PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28137513-6	2017	The kcat/KB value results in DeltaG  of 14.7, 12.6, 6.2, and 6.2 kcal/mol for the 3alpha-HSD/CR catalyzed reaction of cyclohexanol, 2-decalol, androstenol, and androsterone, respectively.	Androstenols	143-154	aldo-keto reductase family 1 member C4	Homo sapiens	82-92
26831808-8	2016	Using this assay system, androstenol and clotrimazole, both of which are inverse agonists of CAR, were classified as an antagonist and weak agonist, respectively.	Androstenols	25-36	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	93-96
25905697-4	2015	For the current paper we characterized the pharmacodynamic interactions of three known CAR inverse agonists/antagonists-PK11195, clotrimazole and androstenol-with the prototype agonist CITCO (6-(4-chlorophenyl)imidazo[2,1-b][1,3] thiazole-5-carbaldehyde-O-(3,4-dichlorobenzyl)oxime) using the TR-FRET LanthaScreen(TM) assay.	Androstenols	146-157	nuclear receptor subfamily 1 group I member 3	Homo sapiens	87-90
20686338-5	2010	Androstenol (Andro) and clotrimazole (CLT), which are both inverse agonists of hCAR, were classified as an antagonist and weak agonist, respectively, in our novel assay system.	Androstenols	0-11	CXADR Ig-like cell adhesion molecule	Homo sapiens	79-83
20686338-5	2010	Androstenol (Andro) and clotrimazole (CLT), which are both inverse agonists of hCAR, were classified as an antagonist and weak agonist, respectively, in our novel assay system.	Androstenols	0-5	CXADR Ig-like cell adhesion molecule	Homo sapiens	79-83
12869636-8	2003	Androstenol repressed the mCAR-mediated constitutive activation of the CYP2C19 promoter in HepG2 cells, whereas the potent mCAR ligand 1,4-bis[2-3,5-dichloropyridyloxyl)] benzene derepressed this response.	Androstenols	0-11	coxsackie virus and adenovirus receptor	Mus musculus	26-30
16415088-6	2006	Androstenol (0.1-1 microM) also potentiated the amplitude of GABA-activated currents in human embryonic kidney 293 cells transfected with recombinant alpha1beta2gamma2 and alpha2beta2gamma2 GABA(A) receptors and, at high concentrations (10-300 microM), directly activated currents in these cells.	Androstenols	0-11	adrenoceptor alpha 1D	Homo sapiens	150-167
15610734-3	2004	We now report the crystal structure of murine CAR bound to the inverse agonist androstenol.	Androstenols	79-90	nuclear receptor subfamily 1, group I, member 3	Mus musculus	46-49
17962186-7	2007	Both Wy-14,643 and ciprofibrate occupied the ligand binding pocket of CAR and adapted a binding mode similar to that of the CAR inverse agonist androstenol.	Androstenols	144-155	nuclear receptor subfamily 1, group I, member 3	Mus musculus	124-127
16635107-8	2006	In contrast, no effect was seen following exposure to the potent murine constitutive androstane receptor-ligand TCPOBOP and the hormonal murine constitutive androstane receptor-ligands androstenol and oestrone.	Androstenols	185-196	nuclear receptor subfamily 1, group I, member 3	Mus musculus	144-176
12948398-2	2003	The high basal activity of mCAR can be modulated by inhibitory steroids related to androstenol and by activating xenobiotic chemicals such as 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene and chlorpromazine.	Androstenols	83-94	coxsackie virus and adenovirus receptor	Mus musculus	27-31
14561088-2	2003	Uniquely among nuclear receptors, mouse CAR (mCAR) can be suppressed by androstenol and activated by structurally diverse drugs, pesticides, and environmental pollutants.	Androstenols	72-83	nuclear receptor subfamily 1, group I, member 3	Mus musculus	40-43
14561088-2	2003	Uniquely among nuclear receptors, mouse CAR (mCAR) can be suppressed by androstenol and activated by structurally diverse drugs, pesticides, and environmental pollutants.	Androstenols	72-83	coxsackie virus and adenovirus receptor	Mus musculus	45-49
14561088-6	2003	Analysis of chimeric and mutant mCAR constructs suggested that androstenol sensitivity is controlled by residues between amino acids 201-263 (helices 5-7) and it does not depend on the residue 350 within helix 12, as previously suggested.	Androstenols	63-74	coxsackie virus and adenovirus receptor	Mus musculus	32-36
12869636-8	2003	Androstenol repressed the mCAR-mediated constitutive activation of the CYP2C19 promoter in HepG2 cells, whereas the potent mCAR ligand 1,4-bis[2-3,5-dichloropyridyloxyl)] benzene derepressed this response.	Androstenols	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
12049174-7	2002	In wild type animals, pretreatment with the CAR inverse agonist androstenol blocks the response of both the CYP2B10 and CYP3A11 genes to PB and TCPOBOP, and decreases basal CYP3A11 expression.	Androstenols	64-75	nuclear receptor subfamily 1, group I, member 3	Mus musculus	44-47
12114525-6	2002	In contrast, an antagonist of CAR, androstenol, alleviated the repression effect.	Androstenols	35-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	30-33
12807759-2	2003	Previously, in vitro studies have shown that the testosterone metabolites, androstenol and androstenol, inhibit the constitutive transcriptional activity of CAR, suggesting that differences might exist in the response to CAR-mediated gene activation between different sexes.	Androstenols	75-86	nuclear receptor subfamily 1, group I, member 3	Mus musculus	157-160
12807759-2	2003	Previously, in vitro studies have shown that the testosterone metabolites, androstenol and androstenol, inhibit the constitutive transcriptional activity of CAR, suggesting that differences might exist in the response to CAR-mediated gene activation between different sexes.	Androstenols	75-86	nuclear receptor subfamily 1, group I, member 3	Mus musculus	221-224
12807759-2	2003	Previously, in vitro studies have shown that the testosterone metabolites, androstenol and androstenol, inhibit the constitutive transcriptional activity of CAR, suggesting that differences might exist in the response to CAR-mediated gene activation between different sexes.	Androstenols	91-102	nuclear receptor subfamily 1, group I, member 3	Mus musculus	157-160
12807759-2	2003	Previously, in vitro studies have shown that the testosterone metabolites, androstenol and androstenol, inhibit the constitutive transcriptional activity of CAR, suggesting that differences might exist in the response to CAR-mediated gene activation between different sexes.	Androstenols	91-102	nuclear receptor subfamily 1, group I, member 3	Mus musculus	221-224
12807759-7	2003	Administration of androstenol to TCPOBOP-treated mice caused a reduction of labelling index, which was accompanied by a decrease of CYP2B10 and CAR mRNA levels.	Androstenols	18-29	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	132-139
12807759-7	2003	Administration of androstenol to TCPOBOP-treated mice caused a reduction of labelling index, which was accompanied by a decrease of CYP2B10 and CAR mRNA levels.	Androstenols	18-29	nuclear receptor subfamily 1, group I, member 3	Mus musculus	144-147
12807759-8	2003	In conclusion, the results show that, in addition to microsomal detoxification, another biological response elicited by the CAR ligand TCPOBOP, namely, hepatocyte proliferation, occurs at higher levels in female than male mice, suggesting that CAR transcriptional activity in males is partially counteracted by physiological higher levels of testosterone metabolites such as androstenol and androstenol.	Androstenols	375-386	nuclear receptor subfamily 1, group I, member 3	Mus musculus	124-127
12807759-8	2003	In conclusion, the results show that, in addition to microsomal detoxification, another biological response elicited by the CAR ligand TCPOBOP, namely, hepatocyte proliferation, occurs at higher levels in female than male mice, suggesting that CAR transcriptional activity in males is partially counteracted by physiological higher levels of testosterone metabolites such as androstenol and androstenol.	Androstenols	375-386	nuclear receptor subfamily 1, group I, member 3	Mus musculus	244-247
12807759-8	2003	In conclusion, the results show that, in addition to microsomal detoxification, another biological response elicited by the CAR ligand TCPOBOP, namely, hepatocyte proliferation, occurs at higher levels in female than male mice, suggesting that CAR transcriptional activity in males is partially counteracted by physiological higher levels of testosterone metabolites such as androstenol and androstenol.	Androstenols	391-402	nuclear receptor subfamily 1, group I, member 3	Mus musculus	124-127
12807759-8	2003	In conclusion, the results show that, in addition to microsomal detoxification, another biological response elicited by the CAR ligand TCPOBOP, namely, hepatocyte proliferation, occurs at higher levels in female than male mice, suggesting that CAR transcriptional activity in males is partially counteracted by physiological higher levels of testosterone metabolites such as androstenol and androstenol.	Androstenols	391-402	nuclear receptor subfamily 1, group I, member 3	Mus musculus	244-247
12631293-0	2003	Assessment of porcine and human 16-ene-synthase, a third activity of P450c17, in the formation of an androstenol precursor.	Androstenols	101-112	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	69-76
12631293-3	2003	In this report, we examine at the molecular level whether the enzyme 17 alpha-hydroxylase/17,20-lyase (P450c17), which possesses dual 17 alpha-hydroxylase and 17,20-lyase activities and catalyzes the production of precursors for glucocorticoids and sex steroids, is also able to catalyze the formation of a third class of active steroids, 16-ene steroids (including androstenol).	Androstenols	366-377	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	103-110
12631293-9	2003	Our results therefore demonstrate that human P450c17, as other enzymes of the classical steroidogenic pathway, is involved in the biosynthetic pathway leading to the formation of androstenol.	Androstenols	179-190	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	45-52
12049174-7	2002	In wild type animals, pretreatment with the CAR inverse agonist androstenol blocks the response of both the CYP2B10 and CYP3A11 genes to PB and TCPOBOP, and decreases basal CYP3A11 expression.	Androstenols	64-75	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	108-115
12049174-7	2002	In wild type animals, pretreatment with the CAR inverse agonist androstenol blocks the response of both the CYP2B10 and CYP3A11 genes to PB and TCPOBOP, and decreases basal CYP3A11 expression.	Androstenols	64-75	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	120-127
12049174-7	2002	In wild type animals, pretreatment with the CAR inverse agonist androstenol blocks the response of both the CYP2B10 and CYP3A11 genes to PB and TCPOBOP, and decreases basal CYP3A11 expression.	Androstenols	64-75	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	173-180
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Androstenols	67-78	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	15-21
11457660-1	2001	It has been shown recently that androstenol and androstanol could modulate gene expression through the nuclear orphan receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor).	Androstenols	32-43	nuclear receptor subfamily 1 group I member 3	Homo sapiens	128-131
11457660-1	2001	It has been shown recently that androstenol and androstanol could modulate gene expression through the nuclear orphan receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor).	Androstenols	32-43	nuclear receptor subfamily 1 group I member 3	Homo sapiens	133-165
11457660-1	2001	It has been shown recently that androstenol and androstanol could modulate gene expression through the nuclear orphan receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor).	Androstenols	32-43	nuclear receptor subfamily 1 group I member 2	Homo sapiens	171-174
11457660-1	2001	It has been shown recently that androstenol and androstanol could modulate gene expression through the nuclear orphan receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor).	Androstenols	32-43	nuclear receptor subfamily 1 group I member 2	Homo sapiens	176-195
11457660-5	2001	It has also been shown recently that androstenol could modulate the activity of CAR and PXR and the expression of some cytochrome P450 drug-metabolizing enzymes.	Androstenols	37-48	nuclear receptor subfamily 1 group I member 3	Homo sapiens	80-83
11457660-5	2001	It has also been shown recently that androstenol could modulate the activity of CAR and PXR and the expression of some cytochrome P450 drug-metabolizing enzymes.	Androstenols	37-48	nuclear receptor subfamily 1 group I member 2	Homo sapiens	88-91
11457660-8	2001	We thus provided evidence that androstenol, the ligand for CAR and PXR, is produced by the biosynthetic pathway of sex steroids.	Androstenols	31-42	nuclear receptor subfamily 1 group I member 3	Homo sapiens	59-62
11457660-8	2001	We thus provided evidence that androstenol, the ligand for CAR and PXR, is produced by the biosynthetic pathway of sex steroids.	Androstenols	31-42	nuclear receptor subfamily 1 group I member 2	Homo sapiens	67-70
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Androstenols	67-78	CXADR pseudogene 1	Homo sapiens	164-167
9783588-3	1998	While searching for potential ligands of CAR-beta, we found that the steroids androstanol and androstenol inhibit the constitutive activity of CAR-beta.	Androstenols	94-105	syntaxin 8	Homo sapiens	41-49
9783588-3	1998	While searching for potential ligands of CAR-beta, we found that the steroids androstanol and androstenol inhibit the constitutive activity of CAR-beta.	Androstenols	94-105	syntaxin 8	Homo sapiens	143-151
8431438-5	1993	Effects of short-chain phosphatidylcholines on Ca2+ binding stoichiometry and on ATPase activity can be reversed by addition of androstenol, oleic acid, methyl oleate, or oleyl alcohol but these molecules have no effect on the ATPase reconstituted with dinervonylphosphatidylcholine (C24:1).	Androstenols	128-139	dynein axonemal heavy chain 8	Homo sapiens	81-87
8431438-5	1993	Effects of short-chain phosphatidylcholines on Ca2+ binding stoichiometry and on ATPase activity can be reversed by addition of androstenol, oleic acid, methyl oleate, or oleyl alcohol but these molecules have no effect on the ATPase reconstituted with dinervonylphosphatidylcholine (C24:1).	Androstenols	128-139	dynein axonemal heavy chain 8	Homo sapiens	227-233