14-16	CD59 molecule (CD59 blood group)	Homo sapiens	71-75
10682113-11	1999	These findings suggest that production of complement components and expression of CD59 on MCs could play a role both in peritoneal cavity infection (decreased complement production) and in peritoneal membrane damage (decreased CD59 expression and reduced remesothelialization owing to MC lysis).	Methylcholanthrene	90-92	CD59 molecule (CD59 blood group)	Homo sapiens	82-86
10682113-11	1999	These findings suggest that production of complement components and expression of CD59 on MCs could play a role both in peritoneal cavity infection (decreased complement production) and in peritoneal membrane damage (decreased CD59 expression and reduced remesothelialization owing to MC lysis).	Methylcholanthrene	90-92	CD59 molecule (CD59 blood group)	Homo sapiens	227-231
10026370-5	1999	Spontaneous secretion of IL-1beta or IL-6 by MC of preterm neonates was less inhibited by dexamethasone as compared with cells from adults.	Methylcholanthrene	45-47	interleukin 6	Homo sapiens	37-41
10026370-7	1999	As for term newborns, MC were more sensitive to the inhibitory effect of the drug on LPS-induced IL-6 production than cells of adults.	Methylcholanthrene	22-24	interleukin 6	Homo sapiens	97-101
10325963-9	1999	In the NCGM-treated MC culture, Western blots of MC proteins also showed a 36% reduction of the Kv4.2 K+ channel protein level.	Methylcholanthrene	20-22	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	96-101
10325963-9	1999	In the NCGM-treated MC culture, Western blots of MC proteins also showed a 36% reduction of the Kv4.2 K+ channel protein level.	Methylcholanthrene	49-51	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	96-101
10325963-10	1999	In addition, the NCGM-induced MC hypertrophy was partially inhibited by anti-insulin-like growth factor-1 (IGF-1) antibody, while it revealed no effects on Ito density and Kv4.2 channel expression.	Methylcholanthrene	30-32	insulin-like growth factor 1	Rattus norvegicus	72-105
10402558-4	1999	The induction of CYP1B1 mRNA by PBO or ACN was higher in DBA/2 (Ahrd) than in C57BL/6 (Ahrb-1) mice, while 3-methylcholanthrene induced CYP1B1 more in C57BL/6 than in DBA/2 mice.	Methylcholanthrene	107-127	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	136-142
23898793-6	1999	doses of methylcholanthrene (MC) prior to a single dose of B[a]P resulted in a 2.4 times increase in CYP1A1 activity in liver tissue and 1.5 times higher levelsof total B[a]P-DNA adducts in lung and liver compared with controls which only received B[a]P. Increased levels of BPDE-I-DNA adducts were significantly correlated to increased CYP1A1 activity in induced lung tissue but not in liver.	Methylcholanthrene	9-27	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-107
23898793-6	1999	doses of methylcholanthrene (MC) prior to a single dose of B[a]P resulted in a 2.4 times increase in CYP1A1 activity in liver tissue and 1.5 times higher levelsof total B[a]P-DNA adducts in lung and liver compared with controls which only received B[a]P. Increased levels of BPDE-I-DNA adducts were significantly correlated to increased CYP1A1 activity in induced lung tissue but not in liver.	Methylcholanthrene	9-27	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	337-343
23898793-6	1999	doses of methylcholanthrene (MC) prior to a single dose of B[a]P resulted in a 2.4 times increase in CYP1A1 activity in liver tissue and 1.5 times higher levelsof total B[a]P-DNA adducts in lung and liver compared with controls which only received B[a]P. Increased levels of BPDE-I-DNA adducts were significantly correlated to increased CYP1A1 activity in induced lung tissue but not in liver.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	101-107
23898793-6	1999	doses of methylcholanthrene (MC) prior to a single dose of B[a]P resulted in a 2.4 times increase in CYP1A1 activity in liver tissue and 1.5 times higher levelsof total B[a]P-DNA adducts in lung and liver compared with controls which only received B[a]P. Increased levels of BPDE-I-DNA adducts were significantly correlated to increased CYP1A1 activity in induced lung tissue but not in liver.	Methylcholanthrene	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	337-343
10023447-3	1998	In this study, we transfected methylcholanthrene-induced fibrosarcoma (MCA-D) with TNF gene and investigated the therapeutic effect of TNF gene-transduced cancer vaccine and whether the vaccination effect is enhanced by systemic administration of recombinant IL-12 (rIL-12), in a murine model.	Methylcholanthrene	30-48	tumor necrosis factor	Mus musculus	83-86
9860486-6	1998	Known prototype inducers such as beta-naphthoflavone and 3-methylcholanthrene exhibited the highest inducing potency quantified with an Imax value (maximal induction of cytochrome P450 1A1 mRNA synthesis) of 5.48 and 10.7 x 10(6) mRNA molecules per 150 ng of total RNA, respectively.	Methylcholanthrene	57-77	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	169-188
9784250-1	1998	Benzimidazole compounds, such as omeprazole and thiabendazole, are a different type of CYP1A1 inducer from Ah receptor-ligands, such as TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and 3-methylcholanthrene.	Methylcholanthrene	183-203	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	87-93
9879553-3	1998	The presence of IL-10 in MC culture supernatants was determined by the capacity of these to inhibit, with or without monoclonal antibodies to IL-10, the NO production of recombinant bovine IFN gamma (rBoIFN gamma) activated monocytes.	Methylcholanthrene	25-27	interleukin-10	Bos taurus	16-21
9891550-3	1998	The results obtained indicate that: a) MC higher than 130 microvessels/mm2 is a cut-off value that distinguished patients who relapsed during the follow up period; b) multivariated analysis indicates that MC (p &lt; 0.00001) is an independent predictor of disease free-survival; c) multivariated analysis selectively done on cases with relapse demonstrates that MC correlates with the presence of metastasis (or/and M) with local relapse (T).	Methylcholanthrene	205-207	PNMA family member 2	Homo sapiens	71-74
9891550-3	1998	The results obtained indicate that: a) MC higher than 130 microvessels/mm2 is a cut-off value that distinguished patients who relapsed during the follow up period; b) multivariated analysis indicates that MC (p &lt; 0.00001) is an independent predictor of disease free-survival; c) multivariated analysis selectively done on cases with relapse demonstrates that MC correlates with the presence of metastasis (or/and M) with local relapse (T).	Methylcholanthrene	205-207	PNMA family member 2	Homo sapiens	71-74
9784250-1	1998	Benzimidazole compounds, such as omeprazole and thiabendazole, are a different type of CYP1A1 inducer from Ah receptor-ligands, such as TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and 3-methylcholanthrene.	Methylcholanthrene	183-203	aryl hydrocarbon receptor	Homo sapiens	107-118
9742071-2	1998	Thus, we examined the amount of phenobarbital (PB)-inducible P-450 isoforms (P-450 2B1/2B2) in hepatocytes from rats injected first with PB and then with 3-methylcholanthrene (MC) (PB+MC-treated animals) by quantitative immunohistochemistry.	Methylcholanthrene	154-174	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	83-90
10323327-2	1998	ALDHI is mainly increased by phenobarbital-type inducers; polycyclic aromatic hydrocarbons (PAHs), such as 3- methylcholanthrene (3MC), increase ALDH3c enzyme activity in all rat species currently tested.	Methylcholanthrene	107-128	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	145-150
10323327-2	1998	ALDHI is mainly increased by phenobarbital-type inducers; polycyclic aromatic hydrocarbons (PAHs), such as 3- methylcholanthrene (3MC), increase ALDH3c enzyme activity in all rat species currently tested.	Methylcholanthrene	130-133	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	145-150
10323327-5	1998	To answer this question, we examined the relationship between the induction of ALDH3c by 3MC and the arachidonic acid cascade.	Methylcholanthrene	89-92	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	79-84
10323327-7	1998	The 3MC-induced ALDH3c activity was significantly diminished by the co-administered anti-inflammatory agents.	Methylcholanthrene	4-7	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-21
10323328-8	1998	3-Methylcholanthrene (3MC) greatly increased ALDH3c levels in both substrains, although it was slightly more pronounced in the rr rats, in which it was assessed either as ALDH3c or as total cytosolic ALDH.	Methylcholanthrene	0-20	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	45-49
10323328-8	1998	3-Methylcholanthrene (3MC) greatly increased ALDH3c levels in both substrains, although it was slightly more pronounced in the rr rats, in which it was assessed either as ALDH3c or as total cytosolic ALDH.	Methylcholanthrene	22-25	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	45-49
9742071-0	1998	Effect of 3-methylcholanthrene administration on expression of cytochrome P-450 isoforms induced by phenobarbital in rat hepatocytes.	Methylcholanthrene	10-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
9742071-5	1998	In PB+MC-treated animals, however, the PB-induced increase in 2B1/2B2 content was suppressed in perivenular hepatocytes but promoted in midzonal hepatocytes.	Methylcholanthrene	6-8	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	62-69
9742071-8	1998	The promotion of the increase in P-450 2B1/2B2 content in midzonal hepatocytes in PB+MC-treated animals probably corresponds to the strong hybridization signal, whereas there appeared to be a divergence between the intensity of the signal and the content in perivenular hepatocytes.	Methylcholanthrene	85-87	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	39-46
9698097-1	1998	Complementary DNA fragments encoding cynomolgus monkey CYP1A2 were amplified by the reverse transcriptase-polymerase chain reaction (RT-PCR) method from the liver total RNA of a 3-methylcholanthrene (3-MC)-treated cynomolgus monkey.	Methylcholanthrene	178-198	cytochrome P450 family 1 subfamily A member 2	Macaca fascicularis	55-61
9783725-8	1998	Treatment with the lower dose (5 mg/kg) of 3-methylcholanthrene (3MC) induced expression of UGT1A6 perivenously.	Methylcholanthrene	43-63	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	92-98
9783725-8	1998	Treatment with the lower dose (5 mg/kg) of 3-methylcholanthrene (3MC) induced expression of UGT1A6 perivenously.	Methylcholanthrene	65-68	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	92-98
9783729-0	1998	Regulation of cytochrome P450 enzymes by aryl hydrocarbon receptor in human cells: CYP1A2 expression in the LS180 colon carcinoma cell line after treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin or 3-methylcholanthrene.	Methylcholanthrene	200-220	aryl hydrocarbon receptor	Homo sapiens	41-66
9783729-0	1998	Regulation of cytochrome P450 enzymes by aryl hydrocarbon receptor in human cells: CYP1A2 expression in the LS180 colon carcinoma cell line after treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin or 3-methylcholanthrene.	Methylcholanthrene	200-220	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	83-89
9783729-2	1998	We found that CYP1A2 can be induced significantly by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (MC), or benz[a]anthracene in the human colon carcinoma cell line LS180.	Methylcholanthrene	97-117	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	14-20
9783729-2	1998	We found that CYP1A2 can be induced significantly by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (MC), or benz[a]anthracene in the human colon carcinoma cell line LS180.	Methylcholanthrene	119-121	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	14-20
9783729-3	1998	TCDD and MC each caused a dramatic elevation of CYP1A2 mRNA, as assessed by reverse transcription-polymerase chain reaction or by northern blot analysis.	Methylcholanthrene	9-11	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	48-54
9683793-9	1998	Terminal cell death was enhanced only in normal ECE cells as evidenced by increased envelope formation and was paralleled by an increase in the level of p53 following 3MC treatment.	Methylcholanthrene	167-170	tumor protein p53	Homo sapiens	153-156
9683793-10	1998	The differentiation status of the 3MC-treated cells was similar to untreated cells as indicated by three independent markers of cell differentiation; transglutaminase, involucrin, keratin expression.	Methylcholanthrene	34-37	involucrin	Homo sapiens	168-178
9797569-9	1998	RESULTS: The presence of specific IgG antibodies to B19 was found in 68% EMC, 56% non-essential MC, 78% HCV-MC, and 78% HCV-no-MC.	Methylcholanthrene	74-76	eva-1 homolog C	Homo sapiens	52-55
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	11-17
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-4
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	aryl hydrocarbon receptor	Homo sapiens	60-85
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	aryl hydrocarbon receptor	Homo sapiens	87-90
9783729-7	1998	CYP1A1 and CYP1B1, additional CYP1 enzymes regulated by the aryl hydrocarbon receptor (AHR), also were inducible by TCDD and MC in LS180 cells; their concentration-dependent induction was highly correlated with induction of CYP1A2 at mRNA, protein, and catalytic levels.	Methylcholanthrene	125-127	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	224-230
9731718-4	1998	AHH inducibility (3-methylcholanthrene-induced/non-induced AHH activity) showed a very wide interindividual variation as well as non-induced AHH activity.	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-3
9731718-4	1998	AHH inducibility (3-methylcholanthrene-induced/non-induced AHH activity) showed a very wide interindividual variation as well as non-induced AHH activity.	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	59-62
9731718-4	1998	AHH inducibility (3-methylcholanthrene-induced/non-induced AHH activity) showed a very wide interindividual variation as well as non-induced AHH activity.	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	59-62
9659583-1	1998	Previous studies from this and other laboratories have shown that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring, the incidence of which correlated with fetal inducibility of Cyp1a1.	Methylcholanthrene	98-118	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	222-228
9659583-1	1998	Previous studies from this and other laboratories have shown that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring, the incidence of which correlated with fetal inducibility of Cyp1a1.	Methylcholanthrene	120-122	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	222-228
9698097-1	1998	Complementary DNA fragments encoding cynomolgus monkey CYP1A2 were amplified by the reverse transcriptase-polymerase chain reaction (RT-PCR) method from the liver total RNA of a 3-methylcholanthrene (3-MC)-treated cynomolgus monkey.	Methylcholanthrene	200-204	cytochrome P450 family 1 subfamily A member 2	Macaca fascicularis	55-61
9705900-0	1998	Developmental regulation of the 3-methylcholanthrene- and dioxin-inducible CYP1A5 gene in chick embryo liver in vivo.	Methylcholanthrene	32-52	cytochrome P450 1A2	Gallus gallus	75-81
9632741-9	1998	These findings strongly suggest that AhR translocates from hepatocyte cytoplasm to the nucleus and forms XRE-BP in the nucleus after MC stimulation.	Methylcholanthrene	133-135	aryl hydrocarbon receptor	Rattus norvegicus	37-40
9636188-5	1998	Using tumor cells derived from methylcholanthrene-treated IFN-gamma-insensitive mice, we found IFN-gamma"s actions to be mediated at least partly through its direct effects on the tumor cell leading to enhanced tumor cell immunogenicity.	Methylcholanthrene	31-49	interferon gamma	Mus musculus	58-67
9636188-5	1998	Using tumor cells derived from methylcholanthrene-treated IFN-gamma-insensitive mice, we found IFN-gamma"s actions to be mediated at least partly through its direct effects on the tumor cell leading to enhanced tumor cell immunogenicity.	Methylcholanthrene	31-49	interferon gamma	Mus musculus	95-104
9624139-9	1998	Dog mastocytoma cells incubated with 12-O-tetradecanoylphorbol-13-acetate increase expression of MC-DPPI mRNA.	Methylcholanthrene	97-99	dipeptidyl peptidase 1	Canis lupus familiaris	100-104
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	52-72	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	174-182
9642136-3	1998	S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by MC occurred in rabbit kidney RK13 cells but not in rabbit lung R9ab cells, while aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (Arnt) mRNAs were expressed in both cells at similar levels.	Methylcholanthrene	73-75	cytochrome P450 1A1	Oryctolagus cuniculus	58-64
9642136-3	1998	S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by MC occurred in rabbit kidney RK13 cells but not in rabbit lung R9ab cells, while aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (Arnt) mRNAs were expressed in both cells at similar levels.	Methylcholanthrene	73-75	aryl hydrocarbon receptor nuclear translocator	Oryctolagus cuniculus	216-220
9642136-4	1998	Interestingly, the treatment of R9ab cells with a DNA demethylating agent, 5-aza-2"-deoxycitidine, resulted in the induction of the expression of the CYP1A1 gene by MC.	Methylcholanthrene	165-167	cytochrome P450 1A1	Oryctolagus cuniculus	150-156
9642136-5	1998	The results indicate that DNA methylation is one of the factors involved in the loss of the MC-induced expression of the CYP1A1 gene.	Methylcholanthrene	92-94	cytochrome P450 1A1	Oryctolagus cuniculus	121-127
9667743-0	1998	Induction of mutations in Ki-ras and INK4a in liver tumors of mice exposed in utero to 3-methylcholanthrene.	Methylcholanthrene	87-107	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	26-32
9667743-0	1998	Induction of mutations in Ki-ras and INK4a in liver tumors of mice exposed in utero to 3-methylcholanthrene.	Methylcholanthrene	87-107	cyclin dependent kinase inhibitor 2A	Mus musculus	37-42
9667743-2	1998	The present study utilized a pharmacogenetic mouse model to assess the role of cytochrome P4501A1 (Cyp1a1) in modulating genetic damage to oncogenic and tumor suppressor loci following in utero exposure to the polycyclic aromatic hydrocarbon, 3-methylcholanthrene (MC).	Methylcholanthrene	243-263	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	79-97
9667743-2	1998	The present study utilized a pharmacogenetic mouse model to assess the role of cytochrome P4501A1 (Cyp1a1) in modulating genetic damage to oncogenic and tumor suppressor loci following in utero exposure to the polycyclic aromatic hydrocarbon, 3-methylcholanthrene (MC).	Methylcholanthrene	243-263	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	99-105
9667743-2	1998	The present study utilized a pharmacogenetic mouse model to assess the role of cytochrome P4501A1 (Cyp1a1) in modulating genetic damage to oncogenic and tumor suppressor loci following in utero exposure to the polycyclic aromatic hydrocarbon, 3-methylcholanthrene (MC).	Methylcholanthrene	265-267	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	79-97
9667743-2	1998	The present study utilized a pharmacogenetic mouse model to assess the role of cytochrome P4501A1 (Cyp1a1) in modulating genetic damage to oncogenic and tumor suppressor loci following in utero exposure to the polycyclic aromatic hydrocarbon, 3-methylcholanthrene (MC).	Methylcholanthrene	265-267	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	99-105
9667749-6	1998	After chemical transformation of mouse liver cells with either MC or MNNG, select cyclin D1-CDK-CDI protein complexes were altered.	Methylcholanthrene	63-65	cyclin D1	Mus musculus	82-91
9667749-7	1998	In MC-transformed cells formation of various binary, tertiary and quaternary cyclin D1-CDK-(CDI) protein complexes was reduced, resulting in decreased CDK4 kinase activity.	Methylcholanthrene	3-5	cyclin D1	Mus musculus	77-86
9667749-7	1998	In MC-transformed cells formation of various binary, tertiary and quaternary cyclin D1-CDK-(CDI) protein complexes was reduced, resulting in decreased CDK4 kinase activity.	Methylcholanthrene	3-5	cyclin-dependent kinase 4	Mus musculus	151-155
9616189-7	1998	The formation of 2-hydroxyemodin was increased in liver microsomes from 3-methylcholanthrene-pretreated rats and was inhibited by alpha-naphthoflavone, by an anti-rat cytochrome P450 1A1/2 antibody, and, to a lesser degree, by an anti-rat cytochrome P450 1A1 antibody.	Methylcholanthrene	72-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	167-186
9616189-7	1998	The formation of 2-hydroxyemodin was increased in liver microsomes from 3-methylcholanthrene-pretreated rats and was inhibited by alpha-naphthoflavone, by an anti-rat cytochrome P450 1A1/2 antibody, and, to a lesser degree, by an anti-rat cytochrome P450 1A1 antibody.	Methylcholanthrene	72-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	239-258
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	52-72	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	202-208
9564844-7	1998	MC receptors in these sites are accessible to circulating MC-R agonists in vivo, as specific binding of [125I]NDP-MSH was observed in exocrine and adrenal glands after systemic injection in vivo.	Methylcholanthrene	0-2	norrin cystine knot growth factor NDP	Rattus norvegicus	110-113
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	52-72	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	223-229
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	174-182
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	74-76	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	202-208
9630843-10	1998	Liver microsomes isolated from rats pretreated with 3-methylcholanthrene (MC-microsomes), however, had increased FMO activity and also enhanced rates of forming the 7 alpha-(CYP1A1/2, and 2A1), 6 beta-(CYP3A1), and 2 beta-(CYP3A1) hydroxytestosterone.	Methylcholanthrene	74-76	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	223-229
9630843-14	1998	Increased productions of CA N-demethylation metabolites (TB, PX, and TP) are, however, catalyzed by the increased activities of CYP1A2 and FMO which are associated uniquely with the MC-microsomes.	Methylcholanthrene	182-184	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	128-134
9630845-5	1998	MC induced new expression of CYP1A, GSTA3 and enhanced expression of GSTA1/2 and UGT.	Methylcholanthrene	0-2	glutathione S-transferase alpha 3	Rattus norvegicus	36-41
9630845-5	1998	MC induced new expression of CYP1A, GSTA3 and enhanced expression of GSTA1/2 and UGT.	Methylcholanthrene	0-2	glutathione S-transferase alpha 1	Rattus norvegicus	69-76
9545515-3	1998	By Northern blotting, using an oligonucleotide specific to CYP3A31, the mRNA for this isozyme was shown to be expressed constitutively in liver and induced by treatment with phenobarbital but repressed by 3-methylcholanthrene or dexamethasone treatments.	Methylcholanthrene	205-225	cytochrome P450 3A31	Mesocricetus auratus	59-66
9607418-5	1998	As judged by a thrombin-dependent protein C activation assay, such MC membrane-bound TM was biologically active.	Methylcholanthrene	67-69	coagulation factor II	Rattus norvegicus	15-23
9607418-5	1998	As judged by a thrombin-dependent protein C activation assay, such MC membrane-bound TM was biologically active.	Methylcholanthrene	67-69	thrombomodulin	Rattus norvegicus	85-87
9607418-8	1998	Our data indicate that MC-mediated expression of TM can be used to augment the anticoagulant properties of the parietal peritoneal surface.	Methylcholanthrene	23-25	thrombomodulin	Rattus norvegicus	49-51
9584330-6	1998	Since only the vitamin D compounds which possess hydroxyl groups both in the position 1 alpha and in the side chain, bind to the vitamin D receptor, we suggest that a local metabolism of MC 1582 and 1 alpha(OH)D3 takes place in the skin to the active, side-chain-hydroxylated species, probably to KH 1060 and 1 alpha,25(OH)2D3.	Methylcholanthrene	187-189	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	129-147
9500848-9	1998	The testosterone 7 alpha-hydroxylase activity and the mRNA level in liver were both decreased moderately by administration of 3-methylcholanthrene and slightly by administration of phenobarbital.	Methylcholanthrene	126-146	cytochrome P450 2A9	Mesocricetus auratus	4-36
9536002-8	1998	Enzymatic activity and de novo protein synthesis of 3-methylcholanthrene-induced CYP1A2 and dexamethasone-induced CYP3A4 were also reduced to a much greater extent by oncostatin M than by other cytokines.	Methylcholanthrene	52-72	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	81-87
9536002-8	1998	Enzymatic activity and de novo protein synthesis of 3-methylcholanthrene-induced CYP1A2 and dexamethasone-induced CYP3A4 were also reduced to a much greater extent by oncostatin M than by other cytokines.	Methylcholanthrene	52-72	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-120
9536002-8	1998	Enzymatic activity and de novo protein synthesis of 3-methylcholanthrene-induced CYP1A2 and dexamethasone-induced CYP3A4 were also reduced to a much greater extent by oncostatin M than by other cytokines.	Methylcholanthrene	52-72	oncostatin M	Homo sapiens	167-179
9566755-3	1998	It has been previously reported that in vivo treatment with CYP1A1 inducer 3-methylcholanthrene (3-MC) suppresses rat hepatic HST-a mRNA expression in a dose-dependent manner.	Methylcholanthrene	97-101	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	60-66
9566755-3	1998	It has been previously reported that in vivo treatment with CYP1A1 inducer 3-methylcholanthrene (3-MC) suppresses rat hepatic HST-a mRNA expression in a dose-dependent manner.	Methylcholanthrene	75-95	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	60-66
9461503-3	1998	Some animals also received 3-methylcholanthrene (MC) to induce hepatic CYP1A2.	Methylcholanthrene	49-51	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	71-77
9461503-6	1998	Treatment with MC increased hepatic CYP1A1 in both mouse lines and hepatic CYP1A2 only in the Cyp1a2(+/+) line, as determined by Western immunoblotting.	Methylcholanthrene	15-17	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	36-42
9461503-6	1998	Treatment with MC increased hepatic CYP1A1 in both mouse lines and hepatic CYP1A2 only in the Cyp1a2(+/+) line, as determined by Western immunoblotting.	Methylcholanthrene	15-17	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	75-81
9461503-6	1998	Treatment with MC increased hepatic CYP1A1 in both mouse lines and hepatic CYP1A2 only in the Cyp1a2(+/+) line, as determined by Western immunoblotting.	Methylcholanthrene	15-17	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	94-100
9461503-7	1998	MC increased hepatic ethoxy- and methoxy-resorufin O-dealkylase activities in both mouse lines, but increased uroporphyrinogen oxidation activity in the Cyp1a2(+/+) wild-type mice only.	Methylcholanthrene	0-2	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	153-159
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	32-52	aryl hydrocarbon receptor	Rattus norvegicus	104-107
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	32-52	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	119-125
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	32-52	aryl hydrocarbon receptor	Rattus norvegicus	221-224
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	54-57	aryl hydrocarbon receptor	Rattus norvegicus	104-107
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	54-57	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	119-125
9514075-3	1998	We had previously observed that 3-methylcholanthrene (3MC) and beta-naphthoflavone (betaNF) induced the AHR-associated CYP1A1/1A2 pair in different liver regions, an effect not explained by the acinar distribution of the AHR protein.	Methylcholanthrene	54-57	aryl hydrocarbon receptor	Rattus norvegicus	221-224
9514075-5	1998	Analysis of samples from periportal and perivenous cell lysates from 3MC-treated animals revealed that ALDH3 mRNA, protein and benzaldehyde-NADP associated activity were all confined to the perivenous region.	Methylcholanthrene	69-72	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	103-108
9514075-7	1998	Immunohistochemically, a peculiar mono- or oligocellular induction pattern of ALDH3 was seen, consistently surrounding terminal hepatic veins after 3MC but mainly in the midzonal region after betaNF.	Methylcholanthrene	148-151	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	78-83
9514075-8	1998	A ligand-specific difference in regional induction of GSTYa1 mRNA was also observed: The constitutive perivenous dominance was preserved after 3MC while induction by betaNF was mainly periportal.	Methylcholanthrene	143-146	glutathione S-transferase alpha 2	Rattus norvegicus	54-60
9514084-4	1998	Treatment with 3-methylcholanthrene caused a transient drop in total cell AHR, but the AHR levels returned to near pretreatment levels within 72 hr after the first exposure.	Methylcholanthrene	15-35	aryl-hydrocarbon receptor	Mus musculus	74-77
9566755-3	1998	It has been previously reported that in vivo treatment with CYP1A1 inducer 3-methylcholanthrene (3-MC) suppresses rat hepatic HST-a mRNA expression in a dose-dependent manner.	Methylcholanthrene	75-95	sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 6	Rattus norvegicus	126-131
9566755-3	1998	It has been previously reported that in vivo treatment with CYP1A1 inducer 3-methylcholanthrene (3-MC) suppresses rat hepatic HST-a mRNA expression in a dose-dependent manner.	Methylcholanthrene	97-101	sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 6	Rattus norvegicus	126-131
9454825-5	1998	When hepatocytes were treated with inducers, marked increases in the specific activities of CYP1A1/2 by 3-methylcholanthrene and CYP3A4 by rifampicin were observed, and these inductive effects were greatly reduced in the presence of HGF.	Methylcholanthrene	104-124	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	92-98
9466818-2	1998	A 3MC response element was recently identified approximately 2.2 kb upstream of the transcription start site of the human CYP1A2 gene.	Methylcholanthrene	2-5	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	122-128
9538619-1	1998	To determine accuracy of quantitative immunohistochemical results, serially diluted liver cell lysates from methylcholanthrene (MC)-treated rats containing cytochrome P-450 (P-450) 1A were immobilized on nitrocellulose (NC) filters and stained by the indirect immunoperoxidase method under saturation conditions.	Methylcholanthrene	108-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	156-172
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	KIT ligand	Homo sapiens	91-94
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-110
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-117
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	CD9 molecule	Homo sapiens	174-177
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	integrin subunit beta 1	Homo sapiens	179-183
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	CD33 molecule	Homo sapiens	185-189
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	sialophorin	Homo sapiens	191-195
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	CD44 molecule (Indian blood group)	Homo sapiens	197-201
9485081-6	1998	RESULTS: In both groups of patients (RA and OA), SyMC were found to react with MAb to IgE, SCF receptor (c-kit, CD117), as well as CD antigens likewise expressed in lung MC (CD9, CD29, CD33, CD43, CD44, CD45).	Methylcholanthrene	51-53	protein tyrosine phosphatase receptor type C	Homo sapiens	203-207
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	59-65
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	193-199
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	229-235
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	hepatocyte growth factor	Homo sapiens	276-279
9454825-7	1998	The observed changes in the activity and protein levels of CYP1A2 and CYP3A4 correlated with a reduction in the specific messenger RNA levels both in control, 3-methylcholanthrene-treated (for CYP1A2) and rifampicin-treated (for CYP3A4) hepatocytes, which thus suggested that HGF could down-regulate CYP expression at a pretranslational level.	Methylcholanthrene	159-179	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	59-62
21639152-5	1997	MC-GC/MIP-AES was validated for the analysis of sediment (PACS-1 and BCR 462) and biological (NIES11) certified reference materials.	Methylcholanthrene	0-2	phosphofurin acidic cluster sorting protein 1	Homo sapiens	58-76
9419452-3	1998	Treatment with daily subcutaneous injections of FL not only caused complete regression of tumors in a significant proportion of mice challenged with a syngeneic methylcholanthrene-induced fibrosarcoma, but also caused a significant decrease in the tumor growth rate in the remaining mice.	Methylcholanthrene	161-179	FMS-like tyrosine kinase 3 ligand	Mus musculus	48-50
10729771-0	1998	c-K-ras overexpression is characteristic for metastases derived from a methylcholanthrene-induced fibrosarcoma.	Methylcholanthrene	71-89	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	0-7
10729771-1	1998	We investigated the relationship between the activation of the c-myc and c-K-ras proto-oncogenes and the acquisition of metastatic potential in a methylcholanthrene-induced BALB/c fibrosarcoma.	Methylcholanthrene	146-164	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	73-80
9509414-2	1997	We have found a prominent augmentation of hepatic FMO1 both at transcription and translation levels by pretreatment of rats with 3MC.	Methylcholanthrene	129-132	flavin containing dimethylaniline monoxygenase 1	Rattus norvegicus	50-54
9509414-3	1997	Liver tissues were used to study the inductive effect of 3MC on the FMO1 isoform, the major form present in rat liver.	Methylcholanthrene	57-60	flavin containing dimethylaniline monoxygenase 1	Rattus norvegicus	68-72
9534358-7	1997	The microcrystals positive (MC+) group had significantly higher values for AST (69.8 +/- 1.7) (mean +/- SEM), ALT (123.3 +/- 28.1), FA (252 +/- 28.1), G-GT (144.6 +/- 26.7) and BT (1.83 +/- 0.37) than the microcrystals negative group: AST (19.6 +/- 2.5), ALT (28.3 +/- 5.8), FA (170.5 +/- 15.1), G-GT (54.3 +/- 10.7) and BT (0.76 +/- 0.09).	Methylcholanthrene	28-31	solute carrier family 17 member 5	Homo sapiens	75-78
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	76-96	upstream transcription factor 1	Homo sapiens	0-29
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	76-96	upstream transcription factor 1	Homo sapiens	31-35
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	76-96	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	61-67
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	98-100	upstream transcription factor 1	Homo sapiens	0-29
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	98-100	upstream transcription factor 1	Homo sapiens	31-35
9388470-0	1997	Upstream stimulatory factor 1 (USF1) suppresses induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) in HepG2 cells.	Methylcholanthrene	98-100	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	61-67
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	90-110	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	75-81
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	90-110	upstream transcription factor 1	Homo sapiens	153-157
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	90-110	macrophage scavenger receptor 1	Homo sapiens	158-166
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	112-114	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	75-81
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	112-114	upstream transcription factor 1	Homo sapiens	153-157
9388470-7	1997	Furthermore, the S1 nuclease protection assay showed that the induction of CYP1A1 mRNA by 3-methylcholanthrene (MC) was depressed by the transfection of USF1-SR alpha into HepG2 cells.	Methylcholanthrene	112-114	macrophage scavenger receptor 1	Homo sapiens	158-166
9366293-4	1997	Finally, the authors evaluated the spontaneous production of prostaglandin E2 (PGE2) and tumor necrosis factor-alpha (TNF-alpha) in culture conditioned mediums of unseparated MC by radioimmunoassay and enzyme-linked immunoadsorbent assay methodology, respectively.	Methylcholanthrene	175-177	tumor necrosis factor	Homo sapiens	118-127
9358337-3	1997	GAD65 was captured via solid phase coated Mc-GAD65-Ab and detected via a second biotin-labelled Mc-GAD65-Ab recognizing a NH2-terminal epitope of the molecule.	Methylcholanthrene	42-44	glutamate decarboxylase 2	Rattus norvegicus	0-5
9358337-3	1997	GAD65 was captured via solid phase coated Mc-GAD65-Ab and detected via a second biotin-labelled Mc-GAD65-Ab recognizing a NH2-terminal epitope of the molecule.	Methylcholanthrene	96-98	glutamate decarboxylase 2	Rattus norvegicus	0-5
9534358-7	1997	The microcrystals positive (MC+) group had significantly higher values for AST (69.8 +/- 1.7) (mean +/- SEM), ALT (123.3 +/- 28.1), FA (252 +/- 28.1), G-GT (144.6 +/- 26.7) and BT (1.83 +/- 0.37) than the microcrystals negative group: AST (19.6 +/- 2.5), ALT (28.3 +/- 5.8), FA (170.5 +/- 15.1), G-GT (54.3 +/- 10.7) and BT (0.76 +/- 0.09).	Methylcholanthrene	28-31	solute carrier family 17 member 5	Homo sapiens	235-238
9512925-4	1997	The CYP1A2 dependent O-demethylation of methoxyresorufin in 3-methylcholanthrene induced hepatocytes was also markedly enhanced when intracellular H2O2 was generated by the mitochondrial monoamine oxidase (MAO) substrates tyramine or kynurenamine.	Methylcholanthrene	60-80	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	4-10
9364010-4	1997	The level of CYP1A2 mRNA in the liver was increased by treatment with 3-methylcholanthrene and polychlorinated biphenyls.	Methylcholanthrene	70-90	cytochrome P450 1A2	Callithrix jacchus	13-19
18982480-5	1997	The treatment of 1 nM 3-methylcholanthrene resulted in two fold increases in CAT protein as well as CAT mRNA compared to untreated control hepa 1 cells.	Methylcholanthrene	22-42	catalase	Mus musculus	77-80
18982480-5	1997	The treatment of 1 nM 3-methylcholanthrene resulted in two fold increases in CAT protein as well as CAT mRNA compared to untreated control hepa 1 cells.	Methylcholanthrene	22-42	catalase	Mus musculus	100-103
18982480-8	1997	3-Methylcholanthrene (1 nM) treatment to hepa 1 cells transfected with troutCYP1A-CAT construct stimulated the level of cyp1a1 mRNA by two folds and the activity of ethoxyresorufin-O-deethylase by two fold compared to that of control cells.	Methylcholanthrene	0-20	catalase	Mus musculus	82-85
18982480-8	1997	3-Methylcholanthrene (1 nM) treatment to hepa 1 cells transfected with troutCYP1A-CAT construct stimulated the level of cyp1a1 mRNA by two folds and the activity of ethoxyresorufin-O-deethylase by two fold compared to that of control cells.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	120-126
18982480-9	1997	In this study we reported that troutCYP1A-CAT reporter gene expression construct could be expressed by 3-methylcholanthrene treatment in mouse hepa 1 cells.	Methylcholanthrene	103-123	catalase	Mus musculus	42-45
9399571-1	1997	A heterodimer of AhR (aryl hydrocarbon receptor) and Arnt (AhR nuclear translocator) conveys a transactivation signal of aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the genes for a group of drug-metabolizing enzymes.	Methylcholanthrene	191-211	aryl hydrocarbon receptor	Homo sapiens	17-20
9399571-1	1997	A heterodimer of AhR (aryl hydrocarbon receptor) and Arnt (AhR nuclear translocator) conveys a transactivation signal of aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the genes for a group of drug-metabolizing enzymes.	Methylcholanthrene	191-211	aryl hydrocarbon receptor	Homo sapiens	22-47
9399571-1	1997	A heterodimer of AhR (aryl hydrocarbon receptor) and Arnt (AhR nuclear translocator) conveys a transactivation signal of aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the genes for a group of drug-metabolizing enzymes.	Methylcholanthrene	191-211	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	53-57
9399571-1	1997	A heterodimer of AhR (aryl hydrocarbon receptor) and Arnt (AhR nuclear translocator) conveys a transactivation signal of aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the genes for a group of drug-metabolizing enzymes.	Methylcholanthrene	191-211	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	59-83
9400724-12	1997	The early MC growth increase was not blocked by antibodies to cytokines, such as platelet-derived growth factor, fibroblast growth factors, or tumor necrosis factor, but was inhibited by anti-keratinocyte growth factor (anti-KGF).	Methylcholanthrene	10-12	fibroblast growth factor 7	Rattus norvegicus	225-228
20654333-0	1997	Comparative study of CYP1A1 induction by 3-methylcholanthrene in various human hepatic and epidermal cell types.	Methylcholanthrene	41-61	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	21-27
20654333-3	1997	In these cell types, the effects of 3-methylcholanthrene (3-MC) were analysed on CYP1A1 gene expression, a crucial CYP subfamily in the activation of chemical carcinogens.	Methylcholanthrene	36-56	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	81-87
20654333-3	1997	In these cell types, the effects of 3-methylcholanthrene (3-MC) were analysed on CYP1A1 gene expression, a crucial CYP subfamily in the activation of chemical carcinogens.	Methylcholanthrene	58-62	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	81-87
20654333-8	1997	This study also demonstrated that 3-MC is capable of significantly inducing CYP1A1 in HaCaT cells (17-fold over control), as in human hepatocytes (six- to 18-fold) and HepG2 (fourfold).	Methylcholanthrene	34-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	76-82
11360624-1	1997	With specific designed primers, CYP2B6 and CYP1A1 cDNA were generated by reverse transcription-polymerase chain reaction(RT-PCR) technique performed on total RNAs isolated from human liver and 3-methylcholanthrene(3-MC) induced human amnion FL cells.	Methylcholanthrene	193-213	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	32-38
11360624-1	1997	With specific designed primers, CYP2B6 and CYP1A1 cDNA were generated by reverse transcription-polymerase chain reaction(RT-PCR) technique performed on total RNAs isolated from human liver and 3-methylcholanthrene(3-MC) induced human amnion FL cells.	Methylcholanthrene	193-213	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	43-49
11360624-1	1997	With specific designed primers, CYP2B6 and CYP1A1 cDNA were generated by reverse transcription-polymerase chain reaction(RT-PCR) technique performed on total RNAs isolated from human liver and 3-methylcholanthrene(3-MC) induced human amnion FL cells.	Methylcholanthrene	214-218	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	32-38
9309387-0	1997	Quantitative analysis of endoplasmic reticulum and cytochrome P-450 in hepatocytes from rats injected with methylcholanthrene.	Methylcholanthrene	107-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
9309387-2	1997	In addition, immunostaining intensity of major MC-inducible cytochrome P-450 (P-450) forms (1A1/1A2) and total P-450 content in the cytoplasm of hepatocytes in the three zones were measured by microphotometry to ascertain whether P-450 is sufficiently induced in each sublobular zone by the administration.	Methylcholanthrene	47-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
9350289-0	1997	Interferon-gamma-induced MHC class I expression and defects in Jak/Stat signalling in methylcholanthrene-induced sarcomas.	Methylcholanthrene	86-104	interferon gamma	Mus musculus	0-16
9400724-13	1997	The results show that an early growth phase of MC after asbestos exposure appears unrelated to particle translocation to the pleura but is associated with cytokine release, most likely KGF, by lung cells.	Methylcholanthrene	47-49	fibroblast growth factor 7	Rattus norvegicus	185-188
9295036-2	1997	In a preimmunization-challenge model, virally-induced ALC lymphoma and methylcholanthrene-induced MC57X fibrosarcoma transplants were rejected similarly by syngeneic CD28 knockout and immunocompetent controls.	Methylcholanthrene	71-89	CD28 antigen	Mus musculus	166-170
9260906-8	1997	3-Methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) markedly increased ethoxyresorufin-O-deethylase activity and the related cytochrome P450 (CYP) 1A1/2 protein, whereas alpha-naphtoflavone antagonized the TCDD-elicited induction.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	141-168
9261130-11	1997	Equally effective in inducing CYP1A1 mRNA were benzo[e]pyrene and 3-methylcholanthrene.	Methylcholanthrene	66-86	cytochrome P450 1A1	Cricetulus griseus	30-36
9260198-3	1997	By a competitive sandwich enzyme-linked immunosorbent assay (ELISA), three binding patterns of mc-GAD-Abs were identified: 5 of 15 mc-GAD-Abs recognized a linear N-terminal epitope (p1), 5 of 15 were reactive with a conformational GAD65 epitope region (p2), and 5 of 15 were cross-reactive with GAD67 (p3).	Methylcholanthrene	95-97	glutamate decarboxylase 1	Homo sapiens	98-101
9260198-3	1997	By a competitive sandwich enzyme-linked immunosorbent assay (ELISA), three binding patterns of mc-GAD-Abs were identified: 5 of 15 mc-GAD-Abs recognized a linear N-terminal epitope (p1), 5 of 15 were reactive with a conformational GAD65 epitope region (p2), and 5 of 15 were cross-reactive with GAD67 (p3).	Methylcholanthrene	95-97	glutamate decarboxylase 1	Homo sapiens	134-137
9260198-4	1997	These patterns of mc-GAD-Abs were tested for islet cell binding by indirect immunofluorescence on pancreatic sections treated with either (1) Bouin"s solution, (2) Zamboni"s solution, or (3) phosphate-buffered formaldehyde for 0.5, 1, 2, and 18 h at 4 degrees C. After fixation for up to 2 h no differentiation of immunoreactivity of patterns was observed using the three fixatives.	Methylcholanthrene	18-20	glutamate decarboxylase 1	Homo sapiens	21-24
9260198-5	1997	mc-GAD-Abs recognizing conformational epitope regions (p2) revealed a marked reduced immunoreactivity on pancreatic sections fixed for 18 h with 4% formaldehyde, while mc-GAD-Abs reactive with linear epitopes (p1, p3) were detectable with strong binding.	Methylcholanthrene	0-2	glutamate decarboxylase 1	Homo sapiens	3-6
9260198-5	1997	mc-GAD-Abs recognizing conformational epitope regions (p2) revealed a marked reduced immunoreactivity on pancreatic sections fixed for 18 h with 4% formaldehyde, while mc-GAD-Abs reactive with linear epitopes (p1, p3) were detectable with strong binding.	Methylcholanthrene	0-2	glutamate decarboxylase 1	Homo sapiens	171-174
9260198-5	1997	mc-GAD-Abs recognizing conformational epitope regions (p2) revealed a marked reduced immunoreactivity on pancreatic sections fixed for 18 h with 4% formaldehyde, while mc-GAD-Abs reactive with linear epitopes (p1, p3) were detectable with strong binding.	Methylcholanthrene	168-170	glutamate decarboxylase 1	Homo sapiens	3-6
9260198-5	1997	mc-GAD-Abs recognizing conformational epitope regions (p2) revealed a marked reduced immunoreactivity on pancreatic sections fixed for 18 h with 4% formaldehyde, while mc-GAD-Abs reactive with linear epitopes (p1, p3) were detectable with strong binding.	Methylcholanthrene	168-170	glutamate decarboxylase 1	Homo sapiens	171-174
9212227-6	1997	During serositis, activated MC, both sessile and detached, expressed an extended spectrum of beta1, beta3 and beta4 integrins compared with resting MC, as shown by immunohistology.	Methylcholanthrene	28-30	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	93-105
9247296-1	1997	A 3-methylcholanthrene-induced fibrosarcoma cell line of BALB/c origin, CMS5j, was co-transfected with cDNA for the p40 and p35 subunits of interleukin-12 (IL-12).	Methylcholanthrene	2-22	interleukin 12b	Mus musculus	116-119
9247296-1	1997	A 3-methylcholanthrene-induced fibrosarcoma cell line of BALB/c origin, CMS5j, was co-transfected with cDNA for the p40 and p35 subunits of interleukin-12 (IL-12).	Methylcholanthrene	2-22	interleukin 12a	Mus musculus	124-127
9202038-4	1997	In comparison, induction with the specific inducer, 3-methylcholanthrene (3-MC), results in maximal levels of UGT1A1 mRNA after 8 h of treatment.	Methylcholanthrene	52-72	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-116
9202038-4	1997	In comparison, induction with the specific inducer, 3-methylcholanthrene (3-MC), results in maximal levels of UGT1A1 mRNA after 8 h of treatment.	Methylcholanthrene	74-78	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-116
9212227-9	1997	MC consistently adhered better than mesothelioma cells to laminin, tenascin, fibronectin and collagen type IV.	Methylcholanthrene	0-2	tenascin C	Homo sapiens	67-75
9212227-9	1997	MC consistently adhered better than mesothelioma cells to laminin, tenascin, fibronectin and collagen type IV.	Methylcholanthrene	0-2	fibronectin 1	Homo sapiens	77-88
9212227-10	1997	Adhesion of MC and mesothelioma cells to these matrix proteins was, at least in part, mediated via beta1 integrins.	Methylcholanthrene	12-14	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	99-104
9195908-6	1997	In addition, IL-1 strongly suppressed the induction of rGSTA2 by 3-methylcholanthrene, oltipraz (a synthetic derivative of 1, 2-dithiole-3-thione), and phenobarbital and that of rGSTM1 by oltipraz and phenobarbital, whereas it was ineffective on rGSTP1 induction by these compounds.	Methylcholanthrene	65-85	glutathione S-transferase alpha 2	Rattus norvegicus	55-61
9210976-8	1997	The content of hepatic cytochrome P-450 (0.751 versus 1.57 nmol/mg protein) and the weight of liver (3.53 versus 4.20% of body weight) increased significantly in 3-MC pretreated rats, suggesting that the metabolizing enzyme(s) for azosemide seemed to be induced by pretreatment with 3-MC.	Methylcholanthrene	162-166	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
9214598-1	1997	A previous study from this laboratory demonstrated that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring at 1 year after birth, the incidence of which correlated with fetal inducibility of Cyp1a1.	Methylcholanthrene	88-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	234-240
9214598-1	1997	A previous study from this laboratory demonstrated that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring at 1 year after birth, the incidence of which correlated with fetal inducibility of Cyp1a1.	Methylcholanthrene	110-112	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	234-240
9143324-2	1997	In addition, all of six inducers, such as dexamethasone, 3-methylcholanthrene, phenobarbital, polychlorinated biphenyl, pregnenolone 16 alpha-carbonitrile, and rifampicin, increased the expression of the Cyp3a11 mRNA more extensively than that of Cyp3a13.	Methylcholanthrene	57-77	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	204-211
9176488-2	1997	Since DCs are pivotal in the induction of immune responses, we tested whether Flt3L treatment of mice challenged with a syngeneic methylcholanthrene (MCA)-induced fibrosarcoma would augment the generation of effective antitumor immune responses in vivo.	Methylcholanthrene	130-148	FMS-like tyrosine kinase 3 ligand	Mus musculus	78-83
9176488-2	1997	Since DCs are pivotal in the induction of immune responses, we tested whether Flt3L treatment of mice challenged with a syngeneic methylcholanthrene (MCA)-induced fibrosarcoma would augment the generation of effective antitumor immune responses in vivo.	Methylcholanthrene	150-153	FMS-like tyrosine kinase 3 ligand	Mus musculus	78-83
9179267-4	1997	RESULTS: The PCNA-positive rates of non-cancerous epithelium of the gallbladder in patients with PBMJ (14.2% in MCA group and 11.6% in M group) were significantly higher than those without PBMJ (3.9% in CA group and 1.5% in N group).	Methylcholanthrene	112-115	proliferating cell nuclear antigen	Homo sapiens	13-17
9143324-2	1997	In addition, all of six inducers, such as dexamethasone, 3-methylcholanthrene, phenobarbital, polychlorinated biphenyl, pregnenolone 16 alpha-carbonitrile, and rifampicin, increased the expression of the Cyp3a11 mRNA more extensively than that of Cyp3a13.	Methylcholanthrene	57-77	cytochrome P450, family 3, subfamily a, polypeptide 13	Mus musculus	247-254
9077486-7	1997	That IgG-anti-MC stimulates an increase in IL-1beta and IFN-gamma production in controls suggests that IgG-anti-MC may play a role in melanocyte destruction mediated by monocytes.	Methylcholanthrene	14-16	interleukin 1 beta	Homo sapiens	43-51
9140468-0	1997	Enhancing effects of phenobarbital and 3-methylcholanthrene on GST-P-positive liver cell foci development in a new medium-term rat liver bioassay using D-galactosamine.	Methylcholanthrene	39-59	glutathione S-transferase pi 1	Rattus norvegicus	63-68
9174229-3	1997	IL-2 levels, tested by radioimmunoassay (RIA), were found to be reduced only in supernatants derived from CBMC of term infants and not in those derived from MC of preterm infants or adults.	Methylcholanthrene	108-110	interleukin 2	Homo sapiens	0-4
9128719-13	1997	Treatment of mice with an inducer of CYP1A2, 3-methylcholanthrene, increases the binding of the 46-kDa protein and decreases the binding of the 37-kDa protein to the mRNA, suggesting that changes in the binding of the proteins to the mRNA could play a role in the upregulation of CYP1A2 mRNA by 3-methylcholanthrene.	Methylcholanthrene	45-65	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	37-43
9128719-13	1997	Treatment of mice with an inducer of CYP1A2, 3-methylcholanthrene, increases the binding of the 46-kDa protein and decreases the binding of the 37-kDa protein to the mRNA, suggesting that changes in the binding of the proteins to the mRNA could play a role in the upregulation of CYP1A2 mRNA by 3-methylcholanthrene.	Methylcholanthrene	45-65	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	280-286
9128719-13	1997	Treatment of mice with an inducer of CYP1A2, 3-methylcholanthrene, increases the binding of the 46-kDa protein and decreases the binding of the 37-kDa protein to the mRNA, suggesting that changes in the binding of the proteins to the mRNA could play a role in the upregulation of CYP1A2 mRNA by 3-methylcholanthrene.	Methylcholanthrene	295-315	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	37-43
9077486-7	1997	That IgG-anti-MC stimulates an increase in IL-1beta and IFN-gamma production in controls suggests that IgG-anti-MC may play a role in melanocyte destruction mediated by monocytes.	Methylcholanthrene	14-16	interferon gamma	Homo sapiens	56-65
9054616-5	1997	The number of foci induced by methylcholanthrene, N-methyl-N"-nitro-N-nitrosoguanidine or quercetin was significantly reduced when the cultures were treated with TGF-beta.	Methylcholanthrene	30-48	transforming growth factor beta 1	Homo sapiens	162-170
9103535-6	1997	Decreases in CYP1A2 activity found after exposure of 3-methylcholanthrene-treated hepatocytes to interferon-gamma were also reversed in the presence of N(G)-monomethyl-L-arginine.	Methylcholanthrene	53-73	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	13-19
9103535-6	1997	Decreases in CYP1A2 activity found after exposure of 3-methylcholanthrene-treated hepatocytes to interferon-gamma were also reversed in the presence of N(G)-monomethyl-L-arginine.	Methylcholanthrene	53-73	interferon gamma	Homo sapiens	97-113
9231341-10	1997	Anti-CYP 2C11 also partially inhibited the N-demethylation of racemic chlorpheniramine in rat-liver microsomes exposed to phenobarbitone and 3-methylcholanthrene.	Methylcholanthrene	141-161	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	5-13
9219504-8	1997	RESULTS: Relative to their untreated counterparts, MCF-7/0 and MCF-7/OAP cells treated with 3-methylcholanthrene or catechol transiently expressed elevated levels of cytosolic class 3 aldehyde dehydrogenase, glutathione S-transferase, DT-diaphorase and UDP-glucuronosyl transferase, and were transiently, more resistant to mafosfamide, melphalan, and mitoxantrone, and more sensitive to EO9.	Methylcholanthrene	92-112	glutathione S-transferase kappa 1	Homo sapiens	208-233
20654295-5	1997	Enzyme inductions were effective throughout the whole culture period: EROD activity increased fivefold after exposure to phenobarbital (PB) and up to 20-fold after 3-methylcholanthrene (3-MC) exposure; GST activity was stimulated approximately twofold by both inducers.	Methylcholanthrene	164-184	hematopoietic prostaglandin D synthase	Rattus norvegicus	202-205
9219504-9	1997	Further, MCF-7/0 and MCF-7/OAP cells treated with 3-methylcholanthrene, but not those treated with catechol, transiently expressed elevated levels of cytochrome P450 1A1 and were transiently more sensitive to ellipticine.	Methylcholanthrene	50-70	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	150-169
9030721-3	1997	We find that the regulation of EpRE-mediated GST Ya gene expression by 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone is associated with an induction of AP-1 DNA-binding activity and that the AP-1 complex induced in hepatoma cells by these chemicals contains members of the Fos and Jun protein families.	Methylcholanthrene	71-91	hematopoietic prostaglandin D synthase	Mus musculus	45-48
9030721-3	1997	We find that the regulation of EpRE-mediated GST Ya gene expression by 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone is associated with an induction of AP-1 DNA-binding activity and that the AP-1 complex induced in hepatoma cells by these chemicals contains members of the Fos and Jun protein families.	Methylcholanthrene	71-91	jun proto-oncogene	Mus musculus	175-179
9030721-3	1997	We find that the regulation of EpRE-mediated GST Ya gene expression by 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone is associated with an induction of AP-1 DNA-binding activity and that the AP-1 complex induced in hepatoma cells by these chemicals contains members of the Fos and Jun protein families.	Methylcholanthrene	71-91	jun proto-oncogene	Mus musculus	214-218
9030721-3	1997	We find that the regulation of EpRE-mediated GST Ya gene expression by 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone is associated with an induction of AP-1 DNA-binding activity and that the AP-1 complex induced in hepatoma cells by these chemicals contains members of the Fos and Jun protein families.	Methylcholanthrene	71-91	FBJ osteosarcoma oncogene	Mus musculus	296-299
9030721-7	1997	Evidence is presented that 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone use a signal transduction pathway to Fos/Jun-dependent GST Ya gene expression via Ras and protein-tyrosine kinase activity.	Methylcholanthrene	27-47	FBJ osteosarcoma oncogene	Mus musculus	133-136
9030721-7	1997	Evidence is presented that 3-methylcholanthrene, tert-butylhydroquinone and beta-naphthoflavone use a signal transduction pathway to Fos/Jun-dependent GST Ya gene expression via Ras and protein-tyrosine kinase activity.	Methylcholanthrene	27-47	hematopoietic prostaglandin D synthase	Mus musculus	151-154
9155049-6	1997	Interestingly, a strong statistical association was observed between p53 nuclear accumulation and MC (P = 0.0003).	Methylcholanthrene	98-100	tumor protein p53	Homo sapiens	69-72
9155049-8	1997	When we analysed the concomitant influence of MC and p53 expression on overall survival, we were able to confirm a real predominant role of MC in comparison with p53.	Methylcholanthrene	140-142	tumor protein p53	Homo sapiens	53-56
9155049-10	1997	These results underline the prognostic impact of MC and p53 protein accumulation in NSCLC and their reciprocal inter-relationship, supporting the hypothesis of a wild-type p53 regulation on the angiogenetic process through a VEGF up-regulation.	Methylcholanthrene	49-51	tumor protein p53	Homo sapiens	172-175
9219504-8	1997	RESULTS: Relative to their untreated counterparts, MCF-7/0 and MCF-7/OAP cells treated with 3-methylcholanthrene or catechol transiently expressed elevated levels of cytosolic class 3 aldehyde dehydrogenase, glutathione S-transferase, DT-diaphorase and UDP-glucuronosyl transferase, and were transiently, more resistant to mafosfamide, melphalan, and mitoxantrone, and more sensitive to EO9.	Methylcholanthrene	92-112	NAD(P)H quinone dehydrogenase 1	Homo sapiens	235-248
9101553-5	1997	Among the phase II enzyme activities, only NADPH-quinone reductase was slightly increased by 3-MC and carotenoids, except beta-carotene.	Methylcholanthrene	93-97	crystallin, zeta	Mus musculus	43-66
9279133-2	1997	In both, PB and 3-MC treatment, the magnitude of increase in microsomal protein content, cytochrome b5 and aminopyrine N-demethylase (APND) activity was less in FR animals than in ad libitum fed; while cytochrome P-450 levels and activities of cytochrome c reductase and acetanilide hydroxylase (ACOH) were higher in FR animals.	Methylcholanthrene	16-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
9279133-3	1997	NADPH dependent lipid peroxidation and cytosolic glutathione-s-transferase activity were also enhanced due to PB and 3-MC treatment but the magnitude of increase was less in FR animals.	Methylcholanthrene	117-121	hematopoietic prostaglandin D synthase	Rattus norvegicus	49-74
8996235-6	1997	Treatment of rats with omeprazole, an atypical nonligand activator of the AHR, caused a zone-specific induction of CYP1A1 in the centrilobular region similar to that seen after pretreatment with the AHR ligand 3-methylcholanthrene.	Methylcholanthrene	210-230	aryl hydrocarbon receptor	Rattus norvegicus	74-77
9115594-7	1997	The increase in the amount of CT and CGRP released by the action of 1 microM dexamethasone was reduced by 1 microM 9-cis retinoic acid, and this effect was enhanced by the addition of 0.1 microM calcitriol or KH 1060, EB 1089 and MC 903.	Methylcholanthrene	230-232	calcitonin-related polypeptide alpha	Rattus norvegicus	30-32
9115594-7	1997	The increase in the amount of CT and CGRP released by the action of 1 microM dexamethasone was reduced by 1 microM 9-cis retinoic acid, and this effect was enhanced by the addition of 0.1 microM calcitriol or KH 1060, EB 1089 and MC 903.	Methylcholanthrene	230-232	calcitonin-related polypeptide alpha	Rattus norvegicus	37-41
9633828-0	1997	Signaling pathways in the induction of c-fos and c-jun proto-oncogenes by 3-methylcholanthrene.	Methylcholanthrene	74-94	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-44
9115594-1	1997	This study examined the action of 9-cis retinoic acid and 1,25-dihydroxyvitamin D3 analogues (KH 1060, EB 1089 and MC 903) on the release of calcitonin (CT) and calcitonin gene-related peptide (CGRP) in the rat C cell line CA-77.	Methylcholanthrene	115-117	calcitonin-related polypeptide alpha	Rattus norvegicus	141-151
9118891-6	1996	Likewise, V79 cells transfected with the 3-MC-inducible rat UGT1.6 cDNA showed a considerable rate of PH and HQ glucuronidation.	Methylcholanthrene	41-45	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	60-66
9633828-0	1997	Signaling pathways in the induction of c-fos and c-jun proto-oncogenes by 3-methylcholanthrene.	Methylcholanthrene	74-94	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-54
9633828-3	1997	Through its epoxide metabolites, MC functions also as an inducer of drug-metabolizing enzyme glutathione S-transferase (GST) gene expression.	Methylcholanthrene	33-35	glutathione S-transferase kappa 1	Homo sapiens	93-118
9633828-3	1997	Through its epoxide metabolites, MC functions also as an inducer of drug-metabolizing enzyme glutathione S-transferase (GST) gene expression.	Methylcholanthrene	33-35	glutathione S-transferase kappa 1	Homo sapiens	120-123
9633828-4	1997	Induction of murine GST Ya gene by MC and a variety of other chemical agents is mediated by a regulatory element composed of two adjacent AP-1-like sites, and activated by the Fos/Jun heterodimeric complex (AP-1).	Methylcholanthrene	35-37	glutathione S-transferase kappa 1	Homo sapiens	20-23
9633828-4	1997	Induction of murine GST Ya gene by MC and a variety of other chemical agents is mediated by a regulatory element composed of two adjacent AP-1-like sites, and activated by the Fos/Jun heterodimeric complex (AP-1).	Methylcholanthrene	35-37	FBJ osteosarcoma oncogene	Mus musculus	176-179
9633828-5	1997	In cultured cells, MC causes the induction of AP-1 activity, which is the result of an increased expression of c-Fos and c-Jun proteins.	Methylcholanthrene	19-21	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	111-116
9633828-5	1997	In cultured cells, MC causes the induction of AP-1 activity, which is the result of an increased expression of c-Fos and c-Jun proteins.	Methylcholanthrene	19-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-126
9633828-6	1997	The mechanisms involved in MC activation of c-fos and c-jun gene expression were examined in the present study.	Methylcholanthrene	27-29	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	44-49
9633828-6	1997	The mechanisms involved in MC activation of c-fos and c-jun gene expression were examined in the present study.	Methylcholanthrene	27-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-59
9633828-7	1997	Evidence is presented that stimulation of c-fos transcription by MC involves a signal transduction pathway, which includes activation of the small G protein Ras, Raf-1 kinase, and the mitogen-activated protein (MAP) kinases, ERK1 and ERK2.	Methylcholanthrene	65-67	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	42-47
9633828-7	1997	Evidence is presented that stimulation of c-fos transcription by MC involves a signal transduction pathway, which includes activation of the small G protein Ras, Raf-1 kinase, and the mitogen-activated protein (MAP) kinases, ERK1 and ERK2.	Methylcholanthrene	65-67	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	162-167
9633828-7	1997	Evidence is presented that stimulation of c-fos transcription by MC involves a signal transduction pathway, which includes activation of the small G protein Ras, Raf-1 kinase, and the mitogen-activated protein (MAP) kinases, ERK1 and ERK2.	Methylcholanthrene	65-67	mitogen-activated protein kinase 3	Homo sapiens	225-229
9633828-7	1997	Evidence is presented that stimulation of c-fos transcription by MC involves a signal transduction pathway, which includes activation of the small G protein Ras, Raf-1 kinase, and the mitogen-activated protein (MAP) kinases, ERK1 and ERK2.	Methylcholanthrene	65-67	mitogen-activated protein kinase 1	Homo sapiens	234-238
9633828-8	1997	Furthermore, we find that phorbol 12-myristate 13-acetate, which uses both protein kinase C and protein-tyrosine kinase activities to induce c-fos promoter, may share a common pathway with MC downstream of Ras.	Methylcholanthrene	189-191	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-146
9633828-9	1997	The signal transduction pathway induced by MC to stimulate c-jun promoter involves Ras activation and the JNK group of MAP-kinases.	Methylcholanthrene	43-45	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-64
9633828-9	1997	The signal transduction pathway induced by MC to stimulate c-jun promoter involves Ras activation and the JNK group of MAP-kinases.	Methylcholanthrene	43-45	mitogen-activated protein kinase 8	Homo sapiens	106-109
8943899-11	1996	Thrombomodulin is present and highly active on cultured and seeded MC.	Methylcholanthrene	67-69	thrombomodulin	Homo sapiens	0-14
8938168-6	1996	Activities of MC-CoA hydratase and HIB-CoA hydrolase in human liver were very high compared with that of branched-chain alpha-keto acid dehydrogenase complex, suggesting an important role for these enzymes in catabolism of a potentially toxic compound, MC-CoA, formed as an intermediate in the catabolism of valine and isobutyrate.	Methylcholanthrene	14-16	3-hydroxyisobutyryl-CoA hydrolase	Homo sapiens	35-52
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
9118891-7	1996	In addition to inducing glucuronidation of phenols, 3-MC treatment (reported to protect rats from the myelotoxicity of benzene) resulted in a decrease of hepatic CYP2E1.	Methylcholanthrene	52-56	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	162-168
9118891-10	1996	In conclusion, the protective effect of 3-MC in rats is probably due to a shift from the labile PH sulfate to the more stable PH glucuronide, and to a decrease in hepatic CYP2E1.	Methylcholanthrene	40-44	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	171-177
8937476-6	1996	In addition, pretreatment of 3T3 fibroblast cells with 3-methylcholanthrene abolished TCDD-induced c-Src kinase activity in AhR-immunoprecipitate.	Methylcholanthrene	55-75	c-src tyrosine kinase	Mus musculus	99-111
9008098-7	1996	CsA directly decreased expression of VCAM-1 on MC.	Methylcholanthrene	47-49	vascular cell adhesion molecule 1	Homo sapiens	37-43
8937476-6	1996	In addition, pretreatment of 3T3 fibroblast cells with 3-methylcholanthrene abolished TCDD-induced c-Src kinase activity in AhR-immunoprecipitate.	Methylcholanthrene	55-75	aryl-hydrocarbon receptor	Mus musculus	124-127
8837752-4	1996	NAD(P)H-supported lipid peroxidation in microsomes with increased DT-diaphorase activity from 3-methylcholanthrene-treated rats was highly susceptible to menadione.	Methylcholanthrene	94-114	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	66-79
8918566-8	1996	Apoptotic cells defined by merocyanine (MC)540 were gradually increased from 12 h to 24 h. Anti-CD3-induced apoptosis of CD28+ T cells was significantly accelerated in SLE, whereas apoptosis of CD28- T cells was hardly detected in both SLE and normal controls.	Methylcholanthrene	40-42	CD28 molecule	Homo sapiens	121-125
8918566-8	1996	Apoptotic cells defined by merocyanine (MC)540 were gradually increased from 12 h to 24 h. Anti-CD3-induced apoptosis of CD28+ T cells was significantly accelerated in SLE, whereas apoptosis of CD28- T cells was hardly detected in both SLE and normal controls.	Methylcholanthrene	40-42	CD28 molecule	Homo sapiens	194-198
8968046-5	1996	Based on our previous evidence that tumour necrosis factor-alpha (TNF-alpha) acts as an endogenous tumour promoter on BALB/3T3 cells initiated with 3-methylcholanthrene, we found that morphine dose-dependently inhibited TnF-alpha release from KATO III cells (IC50, 5.6 mM) and also from BALB/3T3 cells (IC50, 1.3 mM) induced by okadaic acid, one of the non-TPA type tumour promoters.	Methylcholanthrene	148-168	tumor necrosis factor	Mus musculus	66-75
8937980-6	1996	The regulation of beta-galactosidase expression was determined in mock and 3-MC-treated mice in an extensive range of tissues.	Methylcholanthrene	75-79	galactosidase, beta 1	Mus musculus	18-36
8865788-6	1996	MC alpha using unsupervised 8-hour urine collection at home correlated well with CC alpha.	Methylcholanthrene	0-2	fibrillin 2	Homo sapiens	81-89
8952791-11	1996	CONCLUSIONS: New Mc Ab such as JCB 117 (anti-CD79a) might detect a minimal residual disease in the testes of children treated for ALL, particularly on routine histological material.	Methylcholanthrene	17-19	CD79a molecule	Homo sapiens	45-50
8905915-2	1996	Induction of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by aromatic hydrocarbons such as 3-methylcholanthrene (MC) is accompanied by down-regulation of other CYPs that are expressed constitutively in rat liver.	Methylcholanthrene	99-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-28
8905915-2	1996	Induction of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by aromatic hydrocarbons such as 3-methylcholanthrene (MC) is accompanied by down-regulation of other CYPs that are expressed constitutively in rat liver.	Methylcholanthrene	99-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-33
8905915-2	1996	Induction of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by aromatic hydrocarbons such as 3-methylcholanthrene (MC) is accompanied by down-regulation of other CYPs that are expressed constitutively in rat liver.	Methylcholanthrene	121-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-28
8905915-2	1996	Induction of cytochrome P450 (CYP) enzymes of the CYP1A subfamily by aromatic hydrocarbons such as 3-methylcholanthrene (MC) is accompanied by down-regulation of other CYPs that are expressed constitutively in rat liver.	Methylcholanthrene	121-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-33
8905915-4	1996	We examined the time-course of the effects of MC on the expression of CYP2C11 and 3A2 in the liver of male rats at the catalytic activity, apoprotein and mRNA levels.	Methylcholanthrene	46-48	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	70-77
8905915-6	1996	A single intraperitoneal dose of MC (50 mg/kg) caused an increase in total hepatic microsomal CYP and haem content, and a marked induction of CYP1A1 catalytic activity (7-ethoxyresorufin O-deethylase) and apoprotein.	Methylcholanthrene	33-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-97
8905915-6	1996	A single intraperitoneal dose of MC (50 mg/kg) caused an increase in total hepatic microsomal CYP and haem content, and a marked induction of CYP1A1 catalytic activity (7-ethoxyresorufin O-deethylase) and apoprotein.	Methylcholanthrene	33-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	142-148
8905915-9	1996	MC treatment decreased CYP2C11 and 3A catalytic activity (testosterone 16 alpha- and 6 beta-hydroxylase respectively) and apoprotein, and there was a trend for suppression of 2C11 and 3A2 mRNA.	Methylcholanthrene	0-2	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	23-30
8905915-13	1996	CYP2C11 and 3A2 appear to be regulated by MC at a pre-translational level.	Methylcholanthrene	42-44	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	0-7
8765131-0	1996	Characteristic properties of a retinoic acid synthetic cytochrome P-450 purified from liver microsomes of 3-methylcholanthrene-induced rats.	Methylcholanthrene	106-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
8794894-0	1996	Okadaic acid potentiates 3-methylcholanthrene-induced CYP2A8 gene expression in primary cultures of Syrian hamster hepatocytes: possible involvement of activator protein-1.	Methylcholanthrene	25-45	cytochrome P450 2A8	Mesocricetus auratus	54-60
8794894-1	1996	In Syrian hamster liver, treatment with 3-methylcholanthrene (3-MC) markedly induces an isozyme of cytochrome P450 (CYP), CYP2A8.	Methylcholanthrene	40-60	cytochrome P450 2A8	Mesocricetus auratus	122-128
8794894-1	1996	In Syrian hamster liver, treatment with 3-methylcholanthrene (3-MC) markedly induces an isozyme of cytochrome P450 (CYP), CYP2A8.	Methylcholanthrene	62-66	cytochrome P450 2A8	Mesocricetus auratus	122-128
8794894-2	1996	To elucidate the mechanism of this induction, we studied the effect of okadaic acid (OA), an inhibitor of serine threonine protein phosphatases 1 and 2A, on 3-MC-induced CYP2A8 expression in primary cultures of Syrian hamster hepatocytes.	Methylcholanthrene	157-161	cytochrome P450 2A8	Mesocricetus auratus	170-176
8794894-3	1996	The addition of OA to the cultured hepatocytes at a concentration of 1 nM potentiated 3-MC- (0.1 and 1 microM) induced expression of mRNA and protein of CYP2A8 and its associated coumarin 7-hydroxylase activity.	Methylcholanthrene	86-90	cytochrome P450 2A8	Mesocricetus auratus	153-159
8794894-5	1996	The dose-dependent effect of OA on 3-MC-induced CYP2A8 expression corresponded to that of OA on c-fos and jun-D mRNA induction and on the activation of AP-1-dependent gene transcription.	Methylcholanthrene	35-39	cytochrome P450 2A8	Mesocricetus auratus	48-54
8794894-5	1996	The dose-dependent effect of OA on 3-MC-induced CYP2A8 expression corresponded to that of OA on c-fos and jun-D mRNA induction and on the activation of AP-1-dependent gene transcription.	Methylcholanthrene	35-39	proto-oncogene c-Fos	Mesocricetus auratus	96-101
8794894-5	1996	The dose-dependent effect of OA on 3-MC-induced CYP2A8 expression corresponded to that of OA on c-fos and jun-D mRNA induction and on the activation of AP-1-dependent gene transcription.	Methylcholanthrene	35-39	transcription factor jun-D	Mesocricetus auratus	106-111
8794894-6	1996	The expression of c-fos and jun-D mRNA induced by OA preceded the expression of CYP2A8 mRNA potentiated by co-treatment with 3-MC and OA.	Methylcholanthrene	125-129	proto-oncogene c-Fos	Mesocricetus auratus	18-23
8794894-6	1996	The expression of c-fos and jun-D mRNA induced by OA preceded the expression of CYP2A8 mRNA potentiated by co-treatment with 3-MC and OA.	Methylcholanthrene	125-129	transcription factor jun-D	Mesocricetus auratus	28-33
8794894-6	1996	The expression of c-fos and jun-D mRNA induced by OA preceded the expression of CYP2A8 mRNA potentiated by co-treatment with 3-MC and OA.	Methylcholanthrene	125-129	cytochrome P450 2A8	Mesocricetus auratus	80-86
8794894-7	1996	Treatment with anisomycin and cycloheximide also potentiated 0.1 microM 3-MC-induced coumarin 7-hydroxylase activity, induced c-fos and jun-D mRNA expression, and activated AP-1-dependent gene transcription in the hepatocytes.	Methylcholanthrene	72-76	proto-oncogene c-Fos	Mesocricetus auratus	126-131
8794894-7	1996	Treatment with anisomycin and cycloheximide also potentiated 0.1 microM 3-MC-induced coumarin 7-hydroxylase activity, induced c-fos and jun-D mRNA expression, and activated AP-1-dependent gene transcription in the hepatocytes.	Methylcholanthrene	72-76	transcription factor jun-D	Mesocricetus auratus	136-141
8794894-8	1996	Furthermore, 3-MC-induced CYP2A8 expression was potentiated in the hepatocytes transfected with c-Jun expression plasmid.	Methylcholanthrene	13-17	cytochrome P450 2A8	Mesocricetus auratus	26-32
8794894-9	1996	These results suggest that AP-1, inducible by serine threonine protein kinase, may be one of the components of the signal transduction system from 3-MC to CYP2A8 gene expression.	Methylcholanthrene	147-151	cytochrome P450 2A8	Mesocricetus auratus	155-161
8765131-1	1996	An inducible cytochrome P-450 (P-450) catalyzing retinoic acid synthesis was purified from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats, based on the activity of all-trans-retinoic acid formation from all-trans-retinal.	Methylcholanthrene	111-131	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
8765131-1	1996	An inducible cytochrome P-450 (P-450) catalyzing retinoic acid synthesis was purified from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats, based on the activity of all-trans-retinoic acid formation from all-trans-retinal.	Methylcholanthrene	133-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
8878250-11	1996	The distinct difference in the acinar induction pattern of GST Ya between beta-naphthoflavone and 3-methylcholanthrene resembles that reported for cytochrome P450 (CYP1A1 and CYP1A2), also members of the aryl hydrocarbon (Ah) receptor genes, suggesting common regionally acting regulatory elements in the expression of these genes in the liver.	Methylcholanthrene	98-118	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	147-170
8878250-11	1996	The distinct difference in the acinar induction pattern of GST Ya between beta-naphthoflavone and 3-methylcholanthrene resembles that reported for cytochrome P450 (CYP1A1 and CYP1A2), also members of the aryl hydrocarbon (Ah) receptor genes, suggesting common regionally acting regulatory elements in the expression of these genes in the liver.	Methylcholanthrene	98-118	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	175-181
8878250-0	1996	Distribution of glutathione S-transferase isoforms in rat liver after induction by beta-naphthoflavone or 3-methylcholanthrene.	Methylcholanthrene	106-126	hematopoietic prostaglandin D synthase	Rattus norvegicus	16-41
8878250-11	1996	The distinct difference in the acinar induction pattern of GST Ya between beta-naphthoflavone and 3-methylcholanthrene resembles that reported for cytochrome P450 (CYP1A1 and CYP1A2), also members of the aryl hydrocarbon (Ah) receptor genes, suggesting common regionally acting regulatory elements in the expression of these genes in the liver.	Methylcholanthrene	98-118	aryl hydrocarbon receptor	Rattus norvegicus	204-234
8902877-4	1996	Oral administration of TMK688 (30 mg/kg) almost completely suppressed Cyp1a1 mRNA levels in mouse epidermis induced by a topical application of MC (40 mg/kg) or benzo[a]pyrene (200 nmol) to mouse skin.	Methylcholanthrene	144-146	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	70-76
8902877-5	1996	Oral administration of TMK688 (30 mg/kg) also almost completely inhibited induction of epidermal AHH activity caused by a topical application of MC.	Methylcholanthrene	145-147	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	97-100
8697636-5	1996	Recognition of NS5 peptides was not significantly different between MC+ and MC- patients, but while the former mostly reacted either with peptide 1 (residues 2294-2309) (five of 15 sera) or with peptide 2 (residues 2304-2319) (nine of 15 sera), the latter group showed a more scattered reaction.	Methylcholanthrene	68-71	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	15-18
8706258-0	1996	Mouse lung tumors exhibit specific Ki-ras mutations following transplacental exposure to 3-methylcholanthrene.	Methylcholanthrene	89-109	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	35-41
8697636-5	1996	Recognition of NS5 peptides was not significantly different between MC+ and MC- patients, but while the former mostly reacted either with peptide 1 (residues 2294-2309) (five of 15 sera) or with peptide 2 (residues 2304-2319) (nine of 15 sera), the latter group showed a more scattered reaction.	Methylcholanthrene	68-70	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	15-18
8697636-7	1996	However, whereas IgGl antibodies against peptide 21-38 and peptide 1 of NS5 were more frequently found in MC- rather than in MC+ patients (100% versus 63.8%, P = 0.003, and 22.2% versus 4.2%, P = 0.025, respectively), IgG3 antibodies against region 1-28 were more frequent in MC+ patients (53.19% versus 16.6%, P = 0.0078).	Methylcholanthrene	106-108	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	72-75
8697636-7	1996	However, whereas IgGl antibodies against peptide 21-38 and peptide 1 of NS5 were more frequently found in MC- rather than in MC+ patients (100% versus 63.8%, P = 0.003, and 22.2% versus 4.2%, P = 0.025, respectively), IgG3 antibodies against region 1-28 were more frequent in MC+ patients (53.19% versus 16.6%, P = 0.0078).	Methylcholanthrene	125-128	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	72-75
8630083-3	1996	MC-mediated mdr mRNA induction was demonstrated to be dose-dependent; it occurred through enhanced expression of the mdr 1 gene, as indicated by reverse transcriptase-polymerase chain reaction analysis using rat mdr gene-specific primers and paralleled an induction of a 140 kDa P-gp as demonstrated by Western blotting.	Methylcholanthrene	0-2	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	117-122
8665510-2	1996	By contrast, treatment of rats with either of the inducing agents phenobarbital or 3-methylcholanthrene results in an approximate increase of only 1.4-fold in the amount of AFAR in rat liver.	Methylcholanthrene	83-103	aldo-keto reductase family 7 member A3	Rattus norvegicus	173-177
8630083-3	1996	MC-mediated mdr mRNA induction was demonstrated to be dose-dependent; it occurred through enhanced expression of the mdr 1 gene, as indicated by reverse transcriptase-polymerase chain reaction analysis using rat mdr gene-specific primers and paralleled an induction of a 140 kDa P-gp as demonstrated by Western blotting.	Methylcholanthrene	0-2	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	279-283
8630083-4	1996	In addition, MC-induced P-gp appeared to be fully functional because RLE cells exposed to MC displayed enhanced cellular efflux of rhodamine 123, a known P-gp substrate, compared to their untreated counterparts.	Methylcholanthrene	13-15	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	24-28
8630083-4	1996	In addition, MC-induced P-gp appeared to be fully functional because RLE cells exposed to MC displayed enhanced cellular efflux of rhodamine 123, a known P-gp substrate, compared to their untreated counterparts.	Methylcholanthrene	13-15	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	154-158
8630083-4	1996	In addition, MC-induced P-gp appeared to be fully functional because RLE cells exposed to MC displayed enhanced cellular efflux of rhodamine 123, a known P-gp substrate, compared to their untreated counterparts.	Methylcholanthrene	90-92	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	24-28
8630083-4	1996	In addition, MC-induced P-gp appeared to be fully functional because RLE cells exposed to MC displayed enhanced cellular efflux of rhodamine 123, a known P-gp substrate, compared to their untreated counterparts.	Methylcholanthrene	90-92	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	154-158
8681951-5	1996	In addition, B16 and B16A2 cells were unique in that they expressed CYP2E1 mRNA, a species absent from the available human liver cells, including HepG2 hepatoma cells, and 3-methylcholanthrene-inducible CYP1A2 mRNA.	Methylcholanthrene	172-192	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	203-209
8630083-7	1996	In addition, MC-mediated P-gp regulation was not associated with major cellular disturbances such as alteration of protein synthesis and, thereby, differed from the known mdr mRNA induction occurring in response to cycloheximide.	Methylcholanthrene	13-15	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	25-29
8630083-0	1996	P-glycoprotein induction in rat liver epithelial cells in response to acute 3-methylcholanthrene treatment.	Methylcholanthrene	76-96	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
8624249-2	1996	Female strain A/J mice were administered urethane (1 mg/g body wt) intraperitoneally, and when lung tumors were established at 16 weeks, mice were treated with 3-methylcholanthrene to induce CYP1A1.	Methylcholanthrene	160-180	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	191-197
21544462-0	1996	Irrelevance of the mutated p53 gene product to tumor rejection antigen in 3-methylcholanthrene-induced fibrosarcomas.	Methylcholanthrene	74-94	transformation related protein 53, pseudogene	Mus musculus	27-30
21544462-2	1996	p53 gene was found to be altered in nine MC-induced fibrosarcomas of BALB/c origin.	Methylcholanthrene	41-43	transformation related protein 53, pseudogene	Mus musculus	0-3
21544462-3	1996	The mutated p53 cDNA derived from several MC-induced fibrosarcomas was transduced into CMS8 which lacks p53 expression.	Methylcholanthrene	42-44	transformation related protein 53, pseudogene	Mus musculus	12-15
8665957-5	1996	In contrast, the 20-epi analogs, KH 1060 and MC 1288, were much more potent even at lower concentrations, than calcitriol and MC 903 in stimulating alkaline phosphatase activity, osteocalcin mRNA synthesis and osteocalcin secretion.	Methylcholanthrene	45-47	bone gamma-carboxyglutamate protein	Homo sapiens	179-190
8624249-5	1996	Treatment with 3-methylcholanthrene induced increased levels of both CYP1A1 mRNA and protein in lung parenchyma and tumor foci.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	69-75
8639452-3	1996	Histologically, the MC origin of the large cells was evinced by their association with a small mantle cell component in the same tissue, or their distribution in a classic mantle zone pattern, or their development in a patient with previous s-MCL.	Methylcholanthrene	20-22	C-type lectin domain family 4 member D	Homo sapiens	243-246
8625481-4	1996	32P-Postlabeling assays showed that MCL-5 cells (genetically engineered to express five human cytochromes P450 and microsomal epoxide hydrolase) formed characteristic adduct spots with benz[a]pyrene, benzo[g]chrysene, 7,12-dimethylbenz[a]anthracene, benzidine, sterigmatocystin and 3-methylcholanthrene, whereas CCRF cells did not.	Methylcholanthrene	282-302	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	106-143
8604811-8	1996	Two MC cases studied by Southern blotting exhibited rearrangement of the bcl-1 locus.	Methylcholanthrene	4-6	cyclin D1	Homo sapiens	73-78
8632018-4	1996	UGT1A1 is a major 3-methylcholanthrene (MC)-inducible form in rat liver.	Methylcholanthrene	18-38	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	0-6
9273361-11	1996	rIL-1beta-pretreated MCs induced a rapid increase in intracellular Ca2+ in PMNs; actinomycin D blocked this effect and was also able to prevent adhesion of neutrophils to activated MC monolayers.	Methylcholanthrene	21-23	interleukin 1 beta	Rattus norvegicus	0-9
8631144-3	1996	In rabbits we have shown previously that expression of CYP1A2 increases with age and is inducible by 3-methylcholanthrene (MC) from as early as 4 days pre-parturition.	Methylcholanthrene	101-121	cytochrome P450 1A2	Oryctolagus cuniculus	55-61
8631144-3	1996	In rabbits we have shown previously that expression of CYP1A2 increases with age and is inducible by 3-methylcholanthrene (MC) from as early as 4 days pre-parturition.	Methylcholanthrene	123-125	cytochrome P450 1A2	Oryctolagus cuniculus	55-61
8632018-4	1996	UGT1A1 is a major 3-methylcholanthrene (MC)-inducible form in rat liver.	Methylcholanthrene	40-42	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	0-6
8632018-9	1996	When a single base substitution was introduced into the XRE, MC-induced expression of the UGT1A1 gene was completely abolished.	Methylcholanthrene	61-63	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	90-96
8632018-13	1996	These results suggest that the XRE participates in induction of the rat UGT1A1 gene by MC.	Methylcholanthrene	87-89	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	72-78
8908639-4	1996	The binding of the insulin was significantly higher in the patients treated with conventional insulins vs those treated with MC insulins, i.e., 18 +/- 7.1% vs 10.2 +/- 5.2% (p &lt; 0.001).	Methylcholanthrene	125-127	insulin	Homo sapiens	19-26
8742239-3	1996	The relationship between the rate and BTL concentration showed monophasic kinetics (KM = 0.74 +/- 0.13 microM) when microsomes from untreated rats were used, whereas microsomes from 3-MC-treated rats showed biphasic kinetics (KM1 = 0.76 +/- 0.13, KM2 = 646 +/- 16 microM).	Methylcholanthrene	182-186	Kidney mass QTL 1	Rattus norvegicus	226-229
8742239-3	1996	The relationship between the rate and BTL concentration showed monophasic kinetics (KM = 0.74 +/- 0.13 microM) when microsomes from untreated rats were used, whereas microsomes from 3-MC-treated rats showed biphasic kinetics (KM1 = 0.76 +/- 0.13, KM2 = 646 +/- 16 microM).	Methylcholanthrene	182-186	Kidney mass QTL 2	Rattus norvegicus	247-250
8742239-6	1996	Kinetics observed in microsomes from 3-MC-treated rats changed to nearly monophasic, with a KM value corresponding to KM2.	Methylcholanthrene	37-41	Kidney mass QTL 2	Rattus norvegicus	118-121
8742239-7	1996	Anti-P4501A1 IgG, on the other hand, hardly inhibited the reaction conducted by liver microsomes from 3-MC-treated rats when substrate concentrations were low, whereas at higher concentrations, it inhibited up to 50%, resulting in a monophasic kinetics with a KM value corresponding to KM1.	Methylcholanthrene	102-106	Kidney mass QTL 1	Rattus norvegicus	286-289
8874671-5	1996	When 3-methylcholanthrene was given to rats for a week, the augmentation of cytochrome P-450 content and the stimulation of xenobiotic metabolism were observed.	Methylcholanthrene	5-25	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	76-92
8820987-7	1996	Furthermore, the mc-GAD Ab were analyzed for complement-dependent antibody-mediated cytoxicity (C"AMC) to rat islet cells.	Methylcholanthrene	17-19	glutamate-ammonia ligase	Rattus norvegicus	20-23
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-3
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-55
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	18-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-55
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	40-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-3
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	40-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-55
8609043-2	1996	AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P &lt; 0.0001) and age class (P = 0.015), whereas no correlation was found for the Ile-Val polymorphism (P = 0.509).	Methylcholanthrene	40-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	52-55
8849341-2	1995	In contrast to negligible activities in the untreated rat, ALDH3c enzyme activities are induced after a single dose of 3MC.	Methylcholanthrene	119-122	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	59-64
8849341-3	1995	Hepatic ALDH3c induction is decreased 60% to 90% when 3MC is administered together with any of the following ligands: estradiol, testosterone, progesterone, hydrocortisol, diethylstilbestrol, or tamoxifen.	Methylcholanthrene	54-57	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	8-13
8593816-13	1996	A monoclonal antibody directed toward CYP1A1 partially inhibited the 6 alpha-hydroxylation of E2 and the formation of the 7 alpha-OH E2/15 alpha-OH E2 peak by microsomes from adult female rats treated with 3-methylcholanthrene, but the 2-hydroxylation of E2 was not inhibited.	Methylcholanthrene	206-226	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-44
8865864-3	1996	The aim of the present study was to examine differences in interleukin (IL)-8 expression by MC from patients with NRF and from patients with end-stage renal disease (ESRD).	Methylcholanthrene	92-94	C-X-C motif chemokine ligand 8	Homo sapiens	59-77
8865864-5	1996	MC were stimulated with increasing doses of IL-1 beta or tumor necrosis factor-alpha for 24 hours, after which the supernatant was analyzed for IL-8 content.	Methylcholanthrene	0-2	interleukin 1 beta	Homo sapiens	44-84
8865864-6	1996	The IL-8 background level of MC isolated from patients with NRF was significantly lower than the IL-8 background level of MC derived from patients with ESRD.	Methylcholanthrene	29-31	C-X-C motif chemokine ligand 8	Homo sapiens	4-8
8865864-6	1996	The IL-8 background level of MC isolated from patients with NRF was significantly lower than the IL-8 background level of MC derived from patients with ESRD.	Methylcholanthrene	122-124	C-X-C motif chemokine ligand 8	Homo sapiens	97-101
8554318-5	1995	The UGT1A1 and UGT1A2 of the phenol cluster isozymes were significantly induced in 3-methylcholanthrene-treated rats.	Methylcholanthrene	83-103	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	4-10
8554318-5	1995	The UGT1A1 and UGT1A2 of the phenol cluster isozymes were significantly induced in 3-methylcholanthrene-treated rats.	Methylcholanthrene	83-103	UDP glucuronosyltransferase 1 family, polypeptide A2	Rattus norvegicus	15-21
7585637-5	1995	Pretreatment of the cells with 3-methylcholanthrene or rifampicin, inducers of CYP1A2 and CYP3A4, respectively, caused a significant increase in AFB1 metabolism.	Methylcholanthrene	31-51	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	79-85
8787780-1	1995	The number of spleen Mac-1-positive cells was markedly increased in methylcholanthrene-induced Meth-A fibrosarcoma (Meth-A)-implanted mice.	Methylcholanthrene	68-86	integrin alpha M	Mus musculus	21-26
7585637-5	1995	Pretreatment of the cells with 3-methylcholanthrene or rifampicin, inducers of CYP1A2 and CYP3A4, respectively, caused a significant increase in AFB1 metabolism.	Methylcholanthrene	31-51	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	90-96
7585649-4	1995	The strongest response in the TNF-alpha release was always obtained with the corresponding tumor, with very limited cross-reactivity against five other MC tumors or two virally induced B6 lymphomas.	Methylcholanthrene	152-154	tumor necrosis factor	Mus musculus	30-39
7585652-9	1995	In addition, transversion of G to C and A to T was detected at the K-ras gene in four of the seven sarcomas with the amplified c-myc gene, and these mutations are thought to be induced directly by methylcholanthrene.	Methylcholanthrene	197-215	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	67-72
8601480-6	1995	Mutations in two genes, eat-2 and eat-18, eliminated MC neurotransmission.	Methylcholanthrene	53-55	Neuronal acetylcholine receptor subunit eat-2	Caenorhabditis elegans	24-29
8886157-2	1995	In this study, a monoclonal antibody specific for 3-methyl-cholanthrene-inducible cytochrome P450, Mab 1-7-1, was used to detect, localize and quantify CYP1A1/CYP1A2 in livers of C57BL/6 mice.	Methylcholanthrene	50-71	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	152-158
8886157-2	1995	In this study, a monoclonal antibody specific for 3-methyl-cholanthrene-inducible cytochrome P450, Mab 1-7-1, was used to detect, localize and quantify CYP1A1/CYP1A2 in livers of C57BL/6 mice.	Methylcholanthrene	50-71	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	159-165
8601480-6	1995	Mutations in two genes, eat-2 and eat-18, eliminated MC neurotransmission.	Methylcholanthrene	53-55	Uncharacterized protein	Caenorhabditis elegans	34-40
7497454-1	1995	Induction of cytochrome P450 (CYP) isoenzymes in various organs of rats treated with 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF) was immunohistochemically and biochemically investigated.	Methylcholanthrene	107-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-28
7488175-4	1995	The CYP2B1 antipeptide IgG inhibited pentoxyresorufin O-dealkylase activity of microsomes obtained from phenobarbital-treated rats in a dose-dependent manner, whereas it did not inhibit ethoxyresorufin O-deethylase activity of microsomes obtained from 3-methylcholanthrene-treated rats.	Methylcholanthrene	252-272	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	4-10
7497454-0	1995	Induction of CYP isoenzymes in various organs of rats by 3-methylcholanthrene or beta-naphthoflavone.	Methylcholanthrene	57-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-16
7497454-1	1995	Induction of cytochrome P450 (CYP) isoenzymes in various organs of rats treated with 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF) was immunohistochemically and biochemically investigated.	Methylcholanthrene	85-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-28
7497454-1	1995	Induction of cytochrome P450 (CYP) isoenzymes in various organs of rats treated with 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF) was immunohistochemically and biochemically investigated.	Methylcholanthrene	85-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-33
21597856-9	1995	A good correlation was seen between the percentage of MC in S-phase and the number of CFU-GM (R(2)=0.566, p&lt;0.0065) or the number of CD34(+) cells (R(2)=0.625, p&lt;0.0031) in the leukapheresis product.	Methylcholanthrene	54-56	CD34 molecule	Homo sapiens	136-140
8528652-5	1995	There was a difference between 3-methylcholanthrene (MC) and 2,3,7,8-tetraCDD in the concurrent effects of 3-methylsulfone-3",4,4",5-tetraCB (3-MSF-3",4,4",5-tetraCB) on AHH activity.	Methylcholanthrene	31-51	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	170-173
8528652-5	1995	There was a difference between 3-methylcholanthrene (MC) and 2,3,7,8-tetraCDD in the concurrent effects of 3-methylsulfone-3",4,4",5-tetraCB (3-MSF-3",4,4",5-tetraCB) on AHH activity.	Methylcholanthrene	53-55	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	170-173
8528652-6	1995	The concurrent effect of MC with 3-MSF-3",4,4",5-tetraCB on AHH activity was equal to the effect of MC alone while that of 2,3,7,8-tetraCDD and 3-MSF-3",4,4",5-tetraCB on AHH activity was inhibitory.	Methylcholanthrene	25-27	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	60-63
8528652-6	1995	The concurrent effect of MC with 3-MSF-3",4,4",5-tetraCB on AHH activity was equal to the effect of MC alone while that of 2,3,7,8-tetraCDD and 3-MSF-3",4,4",5-tetraCB on AHH activity was inhibitory.	Methylcholanthrene	25-27	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	171-174
7558346-2	1995	The aim of our study was to investigate whether MC are able to produce IL-8 after direct stimulation with clinically relevant bacteria.	Methylcholanthrene	48-50	C-X-C motif chemokine ligand 8	Homo sapiens	71-75
7558346-3	1995	We observed a significant IL-8 response by the MC which were directly stimulated with viable staphylococci.	Methylcholanthrene	47-49	C-X-C motif chemokine ligand 8	Homo sapiens	26-30
8560419-9	1995	TF expression on cultured MC is an in-vitro effect due to culture conditions and the formation of oxygen free radicals.	Methylcholanthrene	26-28	coagulation factor III, tissue factor	Homo sapiens	0-2
8560419-10	1995	By reducing TF expression by 90%, we have established conditions in which MC are a good alternative for EC for seeding on synthetic grafts.	Methylcholanthrene	74-76	coagulation factor III, tissue factor	Homo sapiens	12-14
8731825-4	1995	Out of the 17 patients, MC of PB from 10 expressed plasma cell antigen CD38.	Methylcholanthrene	24-26	CD38 molecule	Homo sapiens	71-75
8731825-6	1995	MC of 9 patients were CD38+ and CD45RO+, 3 were CD38+, CD45RO+ and CD45RA+ and 1 was CD38+, CD45RA+, CD45RO+ and CD10+ in PB.	Methylcholanthrene	0-2	CD38 molecule	Homo sapiens	22-26
7493548-0	1995	3-Methylcholanthrene and pyridine effects on CYP1A1 and CYP1A2 expression in rat renal tissue.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	45-51
7493548-0	1995	3-Methylcholanthrene and pyridine effects on CYP1A1 and CYP1A2 expression in rat renal tissue.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	56-62
7493548-1	1995	The effects of 3-methylcholanthrene (3-MC) and pyridine on rat renal cytochrome P450 (CYP) 1A1 and 1A2 mRNA expression have been examined by Northern-blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR), followed by Southern-blot analysis of the PCR products.	Methylcholanthrene	15-35	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	69-102
7493548-1	1995	The effects of 3-methylcholanthrene (3-MC) and pyridine on rat renal cytochrome P450 (CYP) 1A1 and 1A2 mRNA expression have been examined by Northern-blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR), followed by Southern-blot analysis of the PCR products.	Methylcholanthrene	37-41	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	69-102
7493548-2	1995	Northern-blot hybridization and RT-PCR analyses of kidney poly(A)+ RNA revealed that 3-MC treatment produced a time-dependent increase in the renal CYP1A1 and 1A2 mRNA levels, with CYP1A1 and 1A2 mRNA levels maximally increased at 24 and 18 hr, respectively, after treatment.	Methylcholanthrene	85-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	148-162
7493548-2	1995	Northern-blot hybridization and RT-PCR analyses of kidney poly(A)+ RNA revealed that 3-MC treatment produced a time-dependent increase in the renal CYP1A1 and 1A2 mRNA levels, with CYP1A1 and 1A2 mRNA levels maximally increased at 24 and 18 hr, respectively, after treatment.	Methylcholanthrene	85-89	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	181-195
7493548-7	1995	These results show that expression of CYP1A1 and 1A2 mRNAs is enhanced in renal tissue after exposure to 3-MC or pyridine, and that constitutive expression of CYP1A1 seems to be greater than that of CYP1A2 in renal tissue.	Methylcholanthrene	105-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-52
7493548-7	1995	These results show that expression of CYP1A1 and 1A2 mRNAs is enhanced in renal tissue after exposure to 3-MC or pyridine, and that constitutive expression of CYP1A1 seems to be greater than that of CYP1A2 in renal tissue.	Methylcholanthrene	105-109	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-44
7493548-7	1995	These results show that expression of CYP1A1 and 1A2 mRNAs is enhanced in renal tissue after exposure to 3-MC or pyridine, and that constitutive expression of CYP1A1 seems to be greater than that of CYP1A2 in renal tissue.	Methylcholanthrene	105-109	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	199-205
7635426-9	1995	The methylcholanthrene-induced increase in microsomal levels of CYP1A1 and CYP1A2, total cytochrome P450, and activities of uroporphyrinogen oxidation and ethoxyresorufin deethylase were not affected by the dietary level of ascorbate.	Methylcholanthrene	4-22	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-70
7635426-9	1995	The methylcholanthrene-induced increase in microsomal levels of CYP1A1 and CYP1A2, total cytochrome P450, and activities of uroporphyrinogen oxidation and ethoxyresorufin deethylase were not affected by the dietary level of ascorbate.	Methylcholanthrene	4-22	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	75-81
7627387-6	1995	RESULTS: Multiple sizes of IGF-II mRNAs were expressed in all colon carcinoma cell lines tested (six human cell lines: HCT116, COLO 205, COLO 320 DM, LoVo, DLD-1, and HT29, and one mouse cell line: MC-26).	Methylcholanthrene	198-201	insulin like growth factor 2	Homo sapiens	27-33
7621585-6	1995	Preincubation of MC with human recombinant interferon-gamma (IFN-gamma) up-regulated MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression, but the effect on antigen-presenting function was not consistent.	Methylcholanthrene	17-19	interferon gamma	Homo sapiens	43-59
7621585-6	1995	Preincubation of MC with human recombinant interferon-gamma (IFN-gamma) up-regulated MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression, but the effect on antigen-presenting function was not consistent.	Methylcholanthrene	17-19	interferon gamma	Homo sapiens	61-70
7621585-6	1995	Preincubation of MC with human recombinant interferon-gamma (IFN-gamma) up-regulated MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression, but the effect on antigen-presenting function was not consistent.	Methylcholanthrene	17-19	intercellular adhesion molecule 1	Homo sapiens	102-135
7621585-6	1995	Preincubation of MC with human recombinant interferon-gamma (IFN-gamma) up-regulated MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression, but the effect on antigen-presenting function was not consistent.	Methylcholanthrene	17-19	intercellular adhesion molecule 1	Homo sapiens	137-143
7564075-6	1995	After preincubation with 3.86% glucose containing PD, all negative effects became even more pronounced in the lactate group whereas the MC maintained their integrity, rate of proliferation and IL-1 ra release after pre-exposure to pyruvate containing PD.	Methylcholanthrene	136-138	interleukin 1 receptor antagonist	Homo sapiens	193-200
7564075-7	1995	These results suggest that the acute toxic effects of commercially available PD on the integrity, proliferation and IL-1 ra production of MC can be avoided by the use of sodium pyruvate instead of sodium lactate.	Methylcholanthrene	138-140	interleukin 1 receptor antagonist	Homo sapiens	116-123
7794261-0	1995	CYP1A2 and 2E1 expression in rat liver treated with combined inducers (3-methylcholanthrene and ethanol).	Methylcholanthrene	71-91	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	0-14
7794261-1	1995	The effects of combined ethanol and 3-methylcholanthrene treatment on rat hepatic cytochrome CYP1A2 and CYP2E1 expression were evaluated.	Methylcholanthrene	36-56	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	93-99
7794261-1	1995	The effects of combined ethanol and 3-methylcholanthrene treatment on rat hepatic cytochrome CYP1A2 and CYP2E1 expression were evaluated.	Methylcholanthrene	36-56	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	104-110
7794261-3	1995	Treatments involving 3-methylcholanthrene and combined ethanol + 3-methylcholanthrene decreased both CYP2E1 expression at the mRNA level (0.6 and 0.4 fold versus controls, respectively) and protein level (0.6 and 0.9 fold versus controls, respectively), while dramatically increasing CYP1A2 expression.	Methylcholanthrene	21-41	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	101-107
7794261-3	1995	Treatments involving 3-methylcholanthrene and combined ethanol + 3-methylcholanthrene decreased both CYP2E1 expression at the mRNA level (0.6 and 0.4 fold versus controls, respectively) and protein level (0.6 and 0.9 fold versus controls, respectively), while dramatically increasing CYP1A2 expression.	Methylcholanthrene	21-41	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	284-290
7794261-3	1995	Treatments involving 3-methylcholanthrene and combined ethanol + 3-methylcholanthrene decreased both CYP2E1 expression at the mRNA level (0.6 and 0.4 fold versus controls, respectively) and protein level (0.6 and 0.9 fold versus controls, respectively), while dramatically increasing CYP1A2 expression.	Methylcholanthrene	65-85	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	101-107
7794261-3	1995	Treatments involving 3-methylcholanthrene and combined ethanol + 3-methylcholanthrene decreased both CYP2E1 expression at the mRNA level (0.6 and 0.4 fold versus controls, respectively) and protein level (0.6 and 0.9 fold versus controls, respectively), while dramatically increasing CYP1A2 expression.	Methylcholanthrene	65-85	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	284-290
7788861-10	1995	Treatment of the differentiated HL60 cells with 3-methylcholanthrene, a ligand of AhR, induced the expression of the P450IA1 gene.	Methylcholanthrene	48-68	aryl hydrocarbon receptor	Homo sapiens	82-85
21556657-5	1995	A higly significant correlation between serum IL-10 levels and the corresponding MC was also found in the MM-bearing patients and to a lesser extent, in MGUS patients, indicating that serum IL-10 is parallel to the amount of the activated clone causing the monoclonal gammopathy.	Methylcholanthrene	81-83	interleukin 10	Homo sapiens	46-51
21556657-5	1995	A higly significant correlation between serum IL-10 levels and the corresponding MC was also found in the MM-bearing patients and to a lesser extent, in MGUS patients, indicating that serum IL-10 is parallel to the amount of the activated clone causing the monoclonal gammopathy.	Methylcholanthrene	81-83	interleukin 10	Homo sapiens	190-195
7497454-1	1995	Induction of cytochrome P450 (CYP) isoenzymes in various organs of rats treated with 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF) was immunohistochemically and biochemically investigated.	Methylcholanthrene	107-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-33
7497454-9	1995	3-MC and BNF induced CYP isoenzymes not only in the liver, but also in the small intestine, large intestine, prostate and seminal vesicles.	Methylcholanthrene	0-4	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-24
7622417-6	1995	Furthermore, the inducibility of CYP1A2 by CYP1A inducers such as 3-methoxy-4-aminoazobenzene and 3-methylcholanthrene was also decreased at the mRNA, protein and activity levels.	Methylcholanthrene	98-118	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	33-39
7750092-0	1995	Mutations of the Ki-ras protooncogene in 3-methylcholanthrene and urethan-induced and butylated hydroxytoluene-promoted lung tumors of strain A/J and SWR mice.	Methylcholanthrene	41-61	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	17-23
7750092-1	1995	Mutations of the Ki-ras protooncogene in 190 lung tumors initiated in male A/J and SWR mice by 3-methylcholanthrene(MCA) or urethan and promoted by butylated hydroxytoluene (BHT), were evaluated by utilizing polymerase chain reaction (PCR) and sequencing analysis.	Methylcholanthrene	116-119	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	17-23
7606203-4	1995	Recent research reports that PSK suppresses pulmonary metastasis of methylcholanthrene-induced sarcomas, human prostate cancer DU145M, and lymphatic metastasis of mouse leukemia P388, and that it has prolonged the survival period in spontaneous metastasis models.	Methylcholanthrene	68-86	TAO kinase 2	Homo sapiens	29-32
7752103-4	1995	All the UDP-GT inducers produced a dose-dependent induction of hepatic UDP-GT activity toward T4; the increases produced by PCN (7-fold) and PCB (5-fold) were more pronounced than those produced by PB and 3MC (3-fold).	Methylcholanthrene	205-208	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	8-14
7752103-4	1995	All the UDP-GT inducers produced a dose-dependent induction of hepatic UDP-GT activity toward T4; the increases produced by PCN (7-fold) and PCB (5-fold) were more pronounced than those produced by PB and 3MC (3-fold).	Methylcholanthrene	205-208	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	71-77
7708743-3	1995	In vivo transfection of the human interleukin 6 gene into the tumor site reduced methylcholanthrene-induced fibrosarcoma growth, and a combination of murine tumor necrosis factor alpha and interferon gamma genes inhibited growth of a renal carcinoma tumor model (Renca).	Methylcholanthrene	81-99	interleukin 6	Homo sapiens	34-47
7882362-11	1995	Some analogues of vitamin D3 (EB 1089, MC 903, and KH 1060) that are known to be potent inhibitors of breast cancer cell growth both in vitro and in vivo had similar or more pronounced inducing effects on TGF-beta 1 mRNA levels.	Methylcholanthrene	39-41	transforming growth factor beta 1	Homo sapiens	205-215
7600448-1	1995	In liver of adult responsive C57BL/6J (B6) mice the aromatic hydrocarbon receptor (AHR) has high affinity for specific halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), as well as nonhalogenated aromatic hydrocarbons (PAHs), such as benz[a]anthracene (BA) or 3-methylcholanthrene (MC).	Methylcholanthrene	296-316	aryl-hydrocarbon receptor	Mus musculus	52-81
7734403-4	1995	The RNA for CYP 1A1 was dramatically and completely induced within 2 hours after exposure of immortalized granulosa cells to 3-methyl-cholanthrene (3MC) and expression could be inhibited with 10 microM phorbol myristate acetate.	Methylcholanthrene	125-146	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	12-19
7734403-4	1995	The RNA for CYP 1A1 was dramatically and completely induced within 2 hours after exposure of immortalized granulosa cells to 3-methyl-cholanthrene (3MC) and expression could be inhibited with 10 microM phorbol myristate acetate.	Methylcholanthrene	148-151	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	12-19
7662117-2	1995	Hepatocytes from all 15 individuals tested responded to treatment with 3-methylcholanthrene (MC) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with induction of CYP1A1 mRNA.	Methylcholanthrene	71-91	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	161-167
7662117-2	1995	Hepatocytes from all 15 individuals tested responded to treatment with 3-methylcholanthrene (MC) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with induction of CYP1A1 mRNA.	Methylcholanthrene	93-95	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	161-167
7502762-6	1995	For example, approximately 40-50% of MC in SMG were CD3+ T cells which consisted of an equal distribution of CD4+, CD8- and CD4-, CD8+ T cell subsets.	Methylcholanthrene	37-39	small nuclear ribonucleoprotein polypeptide G	Mus musculus	43-46
7502762-6	1995	For example, approximately 40-50% of MC in SMG were CD3+ T cells which consisted of an equal distribution of CD4+, CD8- and CD4-, CD8+ T cell subsets.	Methylcholanthrene	37-39	CD3 antigen, epsilon polypeptide	Mus musculus	52-55
7756127-3	1995	This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA.	Methylcholanthrene	87-107	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	44-50
7756127-3	1995	This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA.	Methylcholanthrene	87-107	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-58
7756127-5	1995	Using the reverse transcriptase-polymerase chain reaction, we have demonstrated that the effects of 3-methylcholanthrene, dimethylbenz[a]anthracene and RA on CYP1A1 expression correlate with an increase of CYP1A1 mRNA level.	Methylcholanthrene	100-120	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	158-164
7756127-5	1995	Using the reverse transcriptase-polymerase chain reaction, we have demonstrated that the effects of 3-methylcholanthrene, dimethylbenz[a]anthracene and RA on CYP1A1 expression correlate with an increase of CYP1A1 mRNA level.	Methylcholanthrene	100-120	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	206-212
7827108-0	1995	Effects of partial hepatectomy, phenobarbital and 3-methylcholanthrene on kinetic parameters of glucose-6-phosphate and phosphogluconate dehydrogenase in situ in periportal, intermediate and pericentral zones of rat liver lobules.	Methylcholanthrene	50-70	phosphogluconate dehydrogenase	Rattus norvegicus	120-150
7827108-6	1995	The affinity of G6PDH for glucose-6-phosphate was similar in all zones and it was decreased 2-3 fold by PB and 3-MC treatment.	Methylcholanthrene	111-115	glucose-6-phosphate dehydrogenase	Rattus norvegicus	16-21
7600455-1	1995	The aromatic hydrocarbon receptor (AHR) is a soluble intracellular protein that mediates most, if not all, the toxic effects of polycyclic aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene.	Methylcholanthrene	217-237	aryl hydrocarbon receptor	Homo sapiens	4-33
7600455-1	1995	The aromatic hydrocarbon receptor (AHR) is a soluble intracellular protein that mediates most, if not all, the toxic effects of polycyclic aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene.	Methylcholanthrene	217-237	aryl hydrocarbon receptor	Homo sapiens	35-38
7874572-2	1995	In this study, we examined the role of Ca2+ in the regulation of ODC enzyme activity in mouse colon cancer cells (MC-26).	Methylcholanthrene	114-117	ornithine decarboxylase, structural 1	Mus musculus	65-68
7600448-1	1995	In liver of adult responsive C57BL/6J (B6) mice the aromatic hydrocarbon receptor (AHR) has high affinity for specific halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), as well as nonhalogenated aromatic hydrocarbons (PAHs), such as benz[a]anthracene (BA) or 3-methylcholanthrene (MC).	Methylcholanthrene	296-316	aryl-hydrocarbon receptor	Mus musculus	83-86
7600448-1	1995	In liver of adult responsive C57BL/6J (B6) mice the aromatic hydrocarbon receptor (AHR) has high affinity for specific halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), as well as nonhalogenated aromatic hydrocarbons (PAHs), such as benz[a]anthracene (BA) or 3-methylcholanthrene (MC).	Methylcholanthrene	318-320	aryl-hydrocarbon receptor	Mus musculus	52-81
7600448-1	1995	In liver of adult responsive C57BL/6J (B6) mice the aromatic hydrocarbon receptor (AHR) has high affinity for specific halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), as well as nonhalogenated aromatic hydrocarbons (PAHs), such as benz[a]anthracene (BA) or 3-methylcholanthrene (MC).	Methylcholanthrene	318-320	aryl-hydrocarbon receptor	Mus musculus	83-86
7600448-3	1995	Both TCDD and MC induce aryl hydrocarbon hydroxylase (AHH) in adult B6 mice, whereas adult D2 mouse liver is nonresponsive to MC.	Methylcholanthrene	14-16	aryl-hydrocarbon receptor	Mus musculus	24-52
7600448-13	1995	The AHR in D2 fetal cells was able to activate a transfected chloramphenicol acetyltransferase linked to a dioxin-responsive element nucleotide sequence (DRE-CAT) when the cells were treated with TCDD or MC.	Methylcholanthrene	204-206	aryl-hydrocarbon receptor	Mus musculus	4-7
7566582-7	1995	The exposure of MC to TNF alpha or to a lesser extent IL-1 alpha or LPS reduced their fibrinolytic activity by decreasing t-PA production and increasing PAI-1 synthesis.	Methylcholanthrene	16-18	tumor necrosis factor	Homo sapiens	22-31
7566582-7	1995	The exposure of MC to TNF alpha or to a lesser extent IL-1 alpha or LPS reduced their fibrinolytic activity by decreasing t-PA production and increasing PAI-1 synthesis.	Methylcholanthrene	16-18	interleukin 1 alpha	Homo sapiens	54-64
7566582-7	1995	The exposure of MC to TNF alpha or to a lesser extent IL-1 alpha or LPS reduced their fibrinolytic activity by decreasing t-PA production and increasing PAI-1 synthesis.	Methylcholanthrene	16-18	plasminogen activator, tissue type	Homo sapiens	122-126
7566582-7	1995	The exposure of MC to TNF alpha or to a lesser extent IL-1 alpha or LPS reduced their fibrinolytic activity by decreasing t-PA production and increasing PAI-1 synthesis.	Methylcholanthrene	16-18	serpin family E member 1	Homo sapiens	153-158
7706212-12	1994	The carcinogen, 3-methylcholanthrene, and hepatotoxic carbon tetrachloride increased the enzyme activity, and the transcript and protein levels of choline kinase R in rat liver.	Methylcholanthrene	16-36	choline kinase alpha	Rattus norvegicus	147-163
7811300-4	1994	3-Methylcholanthrene induced CYP1A1 protein in perivenous cells, while a low dose of beta-naphthoflavone caused periportal induction.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-35
7811300-6	1994	A corresponding difference in the regional pattern of CYP1A2 induction was seen: induction by beta-naphthoflavone reversed the constitutive perivenous pattern into a periportal CYP1A2 mRNA pattern while induction after 3-methylcholanthrene treatment was more panacinar.	Methylcholanthrene	219-239	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	54-60
7524750-11	1994	Cross linking of either IgE receptor or SCF receptor (c-kit) on CMC resulted in histamine secretion (non-specific release: &lt; 6% of total histamine, alpha IgE induced: 12% to 52%; SCF-induced release: 9% to 18%), whereas neither substance P (a skin MC agonist) nor the basophil agonist FMLP showed an effect on CMC.	Methylcholanthrene	65-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-59
8619122-2	1995	The test consisted of the studies by the technique of Ames of the ability of the S9 preparation obtained from livers of rats induced by nitrofurans to cause the metabolic activation of ethidium bromide (EtBr)--for induction of 3-MC type or cyclophosphamide (CPA) for PB type of cytochrome P-450.	Methylcholanthrene	227-231	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	278-294
8619122-4	1995	It was found that only furazolidone at cumulative dose 3 x 80 mg/kg of body weight induce the 3-MC-type of cytochrome P-450.	Methylcholanthrene	94-98	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
7897703-4	1994	CpG sites with varying mC in different tissues were found in the GFAP promoter and in a CpG island in exon 1.	Methylcholanthrene	23-25	glial fibrillary acidic protein	Rattus norvegicus	65-69
7897703-7	1994	Testis GFAP exon 1 had a gradient of mC from 5" to 3" across the exon that was absent in liver, brain, and cultured neurons and astrocytes.	Methylcholanthrene	37-39	glial fibrillary acidic protein	Rattus norvegicus	7-11
7524750-11	1994	Cross linking of either IgE receptor or SCF receptor (c-kit) on CMC resulted in histamine secretion (non-specific release: &lt; 6% of total histamine, alpha IgE induced: 12% to 52%; SCF-induced release: 9% to 18%), whereas neither substance P (a skin MC agonist) nor the basophil agonist FMLP showed an effect on CMC.	Methylcholanthrene	65-67	KIT ligand	Homo sapiens	40-43
7524447-0	1994	3-Methylcholanthrene-mediated induction of cytochrome P4501A2 in human hepatoma HepG2 cells as quantified by the reverse transcription-polymerase chain reaction.	Methylcholanthrene	0-20	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	43-61
7808430-3	1994	IL-1 beta and TNF-alpha blocked 3-methylcholanthrene (3-MC)-induced EROD activity by up to 25 and 44%, respectively.	Methylcholanthrene	32-52	tumor necrosis factor	Homo sapiens	14-23
7808430-3	1994	IL-1 beta and TNF-alpha blocked 3-methylcholanthrene (3-MC)-induced EROD activity by up to 25 and 44%, respectively.	Methylcholanthrene	54-58	interleukin 1 beta	Homo sapiens	0-9
7808430-3	1994	IL-1 beta and TNF-alpha blocked 3-methylcholanthrene (3-MC)-induced EROD activity by up to 25 and 44%, respectively.	Methylcholanthrene	54-58	tumor necrosis factor	Homo sapiens	14-23
7808430-5	1994	TGF-beta 1 proved to be the most effective cytokine, because 72 hr of treatment with 2 ng/ml TGF-beta 1 produced nearly 100% inhibition of 3-MC- and benzo(a)pyrene-induced CYP1A1 and CYP1A2 mRNAs and EROD activity.	Methylcholanthrene	139-143	transforming growth factor beta 1	Homo sapiens	0-10
7808430-5	1994	TGF-beta 1 proved to be the most effective cytokine, because 72 hr of treatment with 2 ng/ml TGF-beta 1 produced nearly 100% inhibition of 3-MC- and benzo(a)pyrene-induced CYP1A1 and CYP1A2 mRNAs and EROD activity.	Methylcholanthrene	139-143	transforming growth factor beta 1	Homo sapiens	93-103
7808430-5	1994	TGF-beta 1 proved to be the most effective cytokine, because 72 hr of treatment with 2 ng/ml TGF-beta 1 produced nearly 100% inhibition of 3-MC- and benzo(a)pyrene-induced CYP1A1 and CYP1A2 mRNAs and EROD activity.	Methylcholanthrene	139-143	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	172-178
20693085-9	1994	Upon incubation of hepatocytes with 3-methylcholanthrene the levels of immunoreactive CYP1A1 and CYP2B1/2 were paralleled by an increase of the enzymatic activities of EROD and PROD, respectively.	Methylcholanthrene	36-56	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	86-92
20693085-9	1994	Upon incubation of hepatocytes with 3-methylcholanthrene the levels of immunoreactive CYP1A1 and CYP2B1/2 were paralleled by an increase of the enzymatic activities of EROD and PROD, respectively.	Methylcholanthrene	36-56	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	97-103
20693087-3	1994	In addition, vitamin C reduced the activity of aryl hydrocarbon hydroxylase (AHH) in microsomes from aromatic hydrocarbon-responsive (Ah-responsive) and Ah-non-responsive strains of mice that had been pretreated with olive oil (vehicle), 3-methylcholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	238-258	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	47-75
20693087-3	1994	In addition, vitamin C reduced the activity of aryl hydrocarbon hydroxylase (AHH) in microsomes from aromatic hydrocarbon-responsive (Ah-responsive) and Ah-non-responsive strains of mice that had been pretreated with olive oil (vehicle), 3-methylcholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin.	Methylcholanthrene	238-258	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	77-80
7964168-3	1994	Basal levels of alveolar macrophage (m phi) tumor necrosis factor-alpha (TNF-alpha) production were higher (P &lt; .05) for LC- and MC-fed pigs than for CO- and LO-fed pigs.	Methylcholanthrene	132-134	tumor necrosis factor	Sus scrofa	44-71
7964168-3	1994	Basal levels of alveolar macrophage (m phi) tumor necrosis factor-alpha (TNF-alpha) production were higher (P &lt; .05) for LC- and MC-fed pigs than for CO- and LO-fed pigs.	Methylcholanthrene	132-134	tumor necrosis factor	Sus scrofa	73-82
7917307-0	1994	Cell localization and regulation of expression of cytochrome P450 1A1 and 2B1 in rat lung after induction with 3-methylcholanthrene using mRNA hybridization and immunohistochemistry.	Methylcholanthrene	111-131	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-77
8069948-2	1994	CYP2A5 antibody inhibited AFB1 and NDEA metabolism by 40-60% in untreated hamsters and after treatment with phenobarbital (PB) or 3-methylcholanthrene (MC).	Methylcholanthrene	130-150	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
8069948-2	1994	CYP2A5 antibody inhibited AFB1 and NDEA metabolism by 40-60% in untreated hamsters and after treatment with phenobarbital (PB) or 3-methylcholanthrene (MC).	Methylcholanthrene	152-154	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
7808430-3	1994	IL-1 beta and TNF-alpha blocked 3-methylcholanthrene (3-MC)-induced EROD activity by up to 25 and 44%, respectively.	Methylcholanthrene	32-52	interleukin 1 beta	Homo sapiens	0-9
7524447-2	1994	The reverse transcription-polymerase chain reaction (RT-PCR) assay revealed that HepG2 cells constitutively express CYP1A2 and are able to respond to 3-methylcholanthrene (3MC) by an induction of CYP1A2 mRNA.	Methylcholanthrene	150-170	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	116-122
7524447-2	1994	The reverse transcription-polymerase chain reaction (RT-PCR) assay revealed that HepG2 cells constitutively express CYP1A2 and are able to respond to 3-methylcholanthrene (3MC) by an induction of CYP1A2 mRNA.	Methylcholanthrene	150-170	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	196-202
7524447-2	1994	The reverse transcription-polymerase chain reaction (RT-PCR) assay revealed that HepG2 cells constitutively express CYP1A2 and are able to respond to 3-methylcholanthrene (3MC) by an induction of CYP1A2 mRNA.	Methylcholanthrene	172-175	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	116-122
7524447-2	1994	The reverse transcription-polymerase chain reaction (RT-PCR) assay revealed that HepG2 cells constitutively express CYP1A2 and are able to respond to 3-methylcholanthrene (3MC) by an induction of CYP1A2 mRNA.	Methylcholanthrene	172-175	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	196-202
7874758-5	1994	It revealed that the amount of PCNA positive cells in the group with little or no MC was significantly more than that in the other group.	Methylcholanthrene	82-84	proliferating cell nuclear antigen	Rattus norvegicus	31-35
7524301-4	1994	By univariate analysis, expression of the bcl-2 gene product in RS cells was observed in a significantly greater proportion of NS Hodgkin"s disease cases than MC cases (P &lt; .009), a finding that may have implications on the pathogenesis of this disorder.	Methylcholanthrene	159-161	BCL2 apoptosis regulator	Homo sapiens	42-47
7883754-5	1994	External deletion of the upstream region from the reporter gene resulted in a stepwise decrease of the CAT activity, suggesting that XREs were responsible for inducible expression of CYP1A1 gene by 3-methylcholanthrene (MC).	Methylcholanthrene	198-218	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	183-189
7883754-5	1994	External deletion of the upstream region from the reporter gene resulted in a stepwise decrease of the CAT activity, suggesting that XREs were responsible for inducible expression of CYP1A1 gene by 3-methylcholanthrene (MC).	Methylcholanthrene	220-222	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	183-189
7883754-7	1994	Removal of the NRE from the CYP1A1-CAT fusion gene resulted in about 3-fold increase of MC-inducible CAT activity.	Methylcholanthrene	88-90	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	28-34
8063713-5	1994	The first of these substrates, NFF-1 (Mca-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Lys-(Dnp)-Gly, where Mca is (7-methoxycoumarin-4-yl)acetyl and Dnp is 2,4-dinitrophenyl), was hydrolyzed equally well by MMP-3 and MMP-2 (kcat/Km approximately 11,000 s-1 M-1).	Methylcholanthrene	38-41	matrix metallopeptidase 3	Homo sapiens	199-204
8093035-1	1994	The present study examined changes in hepatic CYP2E1 content and (omega-1)-hydroxylation of lauric acid in rats treated with pyridine, pyrazole, acetone, ethanol and 3-methylcholanthrene.	Methylcholanthrene	166-186	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	46-52
7521008-3	1994	NDFs mutagenized strain TA98NR with S9 mix, and the NAD(P)H system plus 3-methylcholanthrene-induced S9 (3-MC-S9) was the most effective.	Methylcholanthrene	72-92	Mammary tumor resistance QTL 2	Rattus norvegicus	107-112
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	13-33	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	52-56
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	13-33	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-70
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	13-33	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	75-81
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	13-33	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	112-118
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	35-38	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	52-56
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	35-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	64-70
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	35-38	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	75-81
8093105-3	1994	The purified 3-methylcholanthrene (3MC)-induced rat P450 forms, CYP1A1 and CYP1A2, and a possible variant form, CYP1A1*, showed substrate selectivities for propoxyresorufin, methoxyresorufin and ethoxyresorufin, respectively.	Methylcholanthrene	35-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	112-118
7820307-9	1994	Exposure of cells to inducers revealed that aryl hydrocarbon hydroxylase activity was mainly increased after treatment with 3-methylcholanthrene and beta-naphtoflavone, and the highest values were found in rat hepatocytes followed by MH1C1 and Fao cells.	Methylcholanthrene	124-144	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	44-72
8093105-8	1994	Anti-P450 antibody and furafylline inhibition of rat liver microsomal AROD confirmed that ethoxyresorufin was a selective probe for CYP1A1 in 3MC-induced and isosafrole (ISF)-induced microsomes and that pentoxy- and benzyloxyresorufins both selectively measured CYP2B1 in PB-induced and ISF-induced microsomes.	Methylcholanthrene	142-145	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-138
8063713-7	1994	The second substrate, NFF-2 (Mca-Arg-Pro-Lys-Pro-Tyr-Ala-Nva-Trp-Met-Lys(Dnp)-NH2, where Nva is norvaline), was hydrolyzed 60 times more rapidly by MMP-3 (kcat/Km = 59,400 s-1 M-1) than MMP-1.	Methylcholanthrene	29-32	matrix metallopeptidase 3	Homo sapiens	148-153
8063713-7	1994	The second substrate, NFF-2 (Mca-Arg-Pro-Lys-Pro-Tyr-Ala-Nva-Trp-Met-Lys(Dnp)-NH2, where Nva is norvaline), was hydrolyzed 60 times more rapidly by MMP-3 (kcat/Km = 59,400 s-1 M-1) than MMP-1.	Methylcholanthrene	29-32	matrix metallopeptidase 1	Homo sapiens	186-191
8063713-5	1994	The first of these substrates, NFF-1 (Mca-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Lys-(Dnp)-Gly, where Mca is (7-methoxycoumarin-4-yl)acetyl and Dnp is 2,4-dinitrophenyl), was hydrolyzed equally well by MMP-3 and MMP-2 (kcat/Km approximately 11,000 s-1 M-1).	Methylcholanthrene	38-41	matrix metallopeptidase 2	Homo sapiens	209-214
8063713-5	1994	The first of these substrates, NFF-1 (Mca-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Lys-(Dnp)-Gly, where Mca is (7-methoxycoumarin-4-yl)acetyl and Dnp is 2,4-dinitrophenyl), was hydrolyzed equally well by MMP-3 and MMP-2 (kcat/Km approximately 11,000 s-1 M-1).	Methylcholanthrene	99-102	matrix metallopeptidase 3	Homo sapiens	199-204
8063713-5	1994	The first of these substrates, NFF-1 (Mca-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Lys-(Dnp)-Gly, where Mca is (7-methoxycoumarin-4-yl)acetyl and Dnp is 2,4-dinitrophenyl), was hydrolyzed equally well by MMP-3 and MMP-2 (kcat/Km approximately 11,000 s-1 M-1).	Methylcholanthrene	99-102	matrix metallopeptidase 2	Homo sapiens	209-214
8062229-7	1994	Stereochemical analysis revealed that the P-450s 1A1, m1A1, m1A2, r2A1, r2B1, PB- and 3MC-treated rat liver microsomes preferentially formed 3R,4R-diol enantiomer (88-97%), whereas rabbit 4B formed the 3S,4S-diol enantiomer (72%).	Methylcholanthrene	86-89	solute carrier family 45 member 2	Homo sapiens	49-52
8044802-0	1994	3-Methylcholanthrene inactivates the p53 gene in Syrian hamster embryo fibroblasts by inducing a specific intronic point mutation.	Methylcholanthrene	0-20	cellular tumor antigen p53	Mesocricetus auratus	37-40
8044802-1	1994	The expression of the tumor suppressor gene p53 was studied in Syrian hamster embryo cells neoplastically initiated with a single dose of 3-methylcholanthrene.	Methylcholanthrene	138-158	cellular tumor antigen p53	Mesocricetus auratus	44-47
8044802-9	1994	The presence of this mutation in both p53- cell lines strongly suggests that it was induced specifically by 3-methyl-cholanthrene treatment and indicates that the resulting splicing malfunction may account for the lack of p53 gene expression.	Methylcholanthrene	108-129	cellular tumor antigen p53	Mesocricetus auratus	38-41
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Methylcholanthrene	88-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Methylcholanthrene	88-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	23-29
8068047-3	1994	Although clearly a type-1 ALDH-3, the MCF-7/0 enzyme, as well as the type-1 ALDH-3 constitutively present in cultured colon C cells and induced in cultured MCF-7/0 cells by methylcholanthrene, does, however, differ from the prototypical human stomach mucosa type-1 ALDH-3 in one, perhaps pharmacologically important, way, viz.	Methylcholanthrene	173-191	aldehyde dehydrogenase 3 family member A1	Homo sapiens	76-82
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Methylcholanthrene	110-112	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Methylcholanthrene	110-112	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	23-29
8070738-7	1994	This induction profile, characterized by the very strong increase of the activity associated with P4501A1, and the co-induction of UGT1, closely resemble that of a classical inducer, 3-methylcholanthrene.	Methylcholanthrene	183-203	UDP glycosyltransferase 1 family, polypeptide A4, pseudogene	Rattus norvegicus	131-135
8067827-2	1994	In an in vitro experiment, methylcholanthrene-induced sarcoma cells were incubated for 48 hours with 42 micrograms/mL of either human or murine TNF.	Methylcholanthrene	27-45	tumor necrosis factor	Mus musculus	144-147
8068047-3	1994	Although clearly a type-1 ALDH-3, the MCF-7/0 enzyme, as well as the type-1 ALDH-3 constitutively present in cultured colon C cells and induced in cultured MCF-7/0 cells by methylcholanthrene, does, however, differ from the prototypical human stomach mucosa type-1 ALDH-3 in one, perhaps pharmacologically important, way, viz.	Methylcholanthrene	173-191	aldehyde dehydrogenase 3 family member A1	Homo sapiens	76-82
8004320-6	1994	N-CPAP (mc) and face mask CPAP (f-CPAP) resulted in significant dose-dependent decreases of SV-24 +/- 5 ml (21%) and 33 +/- 5 ml (28%), respectively--from baseline to 20 cm H2O (p &lt; 0.05).	Methylcholanthrene	8-10	centromere protein J	Homo sapiens	2-6
8053925-6	1994	As expected, PB and MC increased GST activity together with the concentration of subunits 1 and 3 in rats.	Methylcholanthrene	20-22	hematopoietic prostaglandin D synthase	Rattus norvegicus	33-36
8053925-9	1994	In contrast, MC slightly decreased subunit 1 and markedly raised subunits 3 and 4, resulting in a net increase in total GST activity.	Methylcholanthrene	13-15	hematopoietic prostaglandin D synthase	Rattus norvegicus	120-123
8004320-7	1994	HR were unchanged and CO significantly decreased with n-CPAP(mc) and with f-CPAP, 1.6 +/- 0.38 L/min (23%) and 2.29 +/- 0.54 L/min (31%), respectively, from baseline to 20 cm H2O (p &lt; 0.05).	Methylcholanthrene	61-63	centromere protein J	Homo sapiens	56-60
8004320-8	1994	Esophageal pressure measurements verified increasing intrathoracic pressure with increasing levels of f-CPAP and n-CPAP (mc) but not with n-CPAP (mo).	Methylcholanthrene	121-123	centromere protein J	Homo sapiens	115-119
8004320-9	1994	In conclusion, n-CPAP (mc) and f-CPAP resulted in significant and similar dose-dependent decreases in SV and CO.	Methylcholanthrene	23-25	centromere protein J	Homo sapiens	17-21
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	177-197	histocompatibility 2, K1, K region	Mus musculus	57-62
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	177-197	histocompatibility 2, K1, K region	Mus musculus	117-122
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	177-197	histocompatibility 2, K1, K region	Mus musculus	117-122
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	177-197	histocompatibility 2, K1, K region	Mus musculus	117-122
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	199-202	histocompatibility 2, K1, K region	Mus musculus	57-62
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	199-202	histocompatibility 2, K1, K region	Mus musculus	117-122
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	199-202	histocompatibility 2, K1, K region	Mus musculus	117-122
7517974-3	1994	Tumor-infiltrating lymphocytes (TILs) generated from the H-2Kb+ BL6 lesions (Thy 1.2+, CD8+, CD4-) efficiently lysed H-2Kb+ melanoma (CL8-1 and 2Kb38) and the H-2Kb+ nonrelated 3-methylcholanthrene (MCA)-105 sarcoma, but not the H-2Kb- parental melanoma BL6-8.	Methylcholanthrene	199-202	histocompatibility 2, K1, K region	Mus musculus	117-122
7821706-5	1994	In parallel studies, 3-methylcholanthrene, a prototypical polynuclear aromatic hydrocarbon, also inhibited E2-induced PR binding and immunoreactive protein.	Methylcholanthrene	21-41	progesterone receptor	Homo sapiens	118-120
8021296-6	1994	CYP1A1 apoprotein expression was very low in untreated cells, but was markedly induced after treatment with 1 microM 3-methylcholanthrene or 22 microM beta-naphthoflavone.	Methylcholanthrene	117-137	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
8021296-7	1994	CYP1A1 mRNA was not detected in untreated cells and appeared after 3-methylcholanthrene treatment.	Methylcholanthrene	67-87	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
20692934-7	1994	3-MC increased CYP1A1/2 11-fold and eight-fold in 4 and 13% O(2) cultures, respectively, and the EROD activity 37-fold (4% O(2)) and 30-fold (13% O(2)) on day 4.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	15-21
8033271-6	1994	In addition, rat hepatic hydroxysteroid sulfotransferase-a gene expression in mature female rats, although not substantially altered in response to short-term fasting or high-dose dexamethasone treatment, was suppressed after treatment with the polycyclic aromatic hydrocarbon, 3-methylcholanthrene.	Methylcholanthrene	278-298	sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 6	Rattus norvegicus	25-58
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Methylcholanthrene	250-254	glutathione S-transferase alpha 3	Rattus norvegicus	108-115
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Methylcholanthrene	250-254	hematopoietic prostaglandin D synthase	Rattus norvegicus	108-111
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Methylcholanthrene	250-254	glutathione S-transferase alpha 3	Rattus norvegicus	112-115
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Methylcholanthrene	250-254	hematopoietic prostaglandin D synthase	Rattus norvegicus	197-200
8200083-7	1994	Following treatment of cynomolgus monkey with 3-methylcholanthrene, induction of CYP1A1, but not CYP1A2, was evident.	Methylcholanthrene	46-66	cytochrome P450 family 1 subfamily A member 1	Macaca fascicularis	81-87
7945563-12	1994	Our in vitro experiments suggest that high levels of insulin and IGF-I stimulate MC-mediated oxidation of LDL, an effect that is potentially atherogenic.	Methylcholanthrene	81-83	insulin	Homo sapiens	53-60
7945563-12	1994	Our in vitro experiments suggest that high levels of insulin and IGF-I stimulate MC-mediated oxidation of LDL, an effect that is potentially atherogenic.	Methylcholanthrene	81-83	insulin like growth factor 1	Homo sapiens	65-70
8162571-2	1994	Lf inhibited growth in mice of transplantable solid tumors induced by v-ras transformed fibroblasts and a methylcholanthrene-induced fibrosarcoma.	Methylcholanthrene	106-124	lactotransferrin	Mus musculus	0-2
7496962-2	1994	Both CD4 and CD8 T-cell subsets within MC cultures are activated during SLP, as judged by high-density CD25 (CD25bright) expression; it is unclear, however, whether both cell subsets can directly undergo SLP.	Methylcholanthrene	39-41	CD4 molecule	Homo sapiens	5-8
8200083-7	1994	Following treatment of cynomolgus monkey with 3-methylcholanthrene, induction of CYP1A1, but not CYP1A2, was evident.	Methylcholanthrene	46-66	cytochrome P450 family 1 subfamily A member 2	Macaca fascicularis	97-103
7496962-2	1994	Both CD4 and CD8 T-cell subsets within MC cultures are activated during SLP, as judged by high-density CD25 (CD25bright) expression; it is unclear, however, whether both cell subsets can directly undergo SLP.	Methylcholanthrene	39-41	CD8a molecule	Homo sapiens	13-16
7496962-2	1994	Both CD4 and CD8 T-cell subsets within MC cultures are activated during SLP, as judged by high-density CD25 (CD25bright) expression; it is unclear, however, whether both cell subsets can directly undergo SLP.	Methylcholanthrene	39-41	interleukin 2 receptor subunit alpha	Homo sapiens	103-107
7496962-2	1994	Both CD4 and CD8 T-cell subsets within MC cultures are activated during SLP, as judged by high-density CD25 (CD25bright) expression; it is unclear, however, whether both cell subsets can directly undergo SLP.	Methylcholanthrene	39-41	interleukin 2 receptor subunit alpha	Homo sapiens	109-113
8187057-3	1994	To examine the effect of pretreatment with a cytochrome P450 (CYP) inducer on the formation of DNA adduct, these rats were pretreated with 3-methylcholanthrene (MC; CYP1A1/1A2 inducer) or phenobarbital (PB; CYP2B inducer).	Methylcholanthrene	139-159	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	165-171
8163516-5	1994	Using a gel retardation assay, TCDD and MC were shown to be equipotent in causing in vitro transformation of the cytosolic Ah receptor to its DNA-binding form.	Methylcholanthrene	40-42	aryl-hydrocarbon receptor	Mus musculus	123-134
8163516-1	1994	Halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polycyclic aromatic hydrocarbons such as 3-methylcholanthrene (MC) cause transcriptional activation of the CYP1A1 gene via their interaction with the aromatic hydrocarbon (Ah) receptor.	Methylcholanthrene	130-150	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	196-202
8163516-6	1994	In addition, the transformed Ah receptor bound to a specific dioxin-responsive enhancer sequence with the same apparent affinity when MC was the ligand as when TCDD was the ligand.	Methylcholanthrene	134-136	aryl-hydrocarbon receptor	Mus musculus	29-40
8163516-1	1994	Halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polycyclic aromatic hydrocarbons such as 3-methylcholanthrene (MC) cause transcriptional activation of the CYP1A1 gene via their interaction with the aromatic hydrocarbon (Ah) receptor.	Methylcholanthrene	130-150	aryl-hydrocarbon receptor	Mus musculus	239-273
8163516-7	1994	At an early time point (i.e. 2 h) in the CYP1A1 induction process, TCDD was only approximately 4-25-fold more potent than MC in stimulating the nuclear uptake of the ligand-Ah receptor complex, and the two ligands displayed a relatively small difference (&gt; or = 10-fold) in CYP1A1 mRNA induction potency.	Methylcholanthrene	122-124	aryl-hydrocarbon receptor	Mus musculus	173-184
8163516-2	1994	Direct radioligand binding and competitive binding studies demonstrated that the cytosolic Ah receptor from the mouse hepatoma cell line Hepa-1 bound TCDD with an affinity approximately 3-4-fold greater than that for MC.	Methylcholanthrene	217-219	aryl-hydrocarbon receptor	Mus musculus	91-102
8163516-3	1994	However, TCDD was approximately 1,000-fold more potent than MC as an inducer of CYP1A1-mediated aryl hydrocarbon hydroxylase activity in cultured Hepa-1 cells as assessed at 14 h following exposure to inducer.	Methylcholanthrene	60-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	80-86
8185654-2	1994	P450MCX was co-purified with CYP1A1 from 3MC-treated male Sprague-Dawley rats but was resolved by gel electrophoresis.	Methylcholanthrene	41-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-35
8163516-10	1994	Our data are consistent with the idea that TCDD and MC display relatively small differences in their intrinsic abilities to activate Ah receptor-mediated events.	Methylcholanthrene	52-54	aryl-hydrocarbon receptor	Mus musculus	133-144
8163516-4	1994	To understand the basis for this quantitative discrepancy between Ah receptor binding affinity and CYP1A1 induction potency, we systematically compared TCDD and MC for their abilities to activate sequential events in the CYP1A1 induction mechanism that occur subsequent to initial binding to the cytosolic Ah receptor.	Methylcholanthrene	161-163	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	221-227
8163517-1	1994	The aromatic hydrocarbon (Ah) receptor is a cytosolic protein that binds halogenated ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and nonhalogenated ligands such as 3-methylcholanthrene (MC) and benzo[a]pyrene.	Methylcholanthrene	179-199	aryl hydrocarbon receptor	Homo sapiens	4-38
8163517-1	1994	The aromatic hydrocarbon (Ah) receptor is a cytosolic protein that binds halogenated ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and nonhalogenated ligands such as 3-methylcholanthrene (MC) and benzo[a]pyrene.	Methylcholanthrene	201-203	aryl hydrocarbon receptor	Homo sapiens	4-38
8163517-12	1994	In velocity sedimentation assays of mouse cytosol, [3H]MC binds specifically to two cytosolic proteins: the 4 S carcinogen-binding protein and the Ah receptor (9 S).	Methylcholanthrene	55-57	aryl-hydrocarbon receptor	Mus musculus	147-158
8161348-2	1994	Treatment of cells with IL-6 decreased the level of 3-methylcholanthrene-induced CYPIA1 protein and its mRNA.	Methylcholanthrene	52-72	interleukin 6	Homo sapiens	24-28
8174125-4	1994	Whereas methylcholanthrene induced (a) resistance to mafosfamide and (b) class-3 aldehyde dehydrogenase activity, as well as glutathione S-transferase and DT-diaphorase activities, in the estrogen receptor-positive MCF-7/0 cells, it did not do so in two other human breast adenocarcinoma cell lines, MDA-MB-231 and SK-BR-3, each of which is estrogen receptor negative.	Methylcholanthrene	8-26	NAD(P)H quinone dehydrogenase 1	Homo sapiens	155-168
7952395-2	1994	In a pulmonary metastases model using the methylcholanthrene-induced sarcoma MCA-105 anti-CD3 activated TIL were capable of eradicating disease similar to TIL cultured in rIL-2 only.	Methylcholanthrene	42-60	CD3 antigen, epsilon polypeptide	Mus musculus	90-93
7952395-2	1994	In a pulmonary metastases model using the methylcholanthrene-induced sarcoma MCA-105 anti-CD3 activated TIL were capable of eradicating disease similar to TIL cultured in rIL-2 only.	Methylcholanthrene	42-60	interleukin 2	Rattus norvegicus	171-176
8161348-2	1994	Treatment of cells with IL-6 decreased the level of 3-methylcholanthrene-induced CYPIA1 protein and its mRNA.	Methylcholanthrene	52-72	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	81-87
8128488-0	1994	Suppression of hydroxysteroid sulfotransferase-a gene expression by 3-methylcholanthrene.	Methylcholanthrene	68-88	sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 6	Rattus norvegicus	15-48
8118934-5	1994	Pretreatment of rats with 3-methylcholanthrene (MC), a dioxin-type inducer of CYP1A isozymes and phenol UDP-glucuronosyltransferase (UGT1A1), led to a dramatic decrease of N-acetylated (2% of total metabolites) and an increase of N-hydroxylated (54% as free and glucuronidated compound) and ring-hydroxylated (35%) metabolites.	Methylcholanthrene	26-46	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	133-139
8118934-5	1994	Pretreatment of rats with 3-methylcholanthrene (MC), a dioxin-type inducer of CYP1A isozymes and phenol UDP-glucuronosyltransferase (UGT1A1), led to a dramatic decrease of N-acetylated (2% of total metabolites) and an increase of N-hydroxylated (54% as free and glucuronidated compound) and ring-hydroxylated (35%) metabolites.	Methylcholanthrene	48-50	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	133-139
8120057-4	1994	Dissection of the 5"-flanking portion of the CYP1A2 gene identified two regions that contributed to the overall induction by 3-methylcholanthrene.	Methylcholanthrene	125-145	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	45-51
8120057-6	1994	In addition, deletion of this region of the CYP1A2 gene reduces the 3-methylcholanthrene (3-MC)-initiated induction of chloramphenicol acetyltransferase activity in both promoter- and enhancer-specific constructs.	Methylcholanthrene	68-88	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-50
8120057-6	1994	In addition, deletion of this region of the CYP1A2 gene reduces the 3-methylcholanthrene (3-MC)-initiated induction of chloramphenicol acetyltransferase activity in both promoter- and enhancer-specific constructs.	Methylcholanthrene	90-94	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-50
8124689-7	1994	DNA synthesis and interleukin-2 production by spleen cells following stimulation with anti-CD3 antibody are also profoundly depressed in the presence of MCA-38 and HT-29 adenocarcinoma cells.	Methylcholanthrene	153-156	interleukin 2	Mus musculus	18-31
8124689-7	1994	DNA synthesis and interleukin-2 production by spleen cells following stimulation with anti-CD3 antibody are also profoundly depressed in the presence of MCA-38 and HT-29 adenocarcinoma cells.	Methylcholanthrene	153-156	CD3 antigen, epsilon polypeptide	Mus musculus	91-94
8128488-5	1994	Transcription of the rat hepatic CYP1A1 gene is induced in response to treatment with PAH carcinogen 3-methylcholanthrene (3-MC).	Methylcholanthrene	101-121	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	33-39
8128488-5	1994	Transcription of the rat hepatic CYP1A1 gene is induced in response to treatment with PAH carcinogen 3-methylcholanthrene (3-MC).	Methylcholanthrene	123-127	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	33-39
8128488-6	1994	In view of the potential importance of enzymatic sulfation to the complex process of PAH carcinogenesis, the effect of 3-MC on HST-a gene expression was investigated.	Methylcholanthrene	119-123	fibroblast growth factor 4	Rattus norvegicus	127-130
8128488-10	1994	Subsequent Northern blot analyses on liver tissue isolated from female rats aged approximately 55 days confirmed CYP1A1 mRNA induction in 3-MC-treated animals and demonstrated a dose-dependent suppression of HST-a mRNA expression of approximately 25, 50, and 75% in rats treated with 10, 25, and 80 mg/kg 3-MC ip, respectively.	Methylcholanthrene	138-142	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	113-119
8128488-12	1994	A time-course study revealed that hepatic HST-a mRNA levels returned to control levels by 36 hr following 3-MC treatment.	Methylcholanthrene	106-110	fibroblast growth factor 4	Rattus norvegicus	42-45
8128488-13	1994	These results suggest that xenobiotics such as 3-MC modulate HST-a mRNA expression and that HST-a mRNA suppression after 3-MC treatment may occur at the level of transcription.	Methylcholanthrene	47-51	fibroblast growth factor 4	Rattus norvegicus	61-64
8128488-13	1994	These results suggest that xenobiotics such as 3-MC modulate HST-a mRNA expression and that HST-a mRNA suppression after 3-MC treatment may occur at the level of transcription.	Methylcholanthrene	121-125	fibroblast growth factor 4	Rattus norvegicus	92-95
7508708-3	1994	CYP1A1 mRNA was prominently induced after exposure to 3-methylcholanthrene (MCA) throughout the observation period with either type of culture.	Methylcholanthrene	54-74	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-6
8126925-5	1994	In mice, AHH inducibility is under the control of the Ah locus and certain inbred strains of mice are susceptible to AHH induction by 3-methylcholanthrene treatment (Ah responsive strains), while other strains are not (Ah non-responsive strains).	Methylcholanthrene	134-154	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	117-120
8188531-1	1994	Syngeneic BALB/c mice bearing methylcholanthrene-induced fibrosarcoma (Meth-A) cells transduced with a tumor necrosis factor (TNF) gene showed a longer life span and tumor regression as compared with mice carrying TNF-non-producing Meth-A cells.	Methylcholanthrene	30-48	tumor necrosis factor	Mus musculus	103-124
8188531-1	1994	Syngeneic BALB/c mice bearing methylcholanthrene-induced fibrosarcoma (Meth-A) cells transduced with a tumor necrosis factor (TNF) gene showed a longer life span and tumor regression as compared with mice carrying TNF-non-producing Meth-A cells.	Methylcholanthrene	30-48	tumor necrosis factor	Mus musculus	126-129
7906206-0	1994	Differential modulation of P-glycoprotein expression by dexamethasone and 3-methylcholanthrene in rat hepatocyte primary cultures.	Methylcholanthrene	74-94	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	27-41
8126925-5	1994	In mice, AHH inducibility is under the control of the Ah locus and certain inbred strains of mice are susceptible to AHH induction by 3-methylcholanthrene treatment (Ah responsive strains), while other strains are not (Ah non-responsive strains).	Methylcholanthrene	134-154	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	9-12
8166457-3	1994	On the other hand, Progesterone receptor (PR) level in normal glands tended to be lower in group MC than in group FC, which was recovered by chronic treatment with oestradiol benzoate (group OB).	Methylcholanthrene	97-99	progesterone receptor	Mus musculus	19-40
8166457-3	1994	On the other hand, Progesterone receptor (PR) level in normal glands tended to be lower in group MC than in group FC, which was recovered by chronic treatment with oestradiol benzoate (group OB).	Methylcholanthrene	97-99	progesterone receptor	Mus musculus	42-44
7508708-3	1994	CYP1A1 mRNA was prominently induced after exposure to 3-methylcholanthrene (MCA) throughout the observation period with either type of culture.	Methylcholanthrene	76-79	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-6
7508708-10	1994	Activities of aryl hydrocarbon hydroxylase (AHH) and acetanilide-4-hydroxylase (AAH) were elevated with either type of culture after treatment with MCA and the presence of nicotinamide further increased the AAH, resulting in an increment in the activity ratio of AAH vs AHH.	Methylcholanthrene	148-151	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	14-42
7508708-10	1994	Activities of aryl hydrocarbon hydroxylase (AHH) and acetanilide-4-hydroxylase (AAH) were elevated with either type of culture after treatment with MCA and the presence of nicotinamide further increased the AAH, resulting in an increment in the activity ratio of AAH vs AHH.	Methylcholanthrene	148-151	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	44-47
7652933-2	1994	It has been shown that incubation of the MG-PL complexes with MC resulted in the increase in concentrations of all these macroglobulins (MG, PAG, and PAPP-A) in supernatants of cultured MC.	Methylcholanthrene	62-64	pappalysin 1	Homo sapiens	150-156
7732678-5	1994	Participation of MC induced forms of cytochrome P-450 (P-448) in activation of AFB1 is supposed.	Methylcholanthrene	17-19	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
7732678-5	1994	Participation of MC induced forms of cytochrome P-450 (P-448) in activation of AFB1 is supposed.	Methylcholanthrene	17-19	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	55-60
8252472-5	1993	The MC in the preoperative biopsy was assessed by the presence of: (1) malignant-appearing glands disrupted by the presence of abundant extruded intraluminal mucin; (2) pools of mucin in the connective stroma of the adenocarcinoma; and (3) superficial pools of mucin containing ribbons or clusters of neoplastic epithelial cells.	Methylcholanthrene	4-6	LOC100508689	Homo sapiens	158-163
8252472-5	1993	The MC in the preoperative biopsy was assessed by the presence of: (1) malignant-appearing glands disrupted by the presence of abundant extruded intraluminal mucin; (2) pools of mucin in the connective stroma of the adenocarcinoma; and (3) superficial pools of mucin containing ribbons or clusters of neoplastic epithelial cells.	Methylcholanthrene	4-6	LOC100508689	Homo sapiens	178-183
8252472-5	1993	The MC in the preoperative biopsy was assessed by the presence of: (1) malignant-appearing glands disrupted by the presence of abundant extruded intraluminal mucin; (2) pools of mucin in the connective stroma of the adenocarcinoma; and (3) superficial pools of mucin containing ribbons or clusters of neoplastic epithelial cells.	Methylcholanthrene	4-6	LOC100508689	Homo sapiens	178-183
8252472-9	1993	CONCLUSIONS: Colorectal adenocarcinomas showing MC in the preoperative biopsy are significantly more likely to reveal a high mucin content and to be at an advanced stage at resection.	Methylcholanthrene	48-50	LOC100508689	Homo sapiens	125-130
12369753-2	1994	PCB and MC treatments increased 7-ethoxyresorufin and 7-ethoxycoumarin O-deethylase activities related to cytochrome P-448.	Methylcholanthrene	8-10	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	106-122
12369753-6	1994	The ratio between saturated and unsaturated fatty acids (saturation index) decreased in the total microsomes and phospholipids with PCB treatment, whereas MC did not alter the ratio, except that the major effect of MC was observed in the acyl derivatives of microsomal phosphatidylethanolamine.	Methylcholanthrene	215-217	pyruvate carboxylase	Rattus norvegicus	132-135
7504657-8	1993	The steady-state levels of p53 mRNA were decreased in chemically transformed (both MNNG- and MC-transformed) cells.	Methylcholanthrene	93-95	transformation related protein 53, pseudogene	Mus musculus	27-30
7504657-10	1993	The low level of the p53 protein in MC-transformed cells may result from transcriptional depression of the p53 gene.	Methylcholanthrene	36-38	transformation related protein 53, pseudogene	Mus musculus	21-24
7504657-10	1993	The low level of the p53 protein in MC-transformed cells may result from transcriptional depression of the p53 gene.	Methylcholanthrene	36-38	transformation related protein 53, pseudogene	Mus musculus	107-110
8112878-1	1993	Immunohistochemical localization of cytochrome MC-P-448 (form of cytochrome P-450 induced by methylcholanthrene) in rat hepatic lobule and the changes in their distribution pattern in response to cold exposure at 4 degrees C were investigated.	Methylcholanthrene	93-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
8282126-5	1993	The complex has significantly enhanced stability at neutral and slightly alkaline pH, and reduced proteolytic activity against the synthetic substrate Z-Phe-Arg-MCA compared to free cathepsin L.	Methylcholanthrene	161-164	cathepsin L	Homo sapiens	182-193
8130776-1	1993	The effect of carbon tetrachloride (CCl4) on the induction and activity of 3-methylcholanthrene (MC)-inducible P450IA isozymes (P450IA1 and P450IA2) in the liver was examined by treating male Sprague-Dawley rats with simultaneous i.p.	Methylcholanthrene	75-95	C-C motif chemokine ligand 4	Rattus norvegicus	36-40
8130776-1	1993	The effect of carbon tetrachloride (CCl4) on the induction and activity of 3-methylcholanthrene (MC)-inducible P450IA isozymes (P450IA1 and P450IA2) in the liver was examined by treating male Sprague-Dawley rats with simultaneous i.p.	Methylcholanthrene	97-99	C-C motif chemokine ligand 4	Rattus norvegicus	36-40
8130776-4	1993	As determined by a bacterial mutation test using carcinogenic aromatic amines are P450IA enzyme substrates, CCl4 treatment selectively inhibited the activity of P450IA2 in the MC-induced isozymes.	Methylcholanthrene	176-178	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
8263600-2	1993	In rats of all genotypes the hepatic concentration of UDP glucuronosyltransferase (UDPGT) mRNA was increased at 48 and 96 h after the treatment with 3MC.	Methylcholanthrene	149-152	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	54-81
8263600-2	1993	In rats of all genotypes the hepatic concentration of UDP glucuronosyltransferase (UDPGT) mRNA was increased at 48 and 96 h after the treatment with 3MC.	Methylcholanthrene	149-152	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	83-88
8263600-8	1993	The data indicate that the stimulation of the expression of both the 4-nitrophenol and chloramphenicol UDPGT genes plays a key role in the ascorbic acid biosynthesis induced by 3MC and sodium phenobarbital.	Methylcholanthrene	177-180	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	103-108
8282136-5	1993	MC produced PGE2 30 min after the IL-1 stimulation.	Methylcholanthrene	0-2	interleukin 1 complex	Mus musculus	34-38
8282136-9	1993	KT5720 inhibited the IL-1-induced PGE2 production in MC in a dose dependent fashion.	Methylcholanthrene	53-55	interleukin 1 complex	Mus musculus	21-25
8282136-10	1993	Similarly, staurosporin inhibited the IL-1-induced PGE2 production in MC in a dose dependent manner.	Methylcholanthrene	70-72	interleukin 1 complex	Mus musculus	38-42
7691941-3	1993	Human MC progenitors can be detected in the bone marrow as well as in the peripheral blood (pb) and are responsive to the mast cell growth factor SCF, the ligand of the c-kit tyrosine kinase receptor.	Methylcholanthrene	6-8	KIT ligand	Homo sapiens	146-149
8241264-1	1993	Guinea pig CYP1A1 cDNA was isolated from a liver cDNA library of guinea pig treated with 3-methylcholanthrene.	Methylcholanthrene	89-109	cytochrome P450 1A1	Cavia porcellus	11-17
8241264-4	1993	RNA blot and immunoblot analyses revealed that CYP1A1 was constitutively expressed and was induced by 3-methylcholanthrene in guinea pig liver.	Methylcholanthrene	102-122	cytochrome P450 1A1	Cavia porcellus	47-53
8228266-7	1993	MC were first incubated with anti-CD8-coated magnetic beads (4:1 ratio) to obtain a CD8bright-enriched population (97% of all cells CD8+, 83% of all cells CD8bright).	Methylcholanthrene	0-2	CD8a molecule	Homo sapiens	34-37
8228266-7	1993	MC were first incubated with anti-CD8-coated magnetic beads (4:1 ratio) to obtain a CD8bright-enriched population (97% of all cells CD8+, 83% of all cells CD8bright).	Methylcholanthrene	0-2	CD8a molecule	Homo sapiens	84-87
7691941-7	1993	In the presence of rhSCF, MC developed in long term suspension culture from pure CD34+ cells but not from pure Mo, pure Ba, or Ly (MC-tryptase levels on day 42: CD14+ Mo: 3.7 +/- 0.8 vs CD17+ Ba: 3.2 +/- 0.5 vs Ly: 2.0 +/- 1.5 vs control: 196.5 +/- 92.5 ng/ml, p &lt; 0.001).	Methylcholanthrene	26-28	CD34 molecule	Homo sapiens	81-85
7691941-8	1993	Depletion of CD34+ cells from MNC resulted in a loss of MC in long term suspension culture, whereas depletion of either Mo, Ba, or Ly did not.	Methylcholanthrene	56-58	CD34 molecule	Homo sapiens	13-17
7691941-11	1993	The circulating MC progenitor is a CD34+, c-kit+, Ly-, CD14-, CD17- colony-forming cell.	Methylcholanthrene	16-18	CD34 molecule	Homo sapiens	35-39
7691941-11	1993	The circulating MC progenitor is a CD34+, c-kit+, Ly-, CD14-, CD17- colony-forming cell.	Methylcholanthrene	16-18	CD14 molecule	Homo sapiens	55-59
7692844-10	1993	Pretreating rats with the mono-oxygenase inducers phenobarbitone, 3-methylcholanthrene or Aroclor 1254 showed the last-named to be the most potent inducer of CYP1A1.	Methylcholanthrene	66-86	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	158-164
8293789-5	1993	3-Methylcholanthrene induced CYP1A1 in preference to CYP1A2.	Methylcholanthrene	0-20	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-35
7823004-1	1993	Studies were done to determine plasma PRL in response to oral MC 0.2 mg/kg in 17 normal children (NC), 12 males and 5 females aged between 4.7-12.8 years and in 26 idiopathic growth hormone deficient children (IGHD), 15 M, 11 F, between 1.5-14.7 years old.	Methylcholanthrene	62-64	prolactin	Homo sapiens	38-41
7823004-8	1993	The peak serum PRL response to MC ranges were from 33 to 127 ng/ml with the mean +/- SD and +/- SE of 64.45 +/- 24.22 and +/- 5.88 ng/ml respectively giving the cut point-2SD value of 16.01 ng/ml.	Methylcholanthrene	31-33	prolactin	Homo sapiens	15-18
7823004-9	1993	Among 26I GHD, only 2 patients (7.69%) being all male, had peak PRL response to MC below 16.01 ng/ml, whereas, the rest (92.31%) had peak PRL levels above it.	Methylcholanthrene	80-82	prolactin	Homo sapiens	64-67
7823004-10	1993	It is concluded that oral MC 0.2 mg/kg is the potent PRL stimulator in children, which can be safely used to test pituitary PRL secretion effectively.	Methylcholanthrene	26-28	prolactin	Homo sapiens	53-56
7823004-10	1993	It is concluded that oral MC 0.2 mg/kg is the potent PRL stimulator in children, which can be safely used to test pituitary PRL secretion effectively.	Methylcholanthrene	26-28	prolactin	Homo sapiens	124-127
7823004-11	1993	The majority (92.31%) of idiopathic GH deficient children had adequate serum PRL response to oral MC, whilst 7.69 per cent disclosed inadequate response which might indicate different etiologies.	Methylcholanthrene	98-100	prolactin	Homo sapiens	77-80
8334163-7	1993	Treatment of the hepatocyte cultures with phenobarbital (2 mM) or 3-methylcholanthene (5 microM) for 24, 48, or 72 h, beginning 24 h after plating, resulted in significant increases in glutathione S-transferase activity relative to control, with maximal increases of 158 and 164% measured at 72 h following phenobarbital or 3-methylcholanthrene treatment, respectively.	Methylcholanthrene	324-344	hematopoietic prostaglandin D synthase	Rattus norvegicus	185-210
7902259-4	1993	In liver microsomes from 3-methylcholanthrene-treated rats, antibodies specific for cytochrome P-450 1A1 and 1A2 inhibited hydroxylation of dantrolene by 60% and 20%, respectively.	Methylcholanthrene	25-45	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	84-112
7903616-10	1993	Both UGT-(testosterone) and the 3-methylcholanthrene-inducible form previously described in the literature, may be responsible for the activity, whilst a highly specific form (UGT-phenol) is reported here for the first time.	Methylcholanthrene	32-52	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	176-179
8334163-10	1993	1.5- to 2-fold following phenobarbital, or beta-naphthoflavone treatment; 3-methylcholanthrene was less effective in enhancing GST expression in cultured hepatocytes as compared to phenobarbital or beta-naphthoflavone.	Methylcholanthrene	74-94	hematopoietic prostaglandin D synthase	Rattus norvegicus	127-130
8325712-0	1993	A role for the fyn oncogene in metastasis of methylcholanthrene-induced fibrosarcoma A cells.	Methylcholanthrene	45-63	Fyn proto-oncogene	Mus musculus	15-18
8104124-15	1993	The increase in N-demethylation by MC treatment appears to be due to elevation of CYP1A1/1A2 (P-450c/d).	Methylcholanthrene	35-37	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	82-88
8374053-3	1993	BP, 6-FBP, and 6-CH3BP formed adducts with DNA when (1) they were activated by 3-methylcholanthrene-induced rat liver microsomes, (2) they were activated by horseradish peroxidase (HRP), (3) their 7,8-dihydrodiols were activated by microsomes, or (4) the radical cation of BP, 6-FBP, or 6-CH3-BP was directly reacted with DNA.	Methylcholanthrene	79-99	far upstream element binding protein 1	Rattus norvegicus	6-9
8076525-6	1993	Antisense inhibition of EGF expression produces bilaterally symmetrical Fusilli-form dysmorphogenesis of MC and decreases tooth bud size; these effects are reversed by the addition of exogenous EGF to the culture medium.	Methylcholanthrene	105-107	epidermal growth factor	Mus musculus	24-27
8104124-15	1993	The increase in N-demethylation by MC treatment appears to be due to elevation of CYP1A1/1A2 (P-450c/d).	Methylcholanthrene	35-37	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	94-102
8076525-6	1993	Antisense inhibition of EGF expression produces bilaterally symmetrical Fusilli-form dysmorphogenesis of MC and decreases tooth bud size; these effects are reversed by the addition of exogenous EGF to the culture medium.	Methylcholanthrene	105-107	epidermal growth factor	Mus musculus	194-197
8504461-3	1993	The C22 compound was active in completely inhibiting 3-methylcholanthrene-induced transformation at 10(-5) M when added during the post-initiation phase of carcinogenesis.	Methylcholanthrene	53-73	Sp7 transcription factor 7	Mus musculus	4-7
8508499-2	1993	In order to establish the mechanisms by which such compounds may elicit a protective effect at DNA level, the influence of these compounds upon benzo[a]pyrene (BaP) activation by 3-methyl-cholanthrene-stimulated microsomes was also studied.	Methylcholanthrene	179-200	prohibitin 2	Homo sapiens	160-163
8315282-1	1993	We investigated the expression, distribution, and inducibility of 3-methylcholanthrene (MC)-inducible P450 enzymes, CYP1A1 and 1A2, in livers of rabbits at different stages of development, ranging from 4 days before birth (-4 days of age) to adulthood.	Methylcholanthrene	88-90	cytochrome P450 1A1	Oryctolagus cuniculus	116-130
8315282-7	1993	Although CYP1A1 is induced by MC treatment at most ages, there is no change in its distribution.	Methylcholanthrene	30-32	cytochrome P450 1A1	Oryctolagus cuniculus	9-15
8315282-10	1993	The greatest fold-induction of hepatic CYP1A2 by MC in the rabbit is a 9-11 days of age, when, for MC-treated rabbits, CYP1A2 represents &gt; 60% of the total P450 pool.	Methylcholanthrene	49-51	cytochrome P450 1A2	Oryctolagus cuniculus	39-45
8315282-10	1993	The greatest fold-induction of hepatic CYP1A2 by MC in the rabbit is a 9-11 days of age, when, for MC-treated rabbits, CYP1A2 represents &gt; 60% of the total P450 pool.	Methylcholanthrene	49-51	cytochrome P450 1A2	Oryctolagus cuniculus	119-125
8315282-10	1993	The greatest fold-induction of hepatic CYP1A2 by MC in the rabbit is a 9-11 days of age, when, for MC-treated rabbits, CYP1A2 represents &gt; 60% of the total P450 pool.	Methylcholanthrene	99-101	cytochrome P450 1A2	Oryctolagus cuniculus	39-45
8315282-10	1993	The greatest fold-induction of hepatic CYP1A2 by MC in the rabbit is a 9-11 days of age, when, for MC-treated rabbits, CYP1A2 represents &gt; 60% of the total P450 pool.	Methylcholanthrene	99-101	cytochrome P450 1A2	Oryctolagus cuniculus	119-125
8489258-2	1993	GST specific activity toward 1-chloro-2,4-dinitrobenzene increased by 170% in parasites recovered from mice injected with 3-methylcholanthrene and 230% in parasites recovered from mice maintained on a diet containing butylated hydroxyanisole.	Methylcholanthrene	122-142	glutathione S-transferase kappa 1	Homo sapiens	0-3
8315282-0	1993	Ontogenetic development of the distribution of constitutive and 3-methylcholanthrene-induced CYP1A1 and CYP1A2 in rabbit liver.	Methylcholanthrene	64-84	cytochrome P450 1A1	Oryctolagus cuniculus	93-99
8315282-0	1993	Ontogenetic development of the distribution of constitutive and 3-methylcholanthrene-induced CYP1A1 and CYP1A2 in rabbit liver.	Methylcholanthrene	64-84	cytochrome P450 1A2	Oryctolagus cuniculus	104-110
8315282-1	1993	We investigated the expression, distribution, and inducibility of 3-methylcholanthrene (MC)-inducible P450 enzymes, CYP1A1 and 1A2, in livers of rabbits at different stages of development, ranging from 4 days before birth (-4 days of age) to adulthood.	Methylcholanthrene	66-86	cytochrome P450 1A1	Oryctolagus cuniculus	116-130
8415211-6	1993	The development of insulin-binding antibodies during the first year of observation was more rapid in patients treated with MC pork insulin but thereafter it was similar in the two studied groups.	Methylcholanthrene	123-125	insulin	Homo sapiens	19-26
8415211-6	1993	The development of insulin-binding antibodies during the first year of observation was more rapid in patients treated with MC pork insulin but thereafter it was similar in the two studied groups.	Methylcholanthrene	123-125	insulin	Homo sapiens	131-138
8415211-9	1993	In the group of diabetics treated with MC pork insulin after 5 years of observation serum insulin-binding antibodies were found in 12 patients.	Methylcholanthrene	39-41	insulin	Homo sapiens	47-54
8415211-9	1993	In the group of diabetics treated with MC pork insulin after 5 years of observation serum insulin-binding antibodies were found in 12 patients.	Methylcholanthrene	39-41	insulin	Homo sapiens	90-97
8494539-1	1993	Stably expressed human and rat phenol UDP-glucuronosyltransferases (UGTs) of the UGT1 complex (HlugP1, HlugP4 and 3-methylcholanthrene-inducible rat UGT1A1, the latter considered to be an orthologous enzyme to HlugP1) have been used to investigate the role of UGTs in paracetamol glucuronidation.	Methylcholanthrene	116-134	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	81-85
8494539-1	1993	Stably expressed human and rat phenol UDP-glucuronosyltransferases (UGTs) of the UGT1 complex (HlugP1, HlugP4 and 3-methylcholanthrene-inducible rat UGT1A1, the latter considered to be an orthologous enzyme to HlugP1) have been used to investigate the role of UGTs in paracetamol glucuronidation.	Methylcholanthrene	116-134	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	149-155
8494539-1	1993	Stably expressed human and rat phenol UDP-glucuronosyltransferases (UGTs) of the UGT1 complex (HlugP1, HlugP4 and 3-methylcholanthrene-inducible rat UGT1A1, the latter considered to be an orthologous enzyme to HlugP1) have been used to investigate the role of UGTs in paracetamol glucuronidation.	Methylcholanthrene	116-134	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	210-216
8509896-2	1993	In this study, we examined the effects of phenobarbital (PB) and 3-methylcholanthrene (MC), both of which are known to stimulate AsA biosynthesis in rats, on the hepatic levels of GLO activity, GLO mRNA, and AsA.	Methylcholanthrene	87-89	gulonolactone (L-) oxidase	Rattus norvegicus	180-183
8481899-2	1993	Human TNF-alpha at a concentration of 0.6 nM markedly stimulated transformation of BALB/3T3 cells initiated with 3-methylcholanthrene.	Methylcholanthrene	113-133	tumor necrosis factor	Homo sapiens	6-15
8453613-3	1993	We also observed a homozygous, intragenic deletion in the Ptprg gene in all clonal derivatives of the original L-cell strain, a methylcholanthrene-treated mouse connective tissue cell line which produces sarcomas in syngeneic mice.	Methylcholanthrene	128-146	protein tyrosine phosphatase, receptor type, G	Mus musculus	58-63
8390902-1	1993	The administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene (3MC) to mice results in their binding to the ligand binding portion of the cytosolic dioxin-(Ah)-receptor, followed by translocation of the Ah receptor complex to the nucleus where the DNA binding form of the receptor can be measured by gel retardation analysis.	Methylcholanthrene	69-89	aryl-hydrocarbon receptor	Mus musculus	231-242
8390902-1	1993	The administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 3-methylcholanthrene (3MC) to mice results in their binding to the ligand binding portion of the cytosolic dioxin-(Ah)-receptor, followed by translocation of the Ah receptor complex to the nucleus where the DNA binding form of the receptor can be measured by gel retardation analysis.	Methylcholanthrene	91-94	aryl-hydrocarbon receptor	Mus musculus	231-242
8461038-3	1993	The prototype cytochrome P450 inducers, 3-methylcholanthrene (3-MC) and phenobarbital (PB), increased ECOD and GST activities reaching an optimum 7 days after culturing, followed by a decline in activity.	Methylcholanthrene	40-60	glutathione S-transferase kappa 1	Homo sapiens	111-114
8461038-3	1993	The prototype cytochrome P450 inducers, 3-methylcholanthrene (3-MC) and phenobarbital (PB), increased ECOD and GST activities reaching an optimum 7 days after culturing, followed by a decline in activity.	Methylcholanthrene	62-66	glutathione S-transferase kappa 1	Homo sapiens	111-114
8486527-2	1993	CYP1A1 mRNA was substantially induced by treatment with 3-methylcholanthrene during the observation period, independently of the seeded cell density.	Methylcholanthrene	56-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-6
8486528-2	1993	When the cells were cultivated as monolayers on collagen-coated dishes, CYP1A1 mRNA species were prominently induced after treatment with 3-methylcholanthrene (MCA) throughout the observation period.	Methylcholanthrene	138-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	72-78
8486528-2	1993	When the cells were cultivated as monolayers on collagen-coated dishes, CYP1A1 mRNA species were prominently induced after treatment with 3-methylcholanthrene (MCA) throughout the observation period.	Methylcholanthrene	160-163	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	72-78
8486528-6	1993	The time-course of the induced CYP1A2 mRNA amounts after the treatment with MCA or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) followed the same pattern as that of CYP1A1 mRNA.	Methylcholanthrene	76-79	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	31-37
8486528-6	1993	The time-course of the induced CYP1A2 mRNA amounts after the treatment with MCA or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) followed the same pattern as that of CYP1A1 mRNA.	Methylcholanthrene	76-79	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	163-169
8486528-9	1993	Activities of aryl hydrocarbon hydroxylase (AHH) and acetanilide 4-hydroxylase (AAH) were elevated with either type of cultivation after treatment with MCA or TCDD.	Methylcholanthrene	152-155	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	14-42
8486528-9	1993	Activities of aryl hydrocarbon hydroxylase (AHH) and acetanilide 4-hydroxylase (AAH) were elevated with either type of cultivation after treatment with MCA or TCDD.	Methylcholanthrene	152-155	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	44-47
21573632-0	1993	Characterization of oligosaccharides on methylcholanthrene-induced murine oncofetal antigen using biotinylated lectins.	Methylcholanthrene	40-58	oncofetal antigen	Mus musculus	74-91
8474022-7	1993	In contrast, the monoclonal antibody MAb 1-7-1, raised against 3-methylcholanthrene-inducible rat cytochromes 450, almost abolished CYP1A1-mediated phenacetin O-deethylation, but had no effect on human liver microsomal- or CYP1A2-catalyzed phenacetin dealkylation.	Methylcholanthrene	63-83	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-138
8474022-7	1993	In contrast, the monoclonal antibody MAb 1-7-1, raised against 3-methylcholanthrene-inducible rat cytochromes 450, almost abolished CYP1A1-mediated phenacetin O-deethylation, but had no effect on human liver microsomal- or CYP1A2-catalyzed phenacetin dealkylation.	Methylcholanthrene	63-83	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	223-229
8509896-6	1993	However, the level of GLO mRNA and the activity of GLO in the liver tended to be slightly decreased by the administration of PB or MC, though the differences were not significant.	Methylcholanthrene	131-133	gulonolactone (L-) oxidase	Rattus norvegicus	22-25
8509896-6	1993	However, the level of GLO mRNA and the activity of GLO in the liver tended to be slightly decreased by the administration of PB or MC, though the differences were not significant.	Methylcholanthrene	131-133	gulonolactone (L-) oxidase	Rattus norvegicus	51-54
8509896-7	1993	Thus it is clear that the treatment with PB or MC stimulates the biosynthesis of AsA by increasing the activity of some enzyme(s) participating in the synthesis prior to GLO.	Methylcholanthrene	47-49	gulonolactone (L-) oxidase	Rattus norvegicus	170-173
8417813-0	1993	Preferential increase of glutathione S-transferase class alpha transcripts in cultured human hepatocytes by phenobarbital, 3-methylcholanthrene, and dithiolethiones.	Methylcholanthrene	123-143	glutathione S-transferase kappa 1	Homo sapiens	25-50
8430440-1	1993	In vivo administration of 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced much higher hepatic microsomal aryl hydrocarbon hydroxylase (AHH) induction than 7,8-benzoflavone (7,8-BF) in both aromatic hydrocarbon (Ah)-responsive and nonresponsive strains of mice.	Methylcholanthrene	26-46	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	139-167
8430440-1	1993	In vivo administration of 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced much higher hepatic microsomal aryl hydrocarbon hydroxylase (AHH) induction than 7,8-benzoflavone (7,8-BF) in both aromatic hydrocarbon (Ah)-responsive and nonresponsive strains of mice.	Methylcholanthrene	26-46	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	169-172
8430440-1	1993	In vivo administration of 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced much higher hepatic microsomal aryl hydrocarbon hydroxylase (AHH) induction than 7,8-benzoflavone (7,8-BF) in both aromatic hydrocarbon (Ah)-responsive and nonresponsive strains of mice.	Methylcholanthrene	48-50	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	139-167
8430440-1	1993	In vivo administration of 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced much higher hepatic microsomal aryl hydrocarbon hydroxylase (AHH) induction than 7,8-benzoflavone (7,8-BF) in both aromatic hydrocarbon (Ah)-responsive and nonresponsive strains of mice.	Methylcholanthrene	48-50	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	169-172
8430440-2	1993	Simultaneous treatment or pre-treatment with 7,8-BF produced an inhibitory effect on AHH induction by MC or TCDD (i.e., the degrees of the inhibition, with TCDD, were 28% in the Ah-responsive strain C57BL/6N (C57) mice and 45% in the nonresponsive strain DDD;Qdj (DDD) mice).	Methylcholanthrene	102-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	85-88
8430440-3	1993	However, posttreatment with 7,8-BF was inclined to promote the induction of AHH by MC or TCDD (i.e., the degrees of the enhancement, with MC, were 15% in C57 mice and 45% in DDD mice).	Methylcholanthrene	83-85	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	76-79
8010877-0	1993	Recombinant tumor necrosis factor alpha inhibits growth of methylcholanthrene-induced sarcoma and enhances natural killer activity of tumor-infiltrating lymphocytes in aging rats.	Methylcholanthrene	59-77	tumor necrosis factor	Rattus norvegicus	12-39
8493889-0	1993	Tumor-associated aldehyde dehydrogenase (ALDH3): expression in different human tumor cell lines with and without treatment with 3-methylcholanthrene.	Methylcholanthrene	128-148	aldehyde dehydrogenase 3 family member A1	Homo sapiens	41-46
8417813-4	1993	After 3 daily treatments, the two dithiolethiones were the most potent inducers; phenobarbital was also effective but to a lesser extent and 3-methylcholanthrene increased GST mRNA in only 2 of the 6 samples, although it stimulated cytochrome P-450 1A2 mRNA in all cell preparations.	Methylcholanthrene	141-161	glutathione S-transferase kappa 1	Homo sapiens	172-175
8417813-4	1993	After 3 daily treatments, the two dithiolethiones were the most potent inducers; phenobarbital was also effective but to a lesser extent and 3-methylcholanthrene increased GST mRNA in only 2 of the 6 samples, although it stimulated cytochrome P-450 1A2 mRNA in all cell preparations.	Methylcholanthrene	141-161	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	232-252
8417813-8	1993	These results clearly indicate that phenobarbital, 3-methylcholanthrene, and dithiolethiones are able to markedly increase mRNA levels of GST in human hepatocytes and that the GST alpha class is preferentially involved.	Methylcholanthrene	51-71	glutathione S-transferase kappa 1	Homo sapiens	138-141
8417813-8	1993	These results clearly indicate that phenobarbital, 3-methylcholanthrene, and dithiolethiones are able to markedly increase mRNA levels of GST in human hepatocytes and that the GST alpha class is preferentially involved.	Methylcholanthrene	51-71	glutathione S-transferase kappa 1	Homo sapiens	176-179
1335374-5	1992	Only those congeners which bound to the aryl hydrocarbon (Ah) receptor, namely benzo[a]pyrene, benz[a]anthracene, 7,12-dimethylbenz[a]anthracene and MC, caused a decrease in nuclear ER levels.	Methylcholanthrene	149-151	aryl hydrocarbon receptor	Homo sapiens	40-70
8380963-4	1993	3-Methylcholanthrene, beta-naphthoflavone, and benz[alpha]anthracene were strong inducers of CYP1A1, benzo[alpha]pyrene induced CYP1A1 activity only weakly, while benzo[e]pyrene and phenobarbital were essentially inactive as inducers.	Methylcholanthrene	0-20	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	93-99
8380963-4	1993	3-Methylcholanthrene, beta-naphthoflavone, and benz[alpha]anthracene were strong inducers of CYP1A1, benzo[alpha]pyrene induced CYP1A1 activity only weakly, while benzo[e]pyrene and phenobarbital were essentially inactive as inducers.	Methylcholanthrene	0-20	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	128-134
7805614-4	1993	MC increased only the content of cytochrome b5.	Methylcholanthrene	0-2	cytochrome b5 type A	Rattus norvegicus	33-46
7680337-7	1993	Exposure to phenobarbital on Days 3 to 6 increased the total cytochrome P-450 content twofold; exposure to 3-methylcholanthrene increased the activity of the corresponding cytochrome P-450 isoforms to 20 times that observed in untreated cultures and 6 times that observed in freshly isolated cells.	Methylcholanthrene	107-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	172-188
8255142-2	1993	This oxidation is inversely influenced by cytochrome P-450 inducers in the rat such as 3-methylcholantrene (3-MC) and phenobarbital (PB).	Methylcholanthrene	108-112	cytochrome P-450	Oryctolagus cuniculus	42-58
1282830-1	1992	Three cDNAs coding for monkey cytochrome P-450 (P450) 2C, 2E and 3A (MKmp13, MKj1 and MKnf2, respectively) were isolated from a lambda gt11 cDNA library of a liver from a 3-methylcholanthrene (3MC)-treated crab-eating monkey, using cDNA fragments for human P450 2C, 2E and 3A as respective probes.	Methylcholanthrene	171-191	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-67
1282830-1	1992	Three cDNAs coding for monkey cytochrome P-450 (P450) 2C, 2E and 3A (MKmp13, MKj1 and MKnf2, respectively) were isolated from a lambda gt11 cDNA library of a liver from a 3-methylcholanthrene (3MC)-treated crab-eating monkey, using cDNA fragments for human P450 2C, 2E and 3A as respective probes.	Methylcholanthrene	193-196	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-67
1362526-4	1992	gamma-GT immunoreactivity was restricted to the MC and to basolateral and apical membranes of BG acinar and duct cells.	Methylcholanthrene	48-50	gamma-glutamyltransferase 1	Rattus norvegicus	0-8
1362526-7	1992	In the MC, gamma-GT immunoreactivity was associated primarily with brush borders of ciliated cells.	Methylcholanthrene	7-9	gamma-glutamyltransferase 1	Rattus norvegicus	11-19
1335374-8	1992	These data suggest that the Ah receptor liganded with MC and related PAHs induced a broad spectrum of antiestrogenic responses in MCF-7 cells and complements the results of previous studies which report the antiestrogenic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and other halogenated aromatics which are also Ah receptor agonists.	Methylcholanthrene	54-56	aryl hydrocarbon receptor	Homo sapiens	28-39
1335374-8	1992	These data suggest that the Ah receptor liganded with MC and related PAHs induced a broad spectrum of antiestrogenic responses in MCF-7 cells and complements the results of previous studies which report the antiestrogenic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and other halogenated aromatics which are also Ah receptor agonists.	Methylcholanthrene	54-56	aryl hydrocarbon receptor	Homo sapiens	316-327
1335375-2	1992	The expression of 3-methylcholanthrene (MCA)-induced CYP1A1 mRNA remained high during the observation period under both monolayer and spheroid culture conditions.	Methylcholanthrene	18-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	53-59
1335375-2	1992	The expression of 3-methylcholanthrene (MCA)-induced CYP1A1 mRNA remained high during the observation period under both monolayer and spheroid culture conditions.	Methylcholanthrene	40-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	53-59
1435739-0	1992	Mono- and diglucuronide formation from chrysene and benzo(a)pyrene phenols by 3-methylcholanthrene-inducible phenol UDP-glucuronosyltransferase (UGT1A1).	Methylcholanthrene	78-98	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	145-151
1462357-6	1992	These in vivo results suggest organ specificity in modulating the microsomal cytochrome P-450 (MC) content of hepatic and extra-hepatic tissues by the three compounds.	Methylcholanthrene	95-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
1416978-6	1992	Other inducers of xenobiotic metabolism, such as 3-methylcholanthrene and beta-naphthoflavone, also induced ALDH-3 mRNA to a similar level as TCDD, whereas antioxidants or electrophiles, such as tert-butylhydroquinone and dimethyl fumarate, did not show any induction of ALDH-3 mRNA.	Methylcholanthrene	49-69	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	108-114
1416978-6	1992	Other inducers of xenobiotic metabolism, such as 3-methylcholanthrene and beta-naphthoflavone, also induced ALDH-3 mRNA to a similar level as TCDD, whereas antioxidants or electrophiles, such as tert-butylhydroquinone and dimethyl fumarate, did not show any induction of ALDH-3 mRNA.	Methylcholanthrene	49-69	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	271-277
1443430-0	1992	Differences in hepatic microsomal cytochrome P-450 isoenzyme induction by pyrazole, chronic ethanol, 3-methylcholanthrene, and phenobarbital in high alcohol sensitivity (HAS) and low alcohol sensitivity (LAS) rats.	Methylcholanthrene	101-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	34-50
1340118-4	1992	Transgene expression in mice directed by the Cyp1a-1 promoter and enhancer elements can be increased in the liver up to 10,000-fold by administration to the animals of the inducer, 3-methylcholanthrene.	Methylcholanthrene	181-201	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	45-52
1435739-1	1992	Mono- and diphenols of chrysene and benzo(a)pyrene are suspected substrates of a 3-methylcholanthrene (MC)-inducible phenol UDP-glucuronosyltransferase (UGT1A1).	Methylcholanthrene	81-101	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	153-159
1435739-1	1992	Mono- and diphenols of chrysene and benzo(a)pyrene are suspected substrates of a 3-methylcholanthrene (MC)-inducible phenol UDP-glucuronosyltransferase (UGT1A1).	Methylcholanthrene	103-105	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	153-159
1329733-8	1992	Furthermore, our study indicates that CYP 1A1, induced by 3-MC, demonstrates an unusually low oxidase activity.	Methylcholanthrene	58-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-45
1352550-6	1992	In the same cell type, a 24-hr pretreatment with the inducer of cytochrome P-450 3-methylcholanthrene (10 microM) augmented cyclic GMP stimulation by GTN or isoidide dinitrate by up to 102%.	Methylcholanthrene	81-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
1426026-1	1992	The identity of the sigma receptor as a form of cytochrome P-450 was investigated in rats treated with 3-methylcholanthrene or phenobarbital.	Methylcholanthrene	103-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
1398354-9	1992	This study shows that the polychlorinated biphenyl with the 3-methylcholanthrene-type pattern of induction of cytochrome P-450 has more profound effects on B group vitamins and particularly vitamin A homeostasis than does the phenobarbital-type inducer.	Methylcholanthrene	60-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	110-126
1341266-10	1992	The increase in ODC activity led to an increase in polyamine biosynthesis; putrescine, spermidine, and spermine levels in MC-26 cells were significantly elevated by 24 h after treatment with NaB.	Methylcholanthrene	122-124	ornithine decarboxylase, structural 1	Mus musculus	16-19
1641859-7	1992	T4 UDP-GT activity was increased by PB, 3MC, PCN, and CLO 88, 150, 100, and 160%, respectively on a per-milligram-microsomal-protein basis and 138, 125, 100, and 145% on a per-kilogram-body-weight basis, respectively.	Methylcholanthrene	40-43	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	3-9
1638686-14	1992	MC-treated rats, on the other hand, displayed elevated levels of liver cytochrome P450 and ECD at 8 days.	Methylcholanthrene	0-2	ecdysoneless cell cycle regulator	Rattus norvegicus	91-94
1638686-15	1992	In kidney, PB and PCN did not elicit induction of P450 and individual enzymes, but MC increased total P450 content and ECD activity at 1 day, and ECD activity alone at 8 days.	Methylcholanthrene	83-85	ecdysoneless cell cycle regulator	Rattus norvegicus	119-122
1455607-2	1992	The mice had been previously treated with the AHH inducer 3-methylcholanthrene (MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or vehicle (olive oil) alone.	Methylcholanthrene	58-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	46-49
1455607-6	1992	Simultaneous treatment or pre-treatment with 7,8-BF produced an inhibitory effect on AHH induction by MC or TCDD.	Methylcholanthrene	102-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	85-88
1455607-7	1992	Post-treatment with 7,8-BF inclined to promote the induction of AHH by MC or TCDD.	Methylcholanthrene	71-73	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	64-67
1638671-7	1992	Pretreatment with phorone or the carcinogens mirex and 3-methylcholanthrene significantly decreases GRc binding and nuclear uptake in vivo, as well as diminishes intracellular cytosolic GSH levels.	Methylcholanthrene	55-75	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	100-103
1459314-1	1992	Recently, we have documented an abnormal in vivo complement metabolism in Type 1 diabetic children treated with monocomponent porcine insulin Monotard MC and its correction after switch-over to human insulin Protaphane HM.	Methylcholanthrene	151-153	insulin	Homo sapiens	134-141
1302196-4	1992	3-MC treatment elevated rat liver microsomal cytochrome P-448, enhancing S-oxidation of Yekuling.	Methylcholanthrene	0-4	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	45-61
1517151-3	1992	PSK also inhibited the growth of a methylcholanthrene-induced fibrosarcoma BAMC-1, and a methylurethane-induced adenocarcinoma Colon 26 in the double grafted tumor system of syngeneic BALB/c mice.	Methylcholanthrene	35-53	TAO kinase 2	Mus musculus	0-3
1622155-1	1992	It has been previously found that local administration of X63-m-IL-2 cells transformed by interleukin 2 (IL-2) cDNA and constitutively producing large quantities of IL-2 mediated regressions of murine plasmacytomas and 3-methyl-cholanthrene-induced sarcomas transplanted in syngeneic mice.	Methylcholanthrene	219-240	interleukin 2	Mus musculus	64-68
1567206-3	1992	Cytochromes P450IA1 and IA2 were purified from hepatic microsomes from 3-methylcholanthrene (MC)-treated C57BL/6 mice, using a combination of affinity chromatography and high performance liquid chromatography.	Methylcholanthrene	71-91	protein tyrosine phosphatase, receptor type, N	Mus musculus	24-27
1567478-3	1992	"Native" versus optimal detergent-activated T4 UGT activity determination revealed that the latency of T4 UGT in microsomes from 3-MC-treated rats was decreased while the latency of T4 UGT in microsomes from PB-treated rats was increased compared to control, and suggest that the UGT isoenzyme(s) involved in the hepatic glucuronidation of T4 is (are) different in PB-treated rats than in 3-MC-treated rats.	Methylcholanthrene	129-133	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	47-50
1567206-3	1992	Cytochromes P450IA1 and IA2 were purified from hepatic microsomes from 3-methylcholanthrene (MC)-treated C57BL/6 mice, using a combination of affinity chromatography and high performance liquid chromatography.	Methylcholanthrene	93-95	protein tyrosine phosphatase, receptor type, N	Mus musculus	24-27
1413866-2	1992	The content and specific activities of inducible cytochrome P-450 enzymes were determined in liver microsomes of rats of various ages after maximal induction with phenobarbital, isosafrole of 3-methylcholanthrene, and in untreated animals.	Methylcholanthrene	192-212	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
1314586-3	1992	Cotransfection of an expression vector of the Ah receptor with a reporter plasmid pMC6.3k consisting of CYP1A1 promoter and CAT structural gene into CV-1 cells enhanced the CAT expression in response to added 3-methylcholanthrene.	Methylcholanthrene	209-229	aryl-hydrocarbon receptor	Mus musculus	46-57
1567478-6	1992	The results thus extend evidence that both 3-MC and PB induce the synthesis of UGT protein(s) involved in the glucuronidation of T4, 3-MC being a strong and PB a weak inducer.	Methylcholanthrene	43-47	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	79-82
1567478-6	1992	The results thus extend evidence that both 3-MC and PB induce the synthesis of UGT protein(s) involved in the glucuronidation of T4, 3-MC being a strong and PB a weak inducer.	Methylcholanthrene	133-137	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	79-82
1606251-0	1992	Antitumor activity of Toxoplasma lysate antigen against methylcholanthrene-induced tumor-bearing rats.	Methylcholanthrene	56-74	RT1 class Ib, locus T18	Rattus norvegicus	22-47
1593570-3	1992	MC isolated from inflammatory SF produced, in addition to variable levels of IL-1, a specific IL-1 inhibitor of approximately 23 kDa which blocked both IL-1 biological activity and binding to its receptor.	Methylcholanthrene	0-2	interleukin 1 alpha	Homo sapiens	77-81
1593570-3	1992	MC isolated from inflammatory SF produced, in addition to variable levels of IL-1, a specific IL-1 inhibitor of approximately 23 kDa which blocked both IL-1 biological activity and binding to its receptor.	Methylcholanthrene	0-2	interleukin 1 alpha	Homo sapiens	94-98
1593570-3	1992	MC isolated from inflammatory SF produced, in addition to variable levels of IL-1, a specific IL-1 inhibitor of approximately 23 kDa which blocked both IL-1 biological activity and binding to its receptor.	Methylcholanthrene	0-2	interleukin 1 alpha	Homo sapiens	94-98
1545116-4	1992	Forty to fifty percent of MC in submandibular glands were CD3+ T cells, equally divided into CD4+ CD8- and CD4- CD8+ T cell subsets.	Methylcholanthrene	26-28	CD3 antigen, epsilon polypeptide	Mus musculus	58-61
1545116-7	1992	In contrast, approximately 70 to 90% of MC in periglandular lymph nodes and cervical lymph nodes were CD3+ T cells and like the peripheral lymph nodes consisted of fivefold higher numbers of CD4+ CD8- than CD4- CD8+ T cells, with low numbers of DN cells (less than 5%).	Methylcholanthrene	40-42	CD3 antigen, epsilon polypeptide	Mus musculus	102-105
1606251-1	1992	Growth of the tumor autoinduced by 20-methylcholanthrene (MC) in rats was inhibited after administration of Toxoplasma lysate antigen (TLA).	Methylcholanthrene	35-56	RT1 class Ib, locus T18	Rattus norvegicus	108-133
1606251-1	1992	Growth of the tumor autoinduced by 20-methylcholanthrene (MC) in rats was inhibited after administration of Toxoplasma lysate antigen (TLA).	Methylcholanthrene	35-56	RT1 class Ib, locus T18	Rattus norvegicus	135-138
1606251-1	1992	Growth of the tumor autoinduced by 20-methylcholanthrene (MC) in rats was inhibited after administration of Toxoplasma lysate antigen (TLA).	Methylcholanthrene	58-60	RT1 class Ib, locus T18	Rattus norvegicus	108-133
1606251-1	1992	Growth of the tumor autoinduced by 20-methylcholanthrene (MC) in rats was inhibited after administration of Toxoplasma lysate antigen (TLA).	Methylcholanthrene	58-60	RT1 class Ib, locus T18	Rattus norvegicus	135-138
1606251-6	1992	These observations indicate that TLA is a useful modifier of biological responses to MC-induced tumors.	Methylcholanthrene	85-87	RT1 class Ib, locus T18	Rattus norvegicus	33-36
1372830-7	1992	Separation of DT-diaphorase isoforms from control rat liver cytosol using FPLC-chromatofocusing revealed that the induction of the isoforms is not uniform, since isform II was not found and the major isoform was composed of three peaks, whereas the major isoform of DT-diaphorase from liver cytosol of rats treated with 3-methylcholanthrene was composed of only two peaks.	Methylcholanthrene	320-340	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	14-27
1505106-4	1992	The results showed a significant increase in NAP-1 production by synovial fluid MC when compared to peripheral blood MC.	Methylcholanthrene	80-82	C-X-C motif chemokine ligand 8	Homo sapiens	45-50
1373232-3	1992	MC and monocytes from adult and neonatal subjects produced mRNA for GM-CSF, G-CSF, and M-CSF, whereas T cells produced only GM-CSF mRNA.	Methylcholanthrene	0-2	colony stimulating factor 2	Homo sapiens	68-74
1373232-3	1992	MC and monocytes from adult and neonatal subjects produced mRNA for GM-CSF, G-CSF, and M-CSF, whereas T cells produced only GM-CSF mRNA.	Methylcholanthrene	0-2	colony stimulating factor 3	Homo sapiens	76-81
1373232-3	1992	MC and monocytes from adult and neonatal subjects produced mRNA for GM-CSF, G-CSF, and M-CSF, whereas T cells produced only GM-CSF mRNA.	Methylcholanthrene	0-2	colony stimulating factor 1	Homo sapiens	69-74
1373232-6	1992	Neonatal MC also accumulated similar amounts of G-CSF mRNA and somewhat more M-CSF mRNA than did adult MC; results with monocytes were similar to those with MC.	Methylcholanthrene	9-11	colony stimulating factor 3	Homo sapiens	48-53
1373232-6	1992	Neonatal MC also accumulated similar amounts of G-CSF mRNA and somewhat more M-CSF mRNA than did adult MC; results with monocytes were similar to those with MC.	Methylcholanthrene	9-11	colony stimulating factor 1	Homo sapiens	77-82
1553756-1	1992	Glutathione S-transferase (GST) expression was examined in hepatic cytosol from rats and rabbits treated with 4-picoline, pyrrole, pyridine, pyrazine, imidazole, or piperidine using enzymatic activity, SDS-PAGE, and immunoblot analyses and the results were compared to those obtained with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	307-327	hematopoietic prostaglandin D synthase	Rattus norvegicus	27-30
1553756-5	1992	While phenobarbital and 3-methylcholanthrene induce class alpha and mu GST expression in rat hepatic cytosol, one of the most interesting observations was that neither of these agents stimulated GST expression in the rabbit.	Methylcholanthrene	24-44	hematopoietic prostaglandin D synthase	Rattus norvegicus	71-74
1531454-11	1992	In contrast, anti-IFN-gamma resulted in a small decrease in the ability of liver MC to suppress Con A (but not LPS)-stimulated cell proliferation.	Methylcholanthrene	81-83	interferon gamma	Mus musculus	18-27
1573708-5	1992	At 1, 4, and 8 mg/kg i.v., and at 15, 30, 45, and 60 mg/kg orally, MC increased (P less than 0.05) serum PRL concentrations (difference between maximal and basal serum PRL concentrations) and increased (P less than 0.05) areas under the PRL response curves except for 1.0 mg/kg i.v.	Methylcholanthrene	67-69	prolactin	Homo sapiens	105-108
1573708-5	1992	At 1, 4, and 8 mg/kg i.v., and at 15, 30, 45, and 60 mg/kg orally, MC increased (P less than 0.05) serum PRL concentrations (difference between maximal and basal serum PRL concentrations) and increased (P less than 0.05) areas under the PRL response curves except for 1.0 mg/kg i.v.	Methylcholanthrene	67-69	prolactin	Homo sapiens	168-171
1573708-5	1992	At 1, 4, and 8 mg/kg i.v., and at 15, 30, 45, and 60 mg/kg orally, MC increased (P less than 0.05) serum PRL concentrations (difference between maximal and basal serum PRL concentrations) and increased (P less than 0.05) areas under the PRL response curves except for 1.0 mg/kg i.v.	Methylcholanthrene	67-69	prolactin	Homo sapiens	168-171
1573708-7	1992	These studies determined a dose-response to MC in terms of serum PRL concentration and indicate that MC is well tolerated and effective for elevating serum PRL concentrations in steers.	Methylcholanthrene	44-46	prolactin	Homo sapiens	65-68
1573708-7	1992	These studies determined a dose-response to MC in terms of serum PRL concentration and indicate that MC is well tolerated and effective for elevating serum PRL concentrations in steers.	Methylcholanthrene	101-103	prolactin	Homo sapiens	156-159
1373232-2	1992	Because granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) play critical roles in the production of neutrophils from marrow precursors, we assessed the ability of leukocytes from neonates and adults to produce GM-CSF, G-CSF, and, for comparison, macrophage colony-stimulating factor (M-CSF) after stimulation with concanavalin A +/- phorbol myristate acetate [blood mononuclear cells (MC) and T lymphocytes] or lipopolysaccharide (monocytes).	Methylcholanthrene	442-444	colony stimulating factor 3	Homo sapiens	109-114
1553754-6	1992	UDP-GT activity toward T4 was increased by PB, 3MC, PCN, and PCB 270, 400, 570, and 660%, respectively, and was found to correlate with serum T4 levels (total and free).	Methylcholanthrene	47-50	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
1553756-1	1992	Glutathione S-transferase (GST) expression was examined in hepatic cytosol from rats and rabbits treated with 4-picoline, pyrrole, pyridine, pyrazine, imidazole, or piperidine using enzymatic activity, SDS-PAGE, and immunoblot analyses and the results were compared to those obtained with phenobarbital and 3-methylcholanthrene.	Methylcholanthrene	307-327	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-25
1323998-2	1992	The presence of specific binding sites on MC-26 cells for gastrin-releasing peptide (GRP)/BBS-related peptides was recently reported by us.	Methylcholanthrene	42-44	gastrin releasing peptide	Mus musculus	58-83
1323998-2	1992	The presence of specific binding sites on MC-26 cells for gastrin-releasing peptide (GRP)/BBS-related peptides was recently reported by us.	Methylcholanthrene	42-44	gastrin releasing peptide	Mus musculus	85-88
1323998-5	1992	A possible autocrine role of GRP in the growth of MC-26 cells was also investigated.	Methylcholanthrene	50-52	gastrin releasing peptide	Mus musculus	29-32
1606640-5	1992	However, the microsomes from rats treated with 3-methylcholanthrene, an inducer of DT-diaphorase, did not have stimulative effect greater than the control microsomes.	Methylcholanthrene	47-67	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	83-96
1288050-5	1992	3-methylcholanthrene on various cytochrome P450 and P448 dependent hepatic microsomal enzyme activities was studied in male albino Wistar rats.	Methylcholanthrene	0-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-47
1740588-8	1992	These findings suggest that there is no difference in genetic immunoregulation between subjects with SPSTs and MPSTs but that the presence of the DR4 gene product is associated with a decreased risk of an IgE response to MC and protection from MC pollenosis.	Methylcholanthrene	221-223	major histocompatibility complex, class II, DR beta 4	Homo sapiens	146-149
1740588-8	1992	These findings suggest that there is no difference in genetic immunoregulation between subjects with SPSTs and MPSTs but that the presence of the DR4 gene product is associated with a decreased risk of an IgE response to MC and protection from MC pollenosis.	Methylcholanthrene	244-246	major histocompatibility complex, class II, DR beta 4	Homo sapiens	146-149
1558892-0	1992	Therapeutic effects of Toxoplasma lysate antigen on 20-methylcholanthrene-induced BALB/c mouse tumors.	Methylcholanthrene	52-73	histocompatibility 2, T region locus 18	Mus musculus	23-48
1288050-10	1992	The activity of the cytochrome P448 dependent 7-ethoxyresorufin O-deethylase was enhanced by all three substances, but flumecinol"s effect was by far behind that of 3-methylcholanthrene, so the carcinogenic promoter effect of flumecinol can be questioned.	Methylcholanthrene	165-185	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	20-35
1778655-1	1991	Temporal variations in cytochrome P-450 isozymes of rat testis, PB-P-450 (forms of cytochrome P-450 strongly induced by phenobarbital) and MC-P-448 (forms of cytochrome P-450 strongly induced by 3-methylcholanthrene), were investigated immunohistochemically by the avidin-biotin-complex method using specific antibodies against PB-P-450 and MC-P-448 isozymes.	Methylcholanthrene	195-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
1581109-4	1992	1,25-(OH)2D3-dependent alkaline phosphatase and phospholipase A2 activity were correlated with production of PGE2 and PGE1 in the MC-3T3-E1 cells.	Methylcholanthrene	130-132	phospholipase A2 group IB	Homo sapiens	48-64
1764102-0	1991	Oxidative conversion of 6-fluorobenzo(c)phenanthrene to its K-region oxide by liver microsomes from 3-methylcholanthrene treated rats: reversal of stereoselectivity of cytochrome P-450c due to the influence of fluoro group.	Methylcholanthrene	100-120	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	168-185
1959995-1	1991	We have evaluated the relationship between MHC class-I, c-myc and c-fos proto-oncogene expression in several clones of a methylcholanthrene-induced fibrosarcoma (GR9) which originated in a BALB/c mouse.	Methylcholanthrene	121-139	FBJ osteosarcoma oncogene	Mus musculus	66-71
1418947-12	1992	Only MC from treated organ cultures produced nodules under SRC.	Methylcholanthrene	5-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	59-62
1316759-8	1992	Slot-blot analysis of total RNA isolated from these cells indicated that BeP, BaP, and 3-methylcholanthrene increased the level of CYP1A1 mRNA expression.	Methylcholanthrene	87-107	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	131-137
1800893-3	1991	In the genetically engineered cell lines, benzo[a]pyrene was metabolized specifically by the 3-methylcholanthrene inducible rat liver CYP1A1 (cell line XEM2) whereas cyclophosphamide increased the micronucleus frequency only in cultures expressing the phenobarbital inducible CYP2B1 (SD1).	Methylcholanthrene	93-113	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	134-140
1834380-2	1991	Growth of a methylcholanthrene-induced fibrosarcoma in BALB/c mice was accompanied by an increase in the activation state of tumour-associated macrophages (TAM), as measured by their FcIgG receptor expression, phagocytic index and beta-glucuronidase levels.	Methylcholanthrene	12-30	glucuronidase, beta	Mus musculus	231-249
1744582-3	1991	In this report, we demonstrate that antitumor cytotoxic T lymphocytes (CTL) generated by secondary in vitro sensitization of draining lymph node cells in IL-7 are effective in treating 3-day syngeneic methylcholanthrene (MCA) sarcoma pulmonary metastases in mice.	Methylcholanthrene	201-219	interleukin 7	Mus musculus	154-158
1744582-3	1991	In this report, we demonstrate that antitumor cytotoxic T lymphocytes (CTL) generated by secondary in vitro sensitization of draining lymph node cells in IL-7 are effective in treating 3-day syngeneic methylcholanthrene (MCA) sarcoma pulmonary metastases in mice.	Methylcholanthrene	221-224	interleukin 7	Mus musculus	154-158
1790212-3	1991	During the early stages of less than 44 cm crown rump length (CRL), fibronectin (FN) was distributed densely in the MC.	Methylcholanthrene	116-118	fibronectin 1	Bos taurus	68-79
1790212-3	1991	During the early stages of less than 44 cm crown rump length (CRL), fibronectin (FN) was distributed densely in the MC.	Methylcholanthrene	116-118	fibronectin 1	Bos taurus	81-83
1771946-1	1991	A cocktail of four model substances orally administered to humans is used for simultaneous characterization of phenobarbital and 3-methylcholanthrene inducible forms of cytochrome-P450 and two genetic polymorphisms, the debrisoquine hydroxylation and N-acetylation.	Methylcholanthrene	129-149	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	169-184
1769689-9	1991	Treatment with MCA to CD8-positive cells at the beginning of culture did not block proliferation significantly, but treatment either before or after the 5-day culture period blocked CTL responses.	Methylcholanthrene	15-18	CD8a molecule	Homo sapiens	22-25
1800893-3	1991	In the genetically engineered cell lines, benzo[a]pyrene was metabolized specifically by the 3-methylcholanthrene inducible rat liver CYP1A1 (cell line XEM2) whereas cyclophosphamide increased the micronucleus frequency only in cultures expressing the phenobarbital inducible CYP2B1 (SD1).	Methylcholanthrene	93-113	CUP2Q35	Homo sapiens	284-287
1932143-7	1991	P450IA1 and IA2 (3-methylcholanthrene-inducible forms) and P450IIB1 and IIB2 (phenobarbital-inducible forms) were detected at low levels in rats of both sexes at all ages.	Methylcholanthrene	17-37	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	12-15
1949040-2	1991	hUDP-GT activity toward thyroxine (T4; hUDP-GT-T4) was induced by treatment with beta-naphthoflavone, 3-methylcholanthrene (3-MC), polychlorinated biphenyls, or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	102-122	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	0-7
1654865-1	1991	The Ah (aromatic hydrocarbon) receptor mediates induction of aryl hydrocarbon hydroxylase (AHH; an enzyme activity associated with cytochrome P450IA1) by polycyclic aromatic hydrocarbon carcinogens such as 3-methylcholanthrene (MC) and benzo[a]pyrene (BP) and the halogenated toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	206-226	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	61-89
1654865-1	1991	The Ah (aromatic hydrocarbon) receptor mediates induction of aryl hydrocarbon hydroxylase (AHH; an enzyme activity associated with cytochrome P450IA1) by polycyclic aromatic hydrocarbon carcinogens such as 3-methylcholanthrene (MC) and benzo[a]pyrene (BP) and the halogenated toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	206-226	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	91-94
1654865-1	1991	The Ah (aromatic hydrocarbon) receptor mediates induction of aryl hydrocarbon hydroxylase (AHH; an enzyme activity associated with cytochrome P450IA1) by polycyclic aromatic hydrocarbon carcinogens such as 3-methylcholanthrene (MC) and benzo[a]pyrene (BP) and the halogenated toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	228-230	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	61-89
1654865-1	1991	The Ah (aromatic hydrocarbon) receptor mediates induction of aryl hydrocarbon hydroxylase (AHH; an enzyme activity associated with cytochrome P450IA1) by polycyclic aromatic hydrocarbon carcinogens such as 3-methylcholanthrene (MC) and benzo[a]pyrene (BP) and the halogenated toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Methylcholanthrene	228-230	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	91-94
1654865-7	1991	As with Hepa-1, the human LS180 cytosolic AhR sedimented at about 9 S on sucrose gradients when detected with [3H]TCDD, [3H]BP or [3H]MC.	Methylcholanthrene	134-136	aryl hydrocarbon receptor	Homo sapiens	42-45
1654865-13	1991	The lower sensitivity of the LS180 cells to induction of AHH activity by TCDD or BA is consistent with the lower affinity of TCDD and MC for binding to human AhR.	Methylcholanthrene	134-136	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	57-60
1654865-13	1991	The lower sensitivity of the LS180 cells to induction of AHH activity by TCDD or BA is consistent with the lower affinity of TCDD and MC for binding to human AhR.	Methylcholanthrene	134-136	aryl hydrocarbon receptor	Homo sapiens	158-161
1686852-0	1991	[Precancerous and cancerous lesions and their gamma-glutamyl transpeptidase expression in 3-methylcholanthrene-induced lung carcinogenesis in rats].	Methylcholanthrene	90-110	gamma-glutamyltransferase 1	Rattus norvegicus	46-75
1949040-2	1991	hUDP-GT activity toward thyroxine (T4; hUDP-GT-T4) was induced by treatment with beta-naphthoflavone, 3-methylcholanthrene (3-MC), polychlorinated biphenyls, or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	102-122	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	39-46
1949040-2	1991	hUDP-GT activity toward thyroxine (T4; hUDP-GT-T4) was induced by treatment with beta-naphthoflavone, 3-methylcholanthrene (3-MC), polychlorinated biphenyls, or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	124-128	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	0-7
1949040-2	1991	hUDP-GT activity toward thyroxine (T4; hUDP-GT-T4) was induced by treatment with beta-naphthoflavone, 3-methylcholanthrene (3-MC), polychlorinated biphenyls, or pregnenolone-16 alpha-carbonitrile.	Methylcholanthrene	124-128	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	39-46
1949040-5	1991	Moreover, the induction profile of both hUDP-GT-T4 and hUDP-GT-T3 was similar to that of hUDP-GT toward 1-naphthol, but not chloramphenicol, suggesting that T4 and T3 belong to the so-called group-1 substrates which are preferentially glucuronidated by hUDP-GT(s) inducible by treatment with 3-MC.	Methylcholanthrene	292-296	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	40-47
1717446-0	1991	Molecular basis for the lack of bilirubin-specific and 3-methylcholanthrene-inducible UDP-glucuronosyltransferase activities in Gunn rats.	Methylcholanthrene	55-75	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	86-113
1717446-3	1991	In addition, a UDPGT isoform which is active toward 4-nitrophenol and is induced by 3-methylcholanthrene (3-MC) in normal rats, is produced in a nonfunctional truncated form in Gunn rats due to the deletion of a single guanosine residue in the coding region of its mRNA.	Methylcholanthrene	84-104	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	15-20
1949040-5	1991	Moreover, the induction profile of both hUDP-GT-T4 and hUDP-GT-T3 was similar to that of hUDP-GT toward 1-naphthol, but not chloramphenicol, suggesting that T4 and T3 belong to the so-called group-1 substrates which are preferentially glucuronidated by hUDP-GT(s) inducible by treatment with 3-MC.	Methylcholanthrene	292-296	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	55-62
1717446-3	1991	In addition, a UDPGT isoform which is active toward 4-nitrophenol and is induced by 3-methylcholanthrene (3-MC) in normal rats, is produced in a nonfunctional truncated form in Gunn rats due to the deletion of a single guanosine residue in the coding region of its mRNA.	Methylcholanthrene	106-110	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	15-20
1949040-5	1991	Moreover, the induction profile of both hUDP-GT-T4 and hUDP-GT-T3 was similar to that of hUDP-GT toward 1-naphthol, but not chloramphenicol, suggesting that T4 and T3 belong to the so-called group-1 substrates which are preferentially glucuronidated by hUDP-GT(s) inducible by treatment with 3-MC.	Methylcholanthrene	292-296	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	55-62
1717446-6	1991	3" regions of bilirubin- and 3-MC-inducible UDPGT mRNAs have identical nucleotide sequences; the single base deletion in the 3-MC-inducible UDPGT in Gunn rats occurs within this region.	Methylcholanthrene	29-33	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	44-49
1717446-6	1991	3" regions of bilirubin- and 3-MC-inducible UDPGT mRNAs have identical nucleotide sequences; the single base deletion in the 3-MC-inducible UDPGT in Gunn rats occurs within this region.	Methylcholanthrene	29-33	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	140-145
1717446-6	1991	3" regions of bilirubin- and 3-MC-inducible UDPGT mRNAs have identical nucleotide sequences; the single base deletion in the 3-MC-inducible UDPGT in Gunn rats occurs within this region.	Methylcholanthrene	125-129	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	44-49
1717446-6	1991	3" regions of bilirubin- and 3-MC-inducible UDPGT mRNAs have identical nucleotide sequences; the single base deletion in the 3-MC-inducible UDPGT in Gunn rats occurs within this region.	Methylcholanthrene	125-129	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	140-145
1717446-9	1991	Nucleotide sequence determination revealed that bilirubin- and 3-MC-inducible UDPGT mRNAs in Gunn rats contain an identical frame-shift deletion of a single guanosine residue within the common region of their coding sequences.	Methylcholanthrene	63-67	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	78-83
1949040-5	1991	Moreover, the induction profile of both hUDP-GT-T4 and hUDP-GT-T3 was similar to that of hUDP-GT toward 1-naphthol, but not chloramphenicol, suggesting that T4 and T3 belong to the so-called group-1 substrates which are preferentially glucuronidated by hUDP-GT(s) inducible by treatment with 3-MC.	Methylcholanthrene	292-296	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	55-62
1788977-9	1991	Similarly, MC induced 7-ethoxycoumarin O-deethylase activity (up to 2000% increase from 5 to 45 days) as well as immunoreactive P-450c (IA1) in the hepatocyte cultures.	Methylcholanthrene	11-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	128-139
1681808-9	1991	Phenobarbital, methylcholanthrene and dexamethasone were found to increase significantly gamma-glutamyltransferase while tyrosine aminotransferase activity was enhanced by dexamethasone.	Methylcholanthrene	15-33	gamma-glutamyltransferase 1	Rattus norvegicus	89-114
1800796-3	1991	The level of P-450Md mRNA in female rats was increased by phenobarbital or dexamethasone treatment, whereas the level in the males was depressed by methylcholanthrene.	Methylcholanthrene	148-166	cytochrome P450, family 2, subfamily c, polypeptide 22	Rattus norvegicus	13-20
1650214-9	1991	The Mz-Hep-1 Ah receptor sedimented in continuous sucrose gradients at approximately 9 S. Specificity of binding by [3H]TCDD was demonstrated by competitive binding of non-radiolabeled 2,3,7,8-tetrachlorodibenzofuran, 3-methylcholanthrene (MC), and dibenz[a,h]anthracene in 50-fold molar excess.	Methylcholanthrene	218-238	DNL-type zinc finger	Homo sapiens	7-12
1914510-0	1991	Immunocytochemical study of phenobarbital- and 3-methylcholanthrene-inducible cytochrome P450 isozymes in primary cultures of porcine ciliary epithelium.	Methylcholanthrene	47-67	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-93
1761516-6	1991	A fusion gene which was constructed by ligating the upstream region of the human P-450c gene to the chloramphenicol acetyltransferase (CAT) gene expressed the CAT activity in response to the inducer, methylcholanthrene, when transfected into Hepa-1 cells.	Methylcholanthrene	200-218	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	81-87
1650214-9	1991	The Mz-Hep-1 Ah receptor sedimented in continuous sucrose gradients at approximately 9 S. Specificity of binding by [3H]TCDD was demonstrated by competitive binding of non-radiolabeled 2,3,7,8-tetrachlorodibenzofuran, 3-methylcholanthrene (MC), and dibenz[a,h]anthracene in 50-fold molar excess.	Methylcholanthrene	218-238	aryl hydrocarbon receptor	Homo sapiens	13-24
1650214-9	1991	The Mz-Hep-1 Ah receptor sedimented in continuous sucrose gradients at approximately 9 S. Specificity of binding by [3H]TCDD was demonstrated by competitive binding of non-radiolabeled 2,3,7,8-tetrachlorodibenzofuran, 3-methylcholanthrene (MC), and dibenz[a,h]anthracene in 50-fold molar excess.	Methylcholanthrene	240-242	DNL-type zinc finger	Homo sapiens	7-12
1650214-9	1991	The Mz-Hep-1 Ah receptor sedimented in continuous sucrose gradients at approximately 9 S. Specificity of binding by [3H]TCDD was demonstrated by competitive binding of non-radiolabeled 2,3,7,8-tetrachlorodibenzofuran, 3-methylcholanthrene (MC), and dibenz[a,h]anthracene in 50-fold molar excess.	Methylcholanthrene	240-242	aryl hydrocarbon receptor	Homo sapiens	13-24
1906077-1	1991	Stimulation of multiple CD8+ murine tumor infiltrating lymphocyte (TIL) lines and one TIL clone with the tumor of origin of the TIL induced at least three-fold more secretion of TNF and/or INF-gamma than was elicited by other syngeneic, methylcholanthrene (MCA) induced sarcomas.	Methylcholanthrene	237-255	tumor necrosis factor	Mus musculus	178-181
1859448-6	1991	The induction of 7-ethoxyresorufin O-deethylase activity by 3-MC was potentiated whereas induction of 7-pentoxyresorufin- and 7-benzyloxyresorufin O-dealkylases by PB was suppressed by interferon alpha.	Methylcholanthrene	60-64	interferon alpha	Mus musculus	185-201
1906077-1	1991	Stimulation of multiple CD8+ murine tumor infiltrating lymphocyte (TIL) lines and one TIL clone with the tumor of origin of the TIL induced at least three-fold more secretion of TNF and/or INF-gamma than was elicited by other syngeneic, methylcholanthrene (MCA) induced sarcomas.	Methylcholanthrene	257-260	tumor necrosis factor	Mus musculus	178-181
1840486-2	1991	The mutation was found not only to be located in the region where bilirubin UDPGT cDNA shared an identical sequence with 3-methylcholanthrene (3M C)-inducible UDPGT cDNA but also to occur in the same position on the two cDNAs from the mutant rat.	Methylcholanthrene	121-141	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	76-81
1898024-3	1991	Treatment of rats with phenobarbital (PB) or 3-methylcholanthrene (MC) caused a slight reduction or less than a twofold increase, respectively, in the rate of total metabolism (per nanomole of cytochrome P450) of the enantiomeric dihydrodiols compared to microsomes from control rats.	Methylcholanthrene	45-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-208
1898024-3	1991	Treatment of rats with phenobarbital (PB) or 3-methylcholanthrene (MC) caused a slight reduction or less than a twofold increase, respectively, in the rate of total metabolism (per nanomole of cytochrome P450) of the enantiomeric dihydrodiols compared to microsomes from control rats.	Methylcholanthrene	67-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-208
1898024-5	1991	With either enantiomer of triphenylene 1,2-dihydrodiol, both purified cytochrome P450c (P450IA1) and liver microsomes from MC-treated rats formed diol epoxides and phenolic dihydrodiols in approximately equal amounts.	Methylcholanthrene	123-125	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-86
1898024-12	1991	Experiments with antibodies indicate that a large percentage of the metabolism by microsomes from control and PB-treated rats is catalyzed by cytochrome P450p (P450IIIA1), resulting in the altered stereoselectivity of these microsomes compared to that of the liver microsomes from MC-treated rats.	Methylcholanthrene	281-283	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
1840486-2	1991	The mutation was found not only to be located in the region where bilirubin UDPGT cDNA shared an identical sequence with 3-methylcholanthrene (3M C)-inducible UDPGT cDNA but also to occur in the same position on the two cDNAs from the mutant rat.	Methylcholanthrene	121-141	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	159-164
1876635-4	1991	In this study the growth hormone and cortisol responses were smaller in the MC group than the NMC group on both occasions.	Methylcholanthrene	76-78	growth hormone 1	Homo sapiens	18-32
2032239-1	1991	The presence of interleukin 4 receptor (IL-4R) on methylcholanthrene (MCA-106, MCA-102, and MC-38)- and viral DNA (G-2TS and 14-2TS)-induced murine sarcoma cells was demonstrated.	Methylcholanthrene	50-68	interleukin 4 receptor, alpha	Mus musculus	16-38
2032239-1	1991	The presence of interleukin 4 receptor (IL-4R) on methylcholanthrene (MCA-106, MCA-102, and MC-38)- and viral DNA (G-2TS and 14-2TS)-induced murine sarcoma cells was demonstrated.	Methylcholanthrene	50-68	interleukin 4 receptor, alpha	Mus musculus	40-45
1889831-2	1991	In vitro piperine caused concentration related inhibition (50% at 100 microM) of arylhydrocarbon hydroxylase (AHH) and 7-ethoxycourmarin deethylase (7ECDE) activities, which were comparable in control and 3-methylcholanthrene (3MC) treated rats.	Methylcholanthrene	205-225	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-113
1889831-2	1991	In vitro piperine caused concentration related inhibition (50% at 100 microM) of arylhydrocarbon hydroxylase (AHH) and 7-ethoxycourmarin deethylase (7ECDE) activities, which were comparable in control and 3-methylcholanthrene (3MC) treated rats.	Methylcholanthrene	227-230	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-113
1883912-2	1991	We have previously demonstrated that recombinant human interleukin-2 (IL-2) is effective in such an experimental setting involving a methylcholanthrene-induced fibrosarcoma in mice.	Methylcholanthrene	133-151	interleukin 2	Homo sapiens	55-68
1883912-2	1991	We have previously demonstrated that recombinant human interleukin-2 (IL-2) is effective in such an experimental setting involving a methylcholanthrene-induced fibrosarcoma in mice.	Methylcholanthrene	133-151	interleukin 2	Homo sapiens	70-74
2018565-4	1991	Immunoblot analysis revealed that AAF alone, or in concert with MC, induced comparable levels of the P450d form.	Methylcholanthrene	64-66	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	101-106
2018565-5	1991	Induction of cytochrome P450c by dietary MC was detected only when MC was fed together with AAF.	Methylcholanthrene	41-43	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-29
2018565-5	1991	Induction of cytochrome P450c by dietary MC was detected only when MC was fed together with AAF.	Methylcholanthrene	67-69	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-29
2018565-6	1991	As previously found for butylated hydroxytoluene (BHT), the protective effect of dietary MC against hepatocarcinogenesis in AAF-fed rats correlated with a preservation of nuclear envelope cytochrome P450 content and with the induction of cytochrome P450c.	Methylcholanthrene	89-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	238-254
1688125-4	1991	Both isoforms are overexpressed 10-fold in fl2; however, only b-70I is present in De-B30 and Mc, which contain an amount of total b-70 isoforms fivefold higher than in the wild type.	Methylcholanthrene	93-95	luminal-binding protein 2	Zea mays	62-66
1708245-4	1991	Using Northern and slot blot techniques, the induction of steady-state levels of CYPIA1 RNA was shown to occur as early as 4 hr following 3-methylcholanthrene injection.	Methylcholanthrene	138-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-87
2035621-5	1991	ET-1 caused immediate and sustained depolarization of MC and VSMC.	Methylcholanthrene	54-56	endothelin 1	Homo sapiens	0-4
1916587-2	1991	MC-type PCBs such as 3,4,3",4"-tetrachlorobiphenyl (TCB), 3,4,5,3",4"-pentachlorobiphenyl (PenCB) and 3,4,5,3",4",5"-hexachlorobiphenyl (HexCB) exhibited high acute toxicity in parallel with their induction ability of microsomal benzo[a]pyrene 3-hydroxylase and cytosolic DT-diaphorase.	Methylcholanthrene	0-2	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	272-285
1949900-6	1991	The antifungal derivative was a more potent inhibitor of the troleandomycin-nitrosoalkyl-cytochrome P-450 complex formation in DEX-induced microsomes than of the isosafrole-carbene-cytochrome P-450 complex formation in MC-pretreated rats.	Methylcholanthrene	219-221	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
1708245-2	1991	Determination of aryl hydrocarbon hydroxylase activity 24 hr after injection revealed that treatment with 3-methylcholanthrene resulted in a 10.5-fold stimulation of enzymatic activity in liver 800 x g supernatants.	Methylcholanthrene	106-126	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	17-45
1997155-7	1991	With microsomes from 3-methylcholanthrene-induced male rats, P-450 IA1 and/or IA2 were responsible for 60% of 3-hydroxylation and 40% of depentylation.	Methylcholanthrene	21-41	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	78-81
2051622-0	1991	[Immunohistochemical Study of 3-methylcholanthrene inducible cytochrome P-450 in the stomach and liver--a guide of postoperative chemotherapy in gastric cancer].	Methylcholanthrene	30-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	72-77
2051622-1	1991	Immunohistochemical determination of 3-methylcholanthrene (MC) inducible cytochrome P-450 (MC-P-450) was investigated in rat and human tissue, and its clinical availability was discussed.	Methylcholanthrene	37-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
2051622-1	1991	Immunohistochemical determination of 3-methylcholanthrene (MC) inducible cytochrome P-450 (MC-P-450) was investigated in rat and human tissue, and its clinical availability was discussed.	Methylcholanthrene	37-57	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-99
2051622-1	1991	Immunohistochemical determination of 3-methylcholanthrene (MC) inducible cytochrome P-450 (MC-P-450) was investigated in rat and human tissue, and its clinical availability was discussed.	Methylcholanthrene	59-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
2051622-1	1991	Immunohistochemical determination of 3-methylcholanthrene (MC) inducible cytochrome P-450 (MC-P-450) was investigated in rat and human tissue, and its clinical availability was discussed.	Methylcholanthrene	59-61	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-99
2051622-2	1991	Induced by MC, MC-P-450 in rat liver and stomach was well stained immunohistochemically, showing clear contrast against control without induction.	Methylcholanthrene	11-13	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	15-23
1672658-7	1991	These changes in insulin were dependent on the ratio of activated MCs to HIT cells with the effects clearly evident at an activated MC-HIT cell ratio of greater than or equal to 10:1.	Methylcholanthrene	66-68	insulin	Homo sapiens	17-24
1907967-6	1991	Rotational diffusion of cytochrome P-450 was dependent on the drug-induction with PB, MC, and PCB when compared with non-induced CON-microsomes.	Methylcholanthrene	86-88	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
1708163-2	1991	A monoclonal IgM antibody, H17, has been obtained from rats immunized with mouse fibrosarcoma cells from an in vitro established methylcholanthrene (MCA)-induced tumour.	Methylcholanthrene	129-147	H1.7 linker histone	Homo sapiens	27-30
1708163-2	1991	A monoclonal IgM antibody, H17, has been obtained from rats immunized with mouse fibrosarcoma cells from an in vitro established methylcholanthrene (MCA)-induced tumour.	Methylcholanthrene	149-152	H1.7 linker histone	Homo sapiens	27-30
1900006-0	1991	Induction of alkoxyresorufin O-dealkylases and UDP-glucuronosyl transferase by phenobarbital and 3-methylcholanthrene in primary cultures of porcine ciliary epithelial cells.	Methylcholanthrene	97-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-75
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	Methylcholanthrene	20-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
1985961-3	1991	Complex formation among the different forms of P-450 was probed by cross-linking of membrane proteins followed by immunopurification with a monoclonal antibody (mAb) to P-450c, the major 3-methylcholanthrene-inducible form.	Methylcholanthrene	187-207	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	169-175
1989524-6	1991	The inhibition of only 80% of the AHH activity present in MC liver microsomes by MAb 1-7-1 suggests that additional P450 forms are contributing to the overall AHH activity present in methylcholanthrene (MC)-liver microsomes as MAb 1-7-1 almost completely inhibits the AHH activity of expressed mIA1.	Methylcholanthrene	58-60	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	34-37
1988127-4	1991	When IL-2 coupled beads were mixed with methylcholanthrene-induced Mc7 or Mc107 sarcoma cells and injected into normal syngeneic Wistar rats, the growth of the tumor was suppressed.	Methylcholanthrene	40-58	interleukin 2	Rattus norvegicus	5-9
1899224-10	1991	To further test the biological relevancy of GH with respect to synthesis of TNF alpha, hemorrhagic necrosis of TNF alpha-sensitive murine methyl-cholanthrene-induced tumors was assessed in pituitary-intact mice.	Methylcholanthrene	138-157	tumor necrosis factor	Mus musculus	111-120
1985961-2	1991	The quaternary structure of rat liver cytochrome P-450 within microsomal membranes from 3-methyl-cholanthrene-treated rats was examined by a novel chemical cross-linking-monoclonal antibody approach.	Methylcholanthrene	88-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
1994898-3	1991	MAb 1-7-1 against P450IA1/IA2 inhibited markedly o-cresol formation and slightly p-cresol formation but not BA formation only in microsomes from MC-treated rats.	Methylcholanthrene	145-147	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	26-29
2069016-0	1991	Tissue difference in expression of cytochrome P-450 between liver and lung of Syrian golden hamsters treated with 3-methylcholanthrene.	Methylcholanthrene	114-134	cytochrome P450 2A3-like	Mesocricetus auratus	35-51
1846074-7	1991	Specific binding to the Ah receptor was also detected with [3H]MC and, to a lesser extent, with [3H]benzo[alpha]pyrene.	Methylcholanthrene	63-65	aryl hydrocarbon receptor	Homo sapiens	24-35
1914788-6	1991	In a parallel study, a gene for an inducible mouse UDPGT, designated UDPGTm-1, was shown by Northern blotting to be expressed in fetal liver by day 18 of gestation at low levels relative to adults, but was not induced transplacentally by MC, beta NF or phenobarbital (PB).	Methylcholanthrene	238-240	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	51-56
1868487-5	1991	Flow cytometry studies demonstrated that dietary restriction caused a marked increase of the proportion of Thy 1.2+, L3T4+ T cells in MC-treated diet-restricted mice.	Methylcholanthrene	134-136	thymus cell antigen 1, theta	Mus musculus	107-114
1868487-6	1991	Consistent with this result, T cell responses against concanavalin A and interleukin-2 were also potentiated in spleen cells obtained from MC-treated diet-restricted mice, while spleen cells obtained from MC-treated unrestricted mice showed decreased T cell responses because of their tumor burden.	Methylcholanthrene	139-141	interleukin 2	Mus musculus	73-86
1826444-0	1991	Down-regulation of SPARC/osteonectin/BM-40 expression in methylcholanthrene-induced fibrosarcomas and in Kirsten-MSV transformed fibroblasts.	Methylcholanthrene	57-75	secreted protein acidic and cysteine rich	Homo sapiens	19-24
2009865-12	1991	This study showed that 3-chlorodibenzofuran is activated not only by cytochrome P-448, which is induced by 3-methylcholanthrene type inducers, but also by the enzymes existing in normal rat liver.	Methylcholanthrene	107-127	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	69-85
1826444-0	1991	Down-regulation of SPARC/osteonectin/BM-40 expression in methylcholanthrene-induced fibrosarcomas and in Kirsten-MSV transformed fibroblasts.	Methylcholanthrene	57-75	secreted protein acidic and cysteine rich	Homo sapiens	37-42
1826444-2	1991	Northern and slot-blot analyses were used to study SPARC expression in tumours induced in vivo by methylcholanthrene (MCA) and in transformed cells induced in vitro by Kirsten-MSV and SV-40 infection.	Methylcholanthrene	98-116	secreted protein acidic and cysteine rich	Homo sapiens	51-56
1899082-3	1991	Steady-state UDP-glucuronosyltransferase mRNA levels were determined by Northern blot analysis or in situ hybridization of tissue sections using a 30-mer oligonucleotide specific for the 3-methylcholanthrene-inducible UDP-glucuronosyltransferase (which is active toward 4-nitrophenol) or a double-stranded cDNA probe specific for androsterone-UDP-glucuronosyltransferase.	Methylcholanthrene	187-207	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	13-40
1899082-4	1991	For 3-methylcholanthrene-inducible UDP-glucuronosyltransferase, the mRNA level was very low in control liver; there was a 15-fold increase after 3-methylcholanthrene treatment.	Methylcholanthrene	145-165	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	35-62
1899082-7	1991	Similar changes in the level of the 3-methylcholanthrene-inducible UDP-glucuronosyltransferase were also observed by in situ hybridization of tissue sections.	Methylcholanthrene	36-56	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	67-94
1899082-8	1991	Immunocytochemical studies using an antiserum that recognizes the 3-methylcholanthrene-inducible UDP-glucuronosyltransferase showed a marked increase in the concentration of this isoform in preneoplastic nodules compared with the adjacent nonnodular liver.	Methylcholanthrene	66-86	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	97-124
1801846-8	1991	Induction is most effectively achieved by oral administration of the agents, and is rapid--aryl hydrocarbon hydroxylase (AHH) was increased within 1 h of administration of, for example, 3-MC.	Methylcholanthrene	186-190	aryl hydrocarbon receptor repressor	Homo sapiens	84-119
1801846-8	1991	Induction is most effectively achieved by oral administration of the agents, and is rapid--aryl hydrocarbon hydroxylase (AHH) was increased within 1 h of administration of, for example, 3-MC.	Methylcholanthrene	186-190	aryl hydrocarbon receptor repressor	Homo sapiens	121-124
1855887-8	1991	With 3-methylcholanthrene-induced male microsomes, most 3-hydroxylation and some depentylation were due to IA1 or IA2.	Methylcholanthrene	5-25	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	114-117
1899082-3	1991	Steady-state UDP-glucuronosyltransferase mRNA levels were determined by Northern blot analysis or in situ hybridization of tissue sections using a 30-mer oligonucleotide specific for the 3-methylcholanthrene-inducible UDP-glucuronosyltransferase (which is active toward 4-nitrophenol) or a double-stranded cDNA probe specific for androsterone-UDP-glucuronosyltransferase.	Methylcholanthrene	187-207	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	218-245
1899082-3	1991	Steady-state UDP-glucuronosyltransferase mRNA levels were determined by Northern blot analysis or in situ hybridization of tissue sections using a 30-mer oligonucleotide specific for the 3-methylcholanthrene-inducible UDP-glucuronosyltransferase (which is active toward 4-nitrophenol) or a double-stranded cDNA probe specific for androsterone-UDP-glucuronosyltransferase.	Methylcholanthrene	187-207	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	330-370
1899082-4	1991	For 3-methylcholanthrene-inducible UDP-glucuronosyltransferase, the mRNA level was very low in control liver; there was a 15-fold increase after 3-methylcholanthrene treatment.	Methylcholanthrene	4-24	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	35-62
1677496-10	1991	The 3-MC-induced S-9 was the least effective in suppressing growth of salivary glands.	Methylcholanthrene	4-8	ribosomal protein S9	Homo sapiens	17-20
1839629-6	1991	Among the ten drugs, CCl4, alcohol, paraquat, phenobarbital, thiopental and methylcholanthrene caused the TBA values to increase, and the phosphoglucomutase activity to decrease, in the liver 24 h after the doses.	Methylcholanthrene	76-94	C-C motif chemokine ligand 4	Rattus norvegicus	21-25
1768430-7	1991	The Ah-receptor binding compounds, such as coal tar constituents, or 3-methylcholanthrene induce cytochrome P-450-dependent activities such as aryl hydrocarbon hydroxylase or 7-ethoxyresorufin-O-de-ethylase and NQR, whereas butyl hydroxytoluol, which does not bind to the Ah receptor, induces only NQR.	Methylcholanthrene	69-89	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	97-113
1768430-7	1991	The Ah-receptor binding compounds, such as coal tar constituents, or 3-methylcholanthrene induce cytochrome P-450-dependent activities such as aryl hydrocarbon hydroxylase or 7-ethoxyresorufin-O-de-ethylase and NQR, whereas butyl hydroxytoluol, which does not bind to the Ah receptor, induces only NQR.	Methylcholanthrene	69-89	crystallin zeta	Homo sapiens	211-214
1768430-7	1991	The Ah-receptor binding compounds, such as coal tar constituents, or 3-methylcholanthrene induce cytochrome P-450-dependent activities such as aryl hydrocarbon hydroxylase or 7-ethoxyresorufin-O-de-ethylase and NQR, whereas butyl hydroxytoluol, which does not bind to the Ah receptor, induces only NQR.	Methylcholanthrene	69-89	aryl hydrocarbon receptor	Homo sapiens	272-283
1768430-7	1991	The Ah-receptor binding compounds, such as coal tar constituents, or 3-methylcholanthrene induce cytochrome P-450-dependent activities such as aryl hydrocarbon hydroxylase or 7-ethoxyresorufin-O-de-ethylase and NQR, whereas butyl hydroxytoluol, which does not bind to the Ah receptor, induces only NQR.	Methylcholanthrene	69-89	crystallin zeta	Homo sapiens	298-301
1699680-1	1990	Treatment of pregnant mice with 3-methylcholanthrene (MC) causes lung and liver tumors in the offspring, the incidences of which are greatly influenced by the Ah locus regulated induction phenotype for aryl hydrocarbon hydroxylase activity (AHH) in both the mother and fetuses.	Methylcholanthrene	32-52	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	241-244
2085761-6	1990	Administration of 3-methylcholanthrene, selectively induced the levels of ethoxycoumarin O-deethylase (ECD) and arylhydrocarbon hydroxylase, although the levels of total P-450 were not increased.	Methylcholanthrene	18-38	ecdysoneless cell cycle regulator	Rattus norvegicus	74-101
2085761-6	1990	Administration of 3-methylcholanthrene, selectively induced the levels of ethoxycoumarin O-deethylase (ECD) and arylhydrocarbon hydroxylase, although the levels of total P-450 were not increased.	Methylcholanthrene	18-38	ecdysoneless cell cycle regulator	Rattus norvegicus	103-106
1702367-4	1990	However, exposure of the infected cells to 3-MC resulted in a rapid cell transformation with concomitant enhancement of c-Ha-ras and H-2K class I MHC gene expression in the transformed cells.	Methylcholanthrene	43-47	Harvey rat sarcoma virus oncogene	Mus musculus	120-128
1702367-4	1990	However, exposure of the infected cells to 3-MC resulted in a rapid cell transformation with concomitant enhancement of c-Ha-ras and H-2K class I MHC gene expression in the transformed cells.	Methylcholanthrene	43-47	histocompatibility 2, K1, K region	Mus musculus	133-137
2084182-4	1990	The total and covalently bound radioactivity from [14C]-CAT to liver and kidney were decreased significantly in the starling pretreated with the MFO inducer, 3-methylcholanthrene.	Methylcholanthrene	158-178	catalase	Sturnus vulgaris	56-59
2247082-1	1990	We have previously demonstrated that cytochrome P-450d mRNA accumulation is induced at a posttranscriptional level by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium.	Methylcholanthrene	118-138	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	37-54
2247082-1	1990	We have previously demonstrated that cytochrome P-450d mRNA accumulation is induced at a posttranscriptional level by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium.	Methylcholanthrene	140-143	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	37-54
2250663-7	1990	Ethoxyresorufin deethylation by hepatic microsomes from 3-methylcholanthrene-treated rats was decreased by ischemia-reperfusion; however, pentoxyresorufin dealkylation by hepatic microsomes from phenobarbital-treated rats was not, suggesting specific cytochrome P-450 isozyme loss.	Methylcholanthrene	56-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	251-267
1871511-3	1991	We have recently described a monoclonal IgM antibody, H17, to a mouse methylcholanthrene-induced tumor with specificity for a common saccharide, namely alpha-N-acetylgalactosamine.	Methylcholanthrene	70-88	histocompatibility 17	Mus musculus	54-57
1871511-7	1991	Moreover, the uncommon sensitivity to complement-mediated lysis by this methylcholanthrene-induced tumor was blocked by the H17 monoclonal antibody.	Methylcholanthrene	72-90	histocompatibility 17	Mus musculus	124-127
2285245-4	1990	Treatment of hepatocytes from both control and 3-MC-injected rats with 25 microM BHA for 24 or 48 hours increased GSH-S-T activity significantly.	Methylcholanthrene	47-51	glutathione synthetase	Rattus norvegicus	114-119
1699680-1	1990	Treatment of pregnant mice with 3-methylcholanthrene (MC) causes lung and liver tumors in the offspring, the incidences of which are greatly influenced by the Ah locus regulated induction phenotype for aryl hydrocarbon hydroxylase activity (AHH) in both the mother and fetuses.	Methylcholanthrene	54-56	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	241-244
1699680-7	1990	However, 48 h after exposure to MC, the AHH activity in fetal lungs from B6 mothers had declined to practically control values, whereas fetal lungs from D2 mothers still exhibited a high level of AHH activity.	Methylcholanthrene	32-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	40-43
1699680-7	1990	However, 48 h after exposure to MC, the AHH activity in fetal lungs from B6 mothers had declined to practically control values, whereas fetal lungs from D2 mothers still exhibited a high level of AHH activity.	Methylcholanthrene	32-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	196-199
1699680-10	1990	In both organs, treatment with inducing agents for the P450IA1 gene resulted in a rapid and early induction of CYPIA1 RNA by 4 h. Fetuses from D2 mothers, however, showed a more sustained induction of CYPIA1 RNA following exposure to MC than did fetuses from B6 mothers.	Methylcholanthrene	234-236	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	111-117
1699680-10	1990	In both organs, treatment with inducing agents for the P450IA1 gene resulted in a rapid and early induction of CYPIA1 RNA by 4 h. Fetuses from D2 mothers, however, showed a more sustained induction of CYPIA1 RNA following exposure to MC than did fetuses from B6 mothers.	Methylcholanthrene	234-236	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	201-207
1699680-11	1990	These results suggest that the observed increase in tumor susceptibility observed in the offspring of D2 mothers compared to the offspring of B6 mothers was due, at least in part, to the differences in the persistence of induction of the CYPIA1 gene locus, and may be the result of differences in the clearance rates of MC from the fetal and maternal compartments or its pharmacokinetic distribution in the two types of maternal environments.	Methylcholanthrene	320-322	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	238-244
2148358-10	1990	In addition, anti-VLA-5 but not anti-VLA-3 antibodies inhibited significantly the binding of MC to FN, MC demonstrated binding and phagocytosis of FN coated beads and, purified FN inhibited both phenomena.	Methylcholanthrene	93-95	integrin subunit alpha 5	Homo sapiens	18-23
2128752-4	1990	Inducibility of liver microsomal codeine UDPGT activity in rats was examined by pretreatment with phenobarbital and 3-methylcholanthrene and compared with those of other UDPGT activities.	Methylcholanthrene	116-136	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	41-46
2152550-4	1990	In the MC insulin treated group, the percentage of patients showing deterioration in proteinuria was lower (11% vs 34%, P less than 0.05) and the percentage showing improvement was higher (48% vs 29%) compared to the conventional insulin treated group.	Methylcholanthrene	7-9	insulin	Homo sapiens	10-17
2152550-4	1990	In the MC insulin treated group, the percentage of patients showing deterioration in proteinuria was lower (11% vs 34%, P less than 0.05) and the percentage showing improvement was higher (48% vs 29%) compared to the conventional insulin treated group.	Methylcholanthrene	7-9	insulin	Homo sapiens	230-237
2152550-5	1990	Insulin antibody titres decreased significantly in the MC insulin group and serum C-peptide values decreased in both groups on follow-up.	Methylcholanthrene	55-57	insulin	Homo sapiens	0-7
2152550-5	1990	Insulin antibody titres decreased significantly in the MC insulin group and serum C-peptide values decreased in both groups on follow-up.	Methylcholanthrene	55-57	insulin	Homo sapiens	58-65
2148358-10	1990	In addition, anti-VLA-5 but not anti-VLA-3 antibodies inhibited significantly the binding of MC to FN, MC demonstrated binding and phagocytosis of FN coated beads and, purified FN inhibited both phenomena.	Methylcholanthrene	103-105	integrin subunit alpha 5	Homo sapiens	18-23
2148358-13	1990	MC FN receptors (VLA-5) mediate the binding of MC to FN and could mediate the phagocytosis of FN coated antigen or immune complexes by mesangial cells.	Methylcholanthrene	0-2	integrin subunit alpha 5	Homo sapiens	17-22
2267136-3	1990	To further characterize the role of p53 in growing normal Balb/c 3T3 fibroblasts, as well as of p53 in cells of the methylcholanthrene induced fibrosarcoma cell line Meth A, we analysed the effect of inhibition of p53 synthesis by microinjection of p53-specific monoclonal antibody PAb 122 into the nuclei of these cells after release from growth arrest induced by isoleucine starvation (see preceding paper [Steinmeyer et al., this issue] ).	Methylcholanthrene	116-134	transformation related protein 53, pseudogene	Mus musculus	96-99
2267136-3	1990	To further characterize the role of p53 in growing normal Balb/c 3T3 fibroblasts, as well as of p53 in cells of the methylcholanthrene induced fibrosarcoma cell line Meth A, we analysed the effect of inhibition of p53 synthesis by microinjection of p53-specific monoclonal antibody PAb 122 into the nuclei of these cells after release from growth arrest induced by isoleucine starvation (see preceding paper [Steinmeyer et al., this issue] ).	Methylcholanthrene	116-134	transformation related protein 53, pseudogene	Mus musculus	96-99
2267136-3	1990	To further characterize the role of p53 in growing normal Balb/c 3T3 fibroblasts, as well as of p53 in cells of the methylcholanthrene induced fibrosarcoma cell line Meth A, we analysed the effect of inhibition of p53 synthesis by microinjection of p53-specific monoclonal antibody PAb 122 into the nuclei of these cells after release from growth arrest induced by isoleucine starvation (see preceding paper [Steinmeyer et al., this issue] ).	Methylcholanthrene	116-134	transformation related protein 53, pseudogene	Mus musculus	96-99
2283671-1	1990	The oxidation of uroporphyrinogen, an intermediate of the heme biosynthetic pathway, by methylcholanthrene-inducible isozymes(s) of cytochrome P-450 has been proposed to play a role in the development of chemically induced uroporphyria.	Methylcholanthrene	88-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Methylcholanthrene	173-193	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	35-64
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Methylcholanthrene	173-193	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	66-71
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Methylcholanthrene	195-197	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	35-64
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Methylcholanthrene	195-197	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	66-71
2125771-5	1990	MC-type inducers (representing a large number of planar polycyclic aromatics, beta-naphthoflavone and polyhalogenated aromatics) bind with high affinity to the Ah receptor which controls gene expression similar to steroid hormone receptors.	Methylcholanthrene	0-2	aryl hydrocarbon receptor	Rattus norvegicus	160-171
2085792-6	1990	The level of Yb1 was equally induced by MC or PB with no synergistic effect.	Methylcholanthrene	40-42	Y box binding protein 1	Rattus norvegicus	13-16
1981220-8	1990	Both phenobarbital and 3-methylcholanthrene augmented the GGTP activity of NPE cells but not of PE cells.	Methylcholanthrene	23-43	inactive glutathione hydrolase 2	Homo sapiens	58-62
2122607-5	1990	With liver microsomes from both 3-methylcholanthrene (MC)- and phenobarbital (PB)-pretreated rats, reverse type I difference spectra were observed, indicative of a weak interaction between mitomycin c and the substrate binding site of cytochrome P-450.	Methylcholanthrene	32-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
2219115-6	1990	3-Methylcholanthrene pretreatment increased and pretreatment with cobalt chloride and piperonyl butoxide decreased the hepatic covalent binding of 3HAA, indicating the involvement of cytochrome P450 in the formation of the 3HAA reactive metabolite.	Methylcholanthrene	0-20	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	183-198
2228904-3	1990	For us to start investigating the possible mechanisms involved, it was important that we first develop an in vitro model, in which gastrin expresses its trophic effects directly on the MC-26 cells.	Methylcholanthrene	185-187	gastrin	Mus musculus	131-138
2228904-4	1990	The growth-promoting effects of gastrin on the MC-26 cells were examined in various in vitro culture models, in terms of [3H]thymidine incorporation and cell number.	Methylcholanthrene	47-49	gastrin	Mus musculus	32-39
2228904-6	1990	The optimal cell-culture conditions for observing trophic effects of gastrin were defined and included a 24-h period of rapid growth of MC-26 cells in serum-supplemented normal growth medium, followed by a 24-h period of culture in serum-free medium containing an optimal dose (1.0 mM) of thymidine, to achieve growth-arrest of the cells.	Methylcholanthrene	136-139	gastrin	Mus musculus	69-76
2122607-5	1990	With liver microsomes from both 3-methylcholanthrene (MC)- and phenobarbital (PB)-pretreated rats, reverse type I difference spectra were observed, indicative of a weak interaction between mitomycin c and the substrate binding site of cytochrome P-450.	Methylcholanthrene	54-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
2116480-2	1990	We recently reported that the IDO is dramatically (approximately 50-fold) induced in allografted tumor (3-methylcholanthrene-induced ascites type tumor cells) cells undergoing rejection, and that the enzyme is induced by factor(s) released through the interaction of allografted tumor cells with infiltrating leukocytes.	Methylcholanthrene	104-124	indoleamine 2,3-dioxygenase 1	Homo sapiens	30-33
2228904-10	1990	To determine if gastrin was functioning as an autocrine growth factor for MC-26 cells, we examined the effect of gastrin antibodies on the growth of MC-26 cells; no significant effect of the antigastrin IgG on the growth of MC-26 cells was observed.	Methylcholanthrene	74-76	gastrin	Mus musculus	16-23
2116480-5	1990	Approximately 6 U/ml of IFN-gamma was detected by an ELISA assay in the 12-h culture supernatant with 2 x 10(6) leukocytes/ml, and rIFN-gamma at 6 U/ml induced IDO in 3-methylcholanthrene-induced ascites type tumor cells to the same extent as IFN-gamma in the culture supernatant.	Methylcholanthrene	167-187	interferon gamma	Homo sapiens	24-33
2116480-5	1990	Approximately 6 U/ml of IFN-gamma was detected by an ELISA assay in the 12-h culture supernatant with 2 x 10(6) leukocytes/ml, and rIFN-gamma at 6 U/ml induced IDO in 3-methylcholanthrene-induced ascites type tumor cells to the same extent as IFN-gamma in the culture supernatant.	Methylcholanthrene	167-187	interferon gamma	Homo sapiens	132-141
2375769-7	1990	In competition studies, MC 969 was able to inhibit 25-hydroxylation of tritiated vitamin D3 more effectively than 1 alpha-OH-D3 itself, indicating that the vitamin D3-25-hydroxylase may be responsible for generation of one or more of the metabolites observed.	Methylcholanthrene	24-26	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	156-181
2402117-5	1990	MC express IL-6 mRNA as determined by Northern blot.	Methylcholanthrene	0-2	interleukin 6	Rattus norvegicus	11-15
2402117-7	1990	Incubation of subconfluent MC with recombinant IL-6 results in a dose-dependent increase of 3H-thymidine incorporation and number of MCs.	Methylcholanthrene	27-29	interleukin 6	Rattus norvegicus	47-51
2402117-8	1990	Moreover, reverse phase HPLC fractions of MC-CM containing IL-6 activity increase 3H-thymidine incorporation by MC.	Methylcholanthrene	42-44	interleukin 6	Rattus norvegicus	59-63
2377606-1	1990	Cell-surface glycoproteins of 96 kDa (gp96) have been implicated in immunogenicity of methylcholanthrene-induced mouse sarcomas in syngeneic hosts.	Methylcholanthrene	86-104	heat shock protein 90, beta (Grp94), member 1	Mus musculus	0-42
2247996-0	1990	[Experiences with conversion from MC-insulin NOVO to L-insulin S.N.C.	Methylcholanthrene	34-36	insulin	Homo sapiens	37-44
2383252-4	1990	Exposure to 3-methylcholanthrene (MC) resulted in a significant induction of the activity of AHH (102-345%), ECOD (115-150%) and EROD (75-120%) in the neuronal and glial cell preparations.	Methylcholanthrene	12-32	aryl hydrocarbon receptor repressor	Homo sapiens	93-96
2383252-4	1990	Exposure to 3-methylcholanthrene (MC) resulted in a significant induction of the activity of AHH (102-345%), ECOD (115-150%) and EROD (75-120%) in the neuronal and glial cell preparations.	Methylcholanthrene	34-36	aryl hydrocarbon receptor repressor	Homo sapiens	93-96
2117439-2	1990	It was previously shown that uroporphyrinogen oxidation is catalysed by a form of cytochrome P-450 induced by 3-methylcholanthrene [Sinclair, Lambrecht &amp; Sinclair (1987) Biochem.	Methylcholanthrene	110-130	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-98
1692256-3	1990	The AHH activity of cells treated with either benz(a)anthracene, benzo(a)pyrene, 3-methylcholanthrene, or TCDD continuously or 24 h before harvesting was measured during observation periods for up to 5 days.	Methylcholanthrene	81-101	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	4-7
2398265-5	1990	(a) Activities of the methyl cholanthrene-inducible forms of cytochrome P-450 were decreased compared to normal controls, whereas the activities of the phenobarbitone-inducible isozymes were relatively unaffected.	Methylcholanthrene	22-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	61-77
2363175-3	1990	In this study, the effects of fetal versus adult MC exposure were compared with regard to both induction of aryl hydrocarbon hydroxylase activity (AHH) in lung and dependence of lung tumorigenesis on the Ah genotype.	Methylcholanthrene	49-51	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	147-150
2363175-4	1990	In inducible (C57BL/6 X DBA/2)F1 fetal lung supernatants, a single ip injection of 100 mg/kg of MC to the mothers resulted in a maximal 50-fold induction of AHH activity by 8 hr, which persisted for 48 hr.	Methylcholanthrene	96-98	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	157-160
2363175-9	1990	Single ip injections of MC to adult F1 mice revealed that lung AHH activity was increased only 4- to 7-fold in the adult animal compared to the large fetal induction ratio.	Methylcholanthrene	24-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	63-66
2117068-4	1990	A monoclonal antibody (MAb 1-7-1), which recognizes isozymes of cytochrome P-450 induced by 3-methylcholanthrene (P1-450 and P3-450), selectively inhibited the metabolism of 8-MOP (-57%) and covalent binding of its metabolites (-40%) in microsomes from mice pretreated with BNF, but had no effect in microsomes of mice pretreated with phenobarbital or vehicle.	Methylcholanthrene	92-112	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	64-80
2372865-4	1990	In contrast, polycyclic aromatic hydrocarbons, such as 3-methylcholanthrene, benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene, induce an immediate increase of T-ALDH activity in both cultured rat hepatocytes and hepatoma cell lines.	Methylcholanthrene	55-75	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	162-166
2113060-0	1990	Mechanism of the lack of induction of UDP-glucuronosyltransferase activity in Gunn rats by 3-methylcholanthrene.	Methylcholanthrene	91-111	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	38-65
2113060-3	1990	4-Nitrophenol glucuronidation is mediated by several UDPGT isoforms that are distinct from bilirubin-UDPGT, one of which is induced after 3-methylcholanthrene (3-MC) administration in normal, but not in Gunn rats.	Methylcholanthrene	138-158	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	53-58
2113060-3	1990	4-Nitrophenol glucuronidation is mediated by several UDPGT isoforms that are distinct from bilirubin-UDPGT, one of which is induced after 3-methylcholanthrene (3-MC) administration in normal, but not in Gunn rats.	Methylcholanthrene	138-158	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	101-106
2113060-3	1990	4-Nitrophenol glucuronidation is mediated by several UDPGT isoforms that are distinct from bilirubin-UDPGT, one of which is induced after 3-methylcholanthrene (3-MC) administration in normal, but not in Gunn rats.	Methylcholanthrene	160-164	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	53-58
2113060-3	1990	4-Nitrophenol glucuronidation is mediated by several UDPGT isoforms that are distinct from bilirubin-UDPGT, one of which is induced after 3-methylcholanthrene (3-MC) administration in normal, but not in Gunn rats.	Methylcholanthrene	160-164	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	101-106
2113060-4	1990	In normal rats, 3-MC-inducible UDPGT mRNA concentration increased 15-fold in the liver and 3-fold in kidney after 3-MC (140 mg/kg) administration.	Methylcholanthrene	16-20	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-36
2113060-4	1990	In normal rats, 3-MC-inducible UDPGT mRNA concentration increased 15-fold in the liver and 3-fold in kidney after 3-MC (140 mg/kg) administration.	Methylcholanthrene	114-118	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-36
2113060-8	1990	Nuclear run-on studies showed that the transcription rate for 3-MC-inducible UDPGT was 3-fold higher in Gunn rat liver and kidney than in normal and increased 3- to 5-fold after 3-MC administration.	Methylcholanthrene	62-66	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	77-82
2113060-8	1990	Nuclear run-on studies showed that the transcription rate for 3-MC-inducible UDPGT was 3-fold higher in Gunn rat liver and kidney than in normal and increased 3- to 5-fold after 3-MC administration.	Methylcholanthrene	178-182	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	77-82
2113060-9	1990	Immunotransblot studies revealed an Mr = 56,000 3-MC-inducible UDPGT in liver and kidney of normal, but not in Gunn rats.	Methylcholanthrene	48-52	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	63-68
2113060-11	1990	Cell-free translation of kidney mRNA from 3-MC-treated Gunn rats showed that the Mr = 43,000 UDPGT is synthesized as an Mr = 45,000 protein.	Methylcholanthrene	42-46	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	93-98
2113060-13	1990	These results suggest that a sequence abnormality in the 3-MC-inducible UDPGT mRNA in Gunn rats results in reduced mRNA concentration and synthesis of a truncated, enzymically inactive UDPGT.	Methylcholanthrene	57-61	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	72-77
2113060-13	1990	These results suggest that a sequence abnormality in the 3-MC-inducible UDPGT mRNA in Gunn rats results in reduced mRNA concentration and synthesis of a truncated, enzymically inactive UDPGT.	Methylcholanthrene	57-61	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	185-190
1692256-4	1990	Slight induction of AHH activity by benz(a)anthracene, benzo(a)pyrene, and 3-methylcholanthrene was observed in hepatocytes from the CBA and C3H/He strains during the first half of the observation period, followed by a steep increase thereafter.	Methylcholanthrene	75-95	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	20-23
2359409-5	1990	258:5649-5659 (1983)] reported that ANF metabolism by 3-MC-induced rat liver microsomes was only partially inhibited by antibodies against P-450c.	Methylcholanthrene	54-58	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-145
2344366-0	1990	Effect of different doses of 3-methylcholanthrene on the localization of the 3-methylcholanthrene-inducible isoenzymes of cytochrome P450 within the centrilobular and periportal zones of the rat liver.	Methylcholanthrene	29-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-137
2344366-0	1990	Effect of different doses of 3-methylcholanthrene on the localization of the 3-methylcholanthrene-inducible isoenzymes of cytochrome P450 within the centrilobular and periportal zones of the rat liver.	Methylcholanthrene	77-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-137
2344366-1	1990	Immunohistochemical staining techniques were used to investigate the localization of the 3-methylcholanthrene inducible isoenzymes (P450 IA1 and IA2) in the rat liver.	Methylcholanthrene	89-109	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	145-148
2112380-3	1990	The cDNA shares an identical 913-bp sequence (corresponding to the C-terminal 247 amino acid residues) with that for rat liver 3-methylcholanthrene-inducible 4-nitrophenol UDPGT including the locus where a -1 frameshift mutation was found in the 4-nitrophenol UDPGT cDNA from the jaundiced homozygous Gunn rat.	Methylcholanthrene	127-147	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	172-177
2112380-3	1990	The cDNA shares an identical 913-bp sequence (corresponding to the C-terminal 247 amino acid residues) with that for rat liver 3-methylcholanthrene-inducible 4-nitrophenol UDPGT including the locus where a -1 frameshift mutation was found in the 4-nitrophenol UDPGT cDNA from the jaundiced homozygous Gunn rat.	Methylcholanthrene	127-147	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	260-265
2364062-1	1990	To investigate whether cytochrome P-450 catalyzes the covalent binding of substrates to DNA by one-electron oxidation, the ability of both uninduced and 3-methylcholanthrene (MC) induced rat liver microsomes and nuclei to catalyze covalent binding of benzo[a]pyrene (BP) to DNA and formation of the labile adduct 7-(benzo[a]pyren-6-yl)guanine (BP-N7Gua) was investigated.	Methylcholanthrene	175-177	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
2141611-1	1990	In previous studies it was shown that transformation of AKR fibroblasts with 3-methylcholanthrene was associated with a loss of surface fibronectin and that induction of differentiation of the transformed cells with N,N-dimethylformamide (DMF) was associated with reacquisition of surface fibronectin (Chakrabarty et al., J.	Methylcholanthrene	77-97	fibronectin 1	Mus musculus	136-147
2141611-1	1990	In previous studies it was shown that transformation of AKR fibroblasts with 3-methylcholanthrene was associated with a loss of surface fibronectin and that induction of differentiation of the transformed cells with N,N-dimethylformamide (DMF) was associated with reacquisition of surface fibronectin (Chakrabarty et al., J.	Methylcholanthrene	77-97	fibronectin 1	Mus musculus	289-300
2113322-0	1990	Aryl hydrocarbon hydroxylase activity levels in the hepatic microsomal fraction from MC- or TCDD-treated mice: a comparison between aromatic hydrocarbon responsive and non-responsive strains.	Methylcholanthrene	85-87	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-28
2112112-7	1990	Immunoblots showed the presence of cytochromes P-450 UT-A, UT-H, PB-B, ISF-G and PCN-E, the last three isoenzymes being inducible by, respectively, phenobarbital, 3-methylcholanthrene and dexamethasone.	Methylcholanthrene	163-183	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	47-57
2322313-1	1990	The activity of human cytochrome P450 monooxygenases, aryl hydrocarbon hydroxylase and 7-ethoxycoumarin O-deethylase can be increased by 3-methylcholanthrene, phenobarbital and ethanol in human hepatocytes maintained in primary culture.	Methylcholanthrene	137-157	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	54-82
2233817-1	1990	The levels of the messenger RNAs for the cytochromes P450IA1 (CYPIA1) and P450IA2 (CYPIA2) were determined in liver cytoplasmic RNA of rats of various ages after maximal induction with either 3-methylcholanthrene or isosafrole and in untreated rats.	Methylcholanthrene	192-212	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	83-89
2233817-2	1990	An increase in the CYPIA1 mRNA levels was observed only after treatment with 3-methylcholanthrene, whereas both 3-methylcholanthrene and isosafrole were able to induce the levels of CYPIA2 mRNA.	Methylcholanthrene	77-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	19-25
2233817-2	1990	An increase in the CYPIA1 mRNA levels was observed only after treatment with 3-methylcholanthrene, whereas both 3-methylcholanthrene and isosafrole were able to induce the levels of CYPIA2 mRNA.	Methylcholanthrene	112-132	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	182-188
2322313-4	1990	Addition of 3-methylcholanthrene caused a time- and concentration-dependent increase in both monooxygenase activities, aryl hydrocarbon hydroxylase and 7-ethoxycoumarin O-deethylase, while phenobarbital and ethanol increased 7-ethoxycoumarin O-deethylase activity but had no effect on aryl hydrocarbon hydroxylase.	Methylcholanthrene	12-32	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	119-147
2322313-4	1990	Addition of 3-methylcholanthrene caused a time- and concentration-dependent increase in both monooxygenase activities, aryl hydrocarbon hydroxylase and 7-ethoxycoumarin O-deethylase, while phenobarbital and ethanol increased 7-ethoxycoumarin O-deethylase activity but had no effect on aryl hydrocarbon hydroxylase.	Methylcholanthrene	12-32	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	285-313
2346722-11	1990	The stimulatory activities of MC appeared to be mediated through endogenously released IL-1, as the addition of antibodies towards IL-1 at the initiation of cocultures completely abrogated the IL-6 production.	Methylcholanthrene	30-32	interleukin 6	Homo sapiens	193-197
2346722-2	1990	Recombinant human (rh) IL-1 alpha, IL-1 beta and TNF-alpha augmented production of IL-6 in human MC.	Methylcholanthrene	97-99	interleukin 1 alpha	Homo sapiens	23-33
2154492-9	1990	3-Methylcholanthrene treatment induced cholesterol 7 alpha-hydroxylase activity and enzyme level.	Methylcholanthrene	0-20	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	39-70
2346722-2	1990	Recombinant human (rh) IL-1 alpha, IL-1 beta and TNF-alpha augmented production of IL-6 in human MC.	Methylcholanthrene	97-99	interleukin 1 beta	Homo sapiens	35-44
2346722-2	1990	Recombinant human (rh) IL-1 alpha, IL-1 beta and TNF-alpha augmented production of IL-6 in human MC.	Methylcholanthrene	97-99	tumor necrosis factor	Homo sapiens	49-58
2346722-2	1990	Recombinant human (rh) IL-1 alpha, IL-1 beta and TNF-alpha augmented production of IL-6 in human MC.	Methylcholanthrene	97-99	interleukin 6	Homo sapiens	83-87
2346722-6	1990	IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines.	Methylcholanthrene	186-188	interleukin 1 alpha	Homo sapiens	0-10
2346722-6	1990	IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines.	Methylcholanthrene	186-188	interleukin 1 beta	Homo sapiens	12-21
2346722-6	1990	IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines.	Methylcholanthrene	186-188	tumor necrosis factor	Homo sapiens	26-35
2346722-6	1990	IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines.	Methylcholanthrene	186-188	interleukin 6	Homo sapiens	84-88
2346722-6	1990	IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines.	Methylcholanthrene	186-188	interleukin 6	Homo sapiens	107-111
2346722-10	1990	Further data demonstrated that human MC were able to induce IL-6 production in MSC.	Methylcholanthrene	37-39	interleukin 6	Homo sapiens	60-64
2346722-11	1990	The stimulatory activities of MC appeared to be mediated through endogenously released IL-1, as the addition of antibodies towards IL-1 at the initiation of cocultures completely abrogated the IL-6 production.	Methylcholanthrene	30-32	interleukin 1 beta	Homo sapiens	87-91
2346722-11	1990	The stimulatory activities of MC appeared to be mediated through endogenously released IL-1, as the addition of antibodies towards IL-1 at the initiation of cocultures completely abrogated the IL-6 production.	Methylcholanthrene	30-32	interleukin 1 beta	Homo sapiens	131-135
2185902-1	1990	We previously demonstrated that four tumorigenic methylcholanthrene (MCA) transformed cell lines derived from C3H10T1/2 cells each contain a common G34----T nucleotide alteration in the c-Ki-ras gene.	Methylcholanthrene	49-67	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	186-194
2185902-1	1990	We previously demonstrated that four tumorigenic methylcholanthrene (MCA) transformed cell lines derived from C3H10T1/2 cells each contain a common G34----T nucleotide alteration in the c-Ki-ras gene.	Methylcholanthrene	69-72	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	186-194
2169533-11	1990	Western blot analysis with antibodies to P450 isozymes induced with either phenobarbital (Pb) or 3-methylcholanthrene (3-MC) confirmed that both IIB1 and IA2 were induced, but that IA1 was not induced.	Methylcholanthrene	97-117	protein tyrosine phosphatase, receptor type, N	Mus musculus	154-157
2169533-11	1990	Western blot analysis with antibodies to P450 isozymes induced with either phenobarbital (Pb) or 3-methylcholanthrene (3-MC) confirmed that both IIB1 and IA2 were induced, but that IA1 was not induced.	Methylcholanthrene	119-123	protein tyrosine phosphatase, receptor type, N	Mus musculus	154-157
2115161-4	1990	When added to the culture medium simultaneously with TCDD or 3-methylcholanthrene (MC), 3-MSF-3",4,4",5-tetraCB blocked the enhancement of the AHH activity by TCDD but did not that by MC.	Methylcholanthrene	83-85	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	143-146
2382261-1	1990	Cytochrome P-450MC was induced in pulmonary microsomes of 3-methylcholanthrene-treated rats and also at low level in that of isosafrole-treated rats.	Methylcholanthrene	58-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	11-18
1971562-9	1990	From these findings it was concluded that P-450c is the major isozyme responsible for the metabolism of chlorotrianisene to the covalently binding reactive intermediate in MC microsomes.	Methylcholanthrene	172-174	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	42-48
2310418-7	1990	The involvement of cytochrome P-450 isoenzymes in this reaction is supported by the observation that the N-hydroxylation is only observed after pretreatment of the rats with 3-methylcholanthrene or isosafrole.	Methylcholanthrene	174-194	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
1971562-0	1990	Role of P-450c in the formation of a reactive intermediate of chlorotrianisene (TACE) by hepatic microsomes from methylcholanthrene-treated rats.	Methylcholanthrene	113-131	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	8-14
2319474-5	1990	Inducers of cytochrome P-450 enhanced phenytoin covalent binding as follows: phenobarbital greater than 3-methylcholanthrene greater than saline-treated controls.	Methylcholanthrene	104-124	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	12-28
1971562-0	1990	Role of P-450c in the formation of a reactive intermediate of chlorotrianisene (TACE) by hepatic microsomes from methylcholanthrene-treated rats.	Methylcholanthrene	113-131	ADAM metallopeptidase domain 17	Rattus norvegicus	80-84
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	112-130	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	188-194
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	112-130	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	205-211
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	112-130	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	213-216
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	132-134	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	188-194
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	132-134	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	205-211
1971562-4	1990	Covalent binding of chlorotrianisene in hepatic microsomes is dramatically stimulated by treatment of rats with methylcholanthrene (MC), which is known to induce two major P-450 isozymes, P-450c (IA1) and P-450d (IA2).	Methylcholanthrene	132-134	protein tyrosine phosphatase, receptor type, N	Rattus norvegicus	213-216
2158911-7	1990	The rise in plasma cyclic GMP by alpha-hANP was suppressed by MC both in normal subjects and patients with essential hypertension.	Methylcholanthrene	62-64	5'-nucleotidase, cytosolic II	Homo sapiens	26-29
2303445-0	1990	Dexamethasone-mediated regulation of 3-methylcholanthrene-induced cytochrome P-450d mRNA accumulation in primary rat hepatocyte cultures.	Methylcholanthrene	37-57	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	66-83
2303445-1	1990	We have previously demonstrated that cytochrome P-450c and P-450d mRNAs can be induced by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium (HDM) plus minimal salts (Silver, G., and Krauter, K. S. (1988) J. Biol.	Methylcholanthrene	90-110	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-54
2303445-1	1990	We have previously demonstrated that cytochrome P-450c and P-450d mRNAs can be induced by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium (HDM) plus minimal salts (Silver, G., and Krauter, K. S. (1988) J. Biol.	Methylcholanthrene	90-110	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-65
2303445-1	1990	We have previously demonstrated that cytochrome P-450c and P-450d mRNAs can be induced by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium (HDM) plus minimal salts (Silver, G., and Krauter, K. S. (1988) J. Biol.	Methylcholanthrene	112-115	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-54
2303445-1	1990	We have previously demonstrated that cytochrome P-450c and P-450d mRNAs can be induced by 3-methylcholanthrene (MCA) in primary cultures of rat hepatocytes grown in serum-free hormonally defined medium (HDM) plus minimal salts (Silver, G., and Krauter, K. S. (1988) J. Biol.	Methylcholanthrene	112-115	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-65
2306261-3	1990	Following treatment with hydrocarbons such as 3-methylcholanthrene (MC) and isosafrole (ISF) both cytochromes P450c (P450IA1) and P450d (P450IA2) are also induced in rat liver.	Methylcholanthrene	46-66	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-115
2154949-10	1990	Aryl hydrocarbon hydroxylase (AHH) activity was significantly induced after 24 h of incubation with polycyclic aromatic hydrocarbons: the EC50 for AHH induction was 5.3 microM for benz(a)anthracene and 1.3 microM for 3-methylcholanthrene.	Methylcholanthrene	217-237	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	0-28
2154949-10	1990	Aryl hydrocarbon hydroxylase (AHH) activity was significantly induced after 24 h of incubation with polycyclic aromatic hydrocarbons: the EC50 for AHH induction was 5.3 microM for benz(a)anthracene and 1.3 microM for 3-methylcholanthrene.	Methylcholanthrene	217-237	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	30-33
2154949-10	1990	Aryl hydrocarbon hydroxylase (AHH) activity was significantly induced after 24 h of incubation with polycyclic aromatic hydrocarbons: the EC50 for AHH induction was 5.3 microM for benz(a)anthracene and 1.3 microM for 3-methylcholanthrene.	Methylcholanthrene	217-237	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	147-150
2155352-3	1990	Pretreatment with 7,8-BF increased both P450 and cytochrome b5 levels, whereas phenobarbital (PB) and 3-methylcholanthrene (MC) induced P450 but not cytochrome b5.	Methylcholanthrene	102-122	cytochrome b5-like	Mesocricetus auratus	149-162
2072980-1	1990	Monoclonal antibodies (MAb 1-7-1) directed against the isoenzymes of rat liver cytochrome P-450 induced by methylcholanthrene, inhibited benzo(a)pyrene hydroxylase less strongly at low (0.04 mM) than at high (2 mM) NADH concentration.	Methylcholanthrene	107-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-95
2241997-0	1990	Inhibition of arylhydrocarbon hydroxylase and cytochrome P-450 by 20-methylcholanthrene and phenobarbital in guinea pig on excessive doses of ascorbic acid.	Methylcholanthrene	66-87	cytochrome P450 3A14	Cavia porcellus	46-62
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Methylcholanthrene	61-82	cytochrome P450 3A14	Cavia porcellus	179-195
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Methylcholanthrene	61-82	cytochrome b5	Cavia porcellus	200-213
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Methylcholanthrene	84-87	cytochrome P450 3A14	Cavia porcellus	179-195
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Methylcholanthrene	84-87	cytochrome b5	Cavia porcellus	200-213
2106321-0	1990	Aflatoxin B1-specific cytochrome P-450 isozyme (P-450-AFB) inducible by 3-methylcholanthrene in golden hamsters.	Methylcholanthrene	72-92	cytochrome P450 2A3-like	Mesocricetus auratus	22-38
2106321-6	1990	This isozyme constitutes approximately 40% of the total cytochrome P-450 of the hepatic microsomes from 3-methylcholanthrene-treated Golden hamsters but only 1% in the microsomes of phenobarbital-treated hamsters.	Methylcholanthrene	104-124	cytochrome P450 2A3-like	Mesocricetus auratus	56-72
2106321-7	1990	Thus, we conclude that the high activity of Golden hamster livers towards aflatoxin B1 activation was due presumably to this distinct and unique cytochrome P-450 isozyme which was induced mainly by 3-methylcholanthrene in Golden hamsters.	Methylcholanthrene	198-218	cytochrome P450 2A3-like	Mesocricetus auratus	145-161
2306261-3	1990	Following treatment with hydrocarbons such as 3-methylcholanthrene (MC) and isosafrole (ISF) both cytochromes P450c (P450IA1) and P450d (P450IA2) are also induced in rat liver.	Methylcholanthrene	68-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	110-115
2306261-4	1990	Studies with the reconstituted enzymes have shown that both forms of P450 catalyse phenacetin O-deethylation at rates that exceeded that of the high affinity component of activity of hepatic microsomal preparations from 3-methylcholanthrene-treated rats (at 4 microM phenacetin: P450c, 440 +/- 40 pmol/nmol/min; P450d, 1030 +/- 10 pmol/nmol/min; microsomal fraction, 163 pmol/mg/min).	Methylcholanthrene	220-240	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	279-284
2306261-6	1990	These studies have shown that hepatic high affinity POD activity is exclusively catalysed by cytochrome P450d in both untreated rats and in rats pretreated with MC.	Methylcholanthrene	161-163	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	93-109
2306262-4	1990	Only cytochrome P450c (P450IA1) is inducible in rat extrahepatic tissues by MC or isosafrole, whereas in the liver both cytochromes P450c and P450d (P450IA2) are inducible by these compounds.	Methylcholanthrene	76-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	5-21
2306262-4	1990	Only cytochrome P450c (P450IA1) is inducible in rat extrahepatic tissues by MC or isosafrole, whereas in the liver both cytochromes P450c and P450d (P450IA2) are inducible by these compounds.	Methylcholanthrene	76-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	132-147
2306262-6	1990	Whereas cytochrome P450d is responsible for all of the high affinity POD activity in hepatic microsomal fractions of both untreated and MC treated rats, this activity is mediated only by P450c in microsomal fractions from extrahepatic tissues following MC treatment.	Methylcholanthrene	136-138	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	8-24
2306262-6	1990	Whereas cytochrome P450d is responsible for all of the high affinity POD activity in hepatic microsomal fractions of both untreated and MC treated rats, this activity is mediated only by P450c in microsomal fractions from extrahepatic tissues following MC treatment.	Methylcholanthrene	136-138	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	187-192
2252843-3	1990	Incubation of an enantiomeric 1-OH-3MC with rat liver microsomes resulted in the formation of enantiomeric 3MC trans- and cis-1,2-diols; the absolute configurations of the enantiomeric 1-OH-3MC and 3MC cis-1,2-diol were established on the basis of the absolute configuration of an enantiomeric 3MC trans-1,2-diol.	Methylcholanthrene	35-38	cytokine inducible SH2-containing protein	Rattus norvegicus	122-127
2171791-3	1990	The amount of Ah receptor, i.e. the specific cytosolic binding protein of 3-methylcholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in H4IIEC3/T cells was characterized and quantitated by high performance gel filtration.	Methylcholanthrene	74-94	aryl hydrocarbon receptor	Rattus norvegicus	14-25
2252843-3	1990	Incubation of an enantiomeric 1-OH-3MC with rat liver microsomes resulted in the formation of enantiomeric 3MC trans- and cis-1,2-diols; the absolute configurations of the enantiomeric 1-OH-3MC and 3MC cis-1,2-diol were established on the basis of the absolute configuration of an enantiomeric 3MC trans-1,2-diol.	Methylcholanthrene	35-38	cytokine inducible SH2-containing protein	Rattus norvegicus	202-207
2097279-2	1990	To inhibit monooxygenase activities, the monoclonal antibody MAb 1-7-1 recognizing two isoenzymes of methylcholanthrene-induced cytochrome P-450 was applied.	Methylcholanthrene	101-119	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	128-144
2292469-2	1990	Spleen cells from 8-week-old male, Sprague-Dawley (S-D) rats exposed to 1, 10 or 100 micrograms/ml 3-MC in vitro for 18 h exhibited a dose-dependent decrease in natural killer (NK) cell cytotoxicity against the YAC-1 tumor target cells in a 4 h 51Cr-release assay.	Methylcholanthrene	99-103	ADP-ribosyltransferase 1	Mus musculus	211-216
2155194-12	1990	In addition, ethoxycumarin-O-deethylase and aryl hydrocarbon hydroxylase could be induced in vitro by treatment with methyl cholanthrene.	Methylcholanthrene	117-136	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-72
2229923-1	1990	The immunosuppressive effects of in vivo (subcutaneous) exposure to 40 or 80 mg/kg 3-methylcholanthrene (MC) were examined in aryl hydrocarbon hydroxylase (AHH) responsive C57BL/6 (B6) and AHH non-responsive DBA/2 (D2) inbred strains of mice.	Methylcholanthrene	83-103	aryl-hydrocarbon receptor	Mus musculus	172-192
2229923-1	1990	The immunosuppressive effects of in vivo (subcutaneous) exposure to 40 or 80 mg/kg 3-methylcholanthrene (MC) were examined in aryl hydrocarbon hydroxylase (AHH) responsive C57BL/6 (B6) and AHH non-responsive DBA/2 (D2) inbred strains of mice.	Methylcholanthrene	105-107	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	156-159
2229923-6	1990	When antigen-pulsed adherent cells from MC-treated B6 and D2 mice were recombined with control non-adherent cells from syngeneic and B6D2F1 mice, T-cell proliferation was significantly reduced.	Methylcholanthrene	40-42	defensin beta 2	Mus musculus	51-60
2229923-9	1990	These results suggest that MC treatment has a similar suppressive effect on the immune responses of both B6 and D2 mice that involves the quality of accessory cell-T-cell interactions.	Methylcholanthrene	27-29	defensin beta 2	Mus musculus	105-114
2097279-0	1990	[Effect of monoclonal antibody against methylcholanthrene-induced cytochrome P-450 forms on benzo(a)pyrene metabolism in hepatic microsomes of C57BL/10 mice].	Methylcholanthrene	39-57	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	66-82
2324156-0	1990	Antitumor effects of a new interleukin-2 slow delivery system on methylcholanthrene-induced fibrosarcoma in mice.	Methylcholanthrene	65-83	interleukin 2	Mus musculus	27-40
2324156-2	1990	We have evaluated the antitumor effects of the IL-2 mini-pellet on an established solid murine tumor, methylcholanthrene-induced fibrosarcoma (Meth A).	Methylcholanthrene	102-120	interleukin 2	Mus musculus	47-51
2299585-9	1990	The most likely mechanisms for the effects observed are 1) inhibition of acetaminophen reactive metabolite formation in 3-methylcholanthrene-induced animals by each of the methylxanthines, and 2) activation of the phenobarbital-inducible forms of cytochrome(s) P-450 toward formation of acetaminophen reactive metabolites by caffeine and theophylline, but not theobromine.	Methylcholanthrene	120-140	VPS52 subunit of GARP complex	Rattus norvegicus	52-57
2167416-3	1990	The addition of phenobarbital or 3-methylcholanthrene, which induce cytochrome P450, significantly enhanced the formation of Epo.	Methylcholanthrene	33-53	erythropoietin	Homo sapiens	125-128
2157855-10	1990	After the separation of Ah receptor fraction from liver cytosol in the presence of molybdate, 3-MC consistently bound to a greater extent.	Methylcholanthrene	94-98	aryl hydrocarbon receptor	Rattus norvegicus	24-35
2118391-0	1990	[An immunochemical analysis of the induction of cytochrome P-450 isoforms in the liver of fresh-water fishes by 3-methylcholanthrene, beta-naphthoflavone and aroclor 1254].	Methylcholanthrene	112-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
2118391-2	1990	Using the inhibitory analysis of microsomal monooxygenase activities carried out by the specific polyclonal antibodies it has been shown that 3-methylcholanthrene, beta-naphthoflavone and arochlor 1254 induce isoforms immunologically related to cytochrome P-488c but not to the rat cytochrome P-450b in fish liver microsomes.	Methylcholanthrene	142-162	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	282-299
20702269-2	1990	The mice had been previously injected with a fixed amount of the AHH inducer 3-methylcholanthrene (MC) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or with the vehicle (olive oil) alone.	Methylcholanthrene	77-97	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	65-68
2184350-7	1990	Major populations of tumor-infiltrating lymphocytes (TIL) were found to be R1-3B3 (CD5)- and R1-10B5 (CD8)-positive cells in methylcholanthrene-induced autochthonous tumor.	Methylcholanthrene	125-143	Cd5 molecule	Rattus norvegicus	83-86
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	14-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-74
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	14-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	68-74
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	14-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	193-221
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	14-34	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	223-226
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	36-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-74
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	36-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	68-74
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	36-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	193-221
2092329-1	1990	The effect of 3-methylcholanthrene (MC) treatment on the cytochrome P-450c content of various rat tissues was examined by measuring the level of immunodetectable P-450c in conjunction with its aryl hydrocarbon hydroxylase (AHH) activity.	Methylcholanthrene	36-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	223-226
1704145-0	1990	Methylcholanthrene-induced murine fibrosarcoma cell line BMT-11 secretes granulocyte colony-stimulating factor.	Methylcholanthrene	0-18	colony stimulating factor 3 (granulocyte)	Mus musculus	73-110
20837414-10	1990	These results indicate that isomers of Cl-DBFs induce effectively 3-methylcholanthrene-inducible type of cytochrome P-450.	Methylcholanthrene	66-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	105-121
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	0-20	flightless I actin binding protein	Mus musculus	43-47
2220168-1	1990	Caffeine is mainly metabolized by 3-methyl-cholanthrene-inducible cytochrome P-450, whereas metamizol (Analgin) is probably mainly metabolized by phenobarbital inducible cytochromes P-450.	Methylcholanthrene	34-55	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-82
10660102-4	1999	Treatment with both iNOS antisense and missense ODNs during the promotional phase of the C3H10T1/2 transformation assay significantly increased the number of neoplastic foci in 3-methylcholanthrene (MCA) treated cells which corresponded with the ability of the ODN to inhibit NO production.	Methylcholanthrene	177-197	nitric oxide synthase 2, inducible	Mus musculus	20-24
10660102-4	1999	Treatment with both iNOS antisense and missense ODNs during the promotional phase of the C3H10T1/2 transformation assay significantly increased the number of neoplastic foci in 3-methylcholanthrene (MCA) treated cells which corresponded with the ability of the ODN to inhibit NO production.	Methylcholanthrene	199-202	nitric oxide synthase 2, inducible	Mus musculus	20-24
4084315-3	1985	While 3-methylcholanthrene induced a new form of cytochrome P-450 in kidney and lung microsomes, phenobarbital caused no major change in the HPLC profiles of these microsomes.	Methylcholanthrene	6-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
34844338-5	2022	Results showed MC with molar ratio of Co and Zn at 3:1 (Co-CNT/NPC3/1) achieved the maximal adsorption capacity to 118.3 mg g-1.	Methylcholanthrene	15-17	NPC intracellular cholesterol transporter 1	Homo sapiens	63-69
34481160-6	2022	Of these compounds, 20-methylcholanthrene, 7-methylbenz(a)anthracene, 10-methylbenz(a)pyrene, and 7,12-dimethylbenz(a)anthracene exhibited significant AhR-mediated potency.	Methylcholanthrene	20-41	aryl hydrocarbon receptor	Homo sapiens	151-154
34874153-9	2021	Triplet state time-dependent density functional theory calculations showed that the weak luminescence of Ru-1 was mostly due to the population of the non-emissive 3MC state.	Methylcholanthrene	163-166	Scm like with four mbt domains 1	Homo sapiens	105-109
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	0-20	keratin 14	Mus musculus	134-144
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	0-20	SRY (sex determining region Y)-box 9	Mus musculus	175-179
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	0-20	leucine rich repeat (in FLII) interacting protein 1	Mus musculus	230-236
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	22-25	flightless I actin binding protein	Mus musculus	43-47
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	22-25	keratin 14	Mus musculus	134-144
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	22-25	SRY (sex determining region Y)-box 9	Mus musculus	175-179
34948000-10	2021	3-Methylcholanthrene (MCA)-induced cSCC in Flii overexpressing mice showed increased markers of cancer metastasis including talin and keratin-14 and a significant increase in SOX9 alongside a reduction in Flii associated protein (Flap-1).	Methylcholanthrene	22-25	leucine rich repeat (in FLII) interacting protein 1	Mus musculus	230-236
34203324-3	2021	In this work, a pilot docking study aimed at comparing the interaction of two prodrugs, nabumetone (NB) and its tricyclic analog 7-methoxy-2,3-dihydro-1H-cyclopenta(b)naphthalen-1-one (MC), and their common active metabolite 6-methoxy-2-naphthylacetic acid (MNA) with the COX binding site, was carried out.	Methylcholanthrene	185-187	cytochrome c oxidase subunit 8A	Homo sapiens	272-275
34468979-1	2021	Belantamab mafodotin (belamaf) is an antibody-drug conjugate comprising a humanized anti-B-cell maturation antigen (BCMA) monoclonal antibody conjugated to monomethyl auristatin-F (MMAF) via a protease-resistant maleimidocaproyl (mc) linker.	Methylcholanthrene	230-232	TNF receptor superfamily member 17	Homo sapiens	84-114
34280616-0	2021	Activation of the aryl hydrocarbon receptor by 3-methylcholanthrene, but not by indirubin, suppresses mammosphere formation via downregulation of CDC20 expression in breast cancer cells.	Methylcholanthrene	47-67	aryl hydrocarbon receptor	Homo sapiens	18-43
34280616-0	2021	Activation of the aryl hydrocarbon receptor by 3-methylcholanthrene, but not by indirubin, suppresses mammosphere formation via downregulation of CDC20 expression in breast cancer cells.	Methylcholanthrene	47-67	cell division cycle 20	Homo sapiens	146-151
34280616-2	2021	We reported previously that 3-methylcholanthrene (3MC), an exogenous AhR agonist, inhibited tumorsphere (mammosphere) formation from breast cancer cell lines, while the endogenous AhR agonist, indirubin, very weakly inhibited this process.	Methylcholanthrene	28-48	aryl hydrocarbon receptor	Homo sapiens	69-72
34280616-2	2021	We reported previously that 3-methylcholanthrene (3MC), an exogenous AhR agonist, inhibited tumorsphere (mammosphere) formation from breast cancer cell lines, while the endogenous AhR agonist, indirubin, very weakly inhibited this process.	Methylcholanthrene	50-53	aryl hydrocarbon receptor	Homo sapiens	69-72
34411815-6	2021	Exposure to the MC diet also significantly decreased the thickness of smooth muscle layer and SMCs contractile markers expression (myosin heavy chain 11, smooth muscle actin gamma 2, transgelin, calponin 1) in jejunum and ileum of piglets.	Methylcholanthrene	16-18	myosin heavy chain 11	Homo sapiens	131-181
34411815-6	2021	Exposure to the MC diet also significantly decreased the thickness of smooth muscle layer and SMCs contractile markers expression (myosin heavy chain 11, smooth muscle actin gamma 2, transgelin, calponin 1) in jejunum and ileum of piglets.	Methylcholanthrene	16-18	transgelin	Homo sapiens	183-193
34411815-6	2021	Exposure to the MC diet also significantly decreased the thickness of smooth muscle layer and SMCs contractile markers expression (myosin heavy chain 11, smooth muscle actin gamma 2, transgelin, calponin 1) in jejunum and ileum of piglets.	Methylcholanthrene	16-18	calponin 1	Homo sapiens	195-205
34627522-4	2021	When it was competitively replaced by thiamethoxam and dissociated out of beta-CD, it would be converted to MC, which could be excited by visible light around 550 nm to produce red fluorescence.	Methylcholanthrene	108-110	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	74-81