PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
8461288-2	1993	With the exception of chlorophyll b, which is known to be associated with the complexes comprising the outer antenna (LHCII, CP24, CP26, CP29), the spectral forms occur with similar absorption maxima and are present in rather similar amounts in each of the antenna complexes.	chlorophyll b	22-35	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-135
33233443-0	2020	CYP26A1 Is a Novel Biomarker for Betel Quid-Related Oral and Pharyngeal Cancers.	betel	33-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
1864384-3	1991	Based on the assumption that there is 1 cytochrome b559 per reaction centre it has been found that oxygen-evolving complexes containing CP26 and CP29 bind 42 chlorophyll molecules.	Oxygen	99-105	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	136-140
1864384-3	1991	Based on the assumption that there is 1 cytochrome b559 per reaction centre it has been found that oxygen-evolving complexes containing CP26 and CP29 bind 42 chlorophyll molecules.	Chlorophyll	158-169	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	136-140
1864384-4	1991	When CP26 and CP29 are stripped away, the resulting PSII cores bind 30 chlorophyll molecules while CP43-less cores bind approximately 18 chlorophylls.	Chlorophyll	71-82	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	5-9
1864384-4	1991	When CP26 and CP29 are stripped away, the resulting PSII cores bind 30 chlorophyll molecules while CP43-less cores bind approximately 18 chlorophylls.	cp43	99-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	5-9
33233443-9	2020	We found that CYP26A1 was downregulated as the arecoline dose increased.	Arecoline	47-56	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-21
33233443-11	2020	Arecoline appears to modulate CYP26A1 expression through specific pathways.	Arecoline	0-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	30-37
34389675-5	2021	There were two unexpected findings: 1) a strong induction of CYPs involved in activation of fatty acids (CYP4), and in inactivation of calcitriol (CYP24A1) and retinoic acid (CYP26A1); and 2) a marked down-regulation of FOS, FRA1, and JUN, known tethering partners of ERbeta.	Calcitriol	135-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	175-182
19525031-0	2009	Retinoic acid 4-hydroxylase inducibility and clinical response to isotretinoin in patients with acne.	Isotretinoin	66-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-27
19525031-2	2009	The CYP26 enzyme acts specifically on tRA, but not 13-cis RA (isotretinoin), a retinoid used to treat severe acne.	Isotretinoin	62-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19525031-2	2009	The CYP26 enzyme acts specifically on tRA, but not 13-cis RA (isotretinoin), a retinoid used to treat severe acne.	Retinoids	79-87	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19525031-3	2009	However, 13-cis RA can isomerize to tRA, which can then be metabolized by CYP26.	Tretinoin	16-18	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	74-79
19525031-5	2009	We then investigated whether response to oral 13-cis RA among patients with acne correlates with variability in CYP26 expression.	Tretinoin	53-55	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	112-117
34389675-5	2021	There were two unexpected findings: 1) a strong induction of CYPs involved in activation of fatty acids (CYP4), and in inactivation of calcitriol (CYP24A1) and retinoic acid (CYP26A1); and 2) a marked down-regulation of FOS, FRA1, and JUN, known tethering partners of ERbeta.	Tretinoin	160-173	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	175-182
33472949-3	2021	Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs).	Tretinoin	164-177	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	229-236
35565751-0	2022	CRABPs Alter all-trans-Retinoic Acid Metabolism by CYP26A1 via Protein-Protein Interactions.	Tretinoin	13-36	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-58
35565751-3	2022	We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family.	Tretinoin	50-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-90
35565751-3	2022	We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family.	Tretinoin	106-110	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-90
35565751-5	2022	The unbound atRA Km values for 4-OH-atRA formation by CYP26A1 were 4.7 +- 0.8 nM with atRA, 6.8 +- 1.7 nM with holo-CRABP1 and 6.1 +- 2.7 nM with holo-CRABP2 as a substrate.	4-oh-atra	31-40	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-61
35565751-5	2022	The unbound atRA Km values for 4-OH-atRA formation by CYP26A1 were 4.7 +- 0.8 nM with atRA, 6.8 +- 1.7 nM with holo-CRABP1 and 6.1 +- 2.7 nM with holo-CRABP2 as a substrate.	Tretinoin	86-90	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-61
33909340-2	2021	BRIEF METHODS: In the present study we have tested human CYPs for metabolization of five proluciferin ester substrates which had previously only been known to be hydroxylated by CYP26A1.	proluciferin ester	89-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
33724958-5	2021	Specifically, high expression of the ATRA-catabolizing enzyme, CYP26A1, in human IDCM could dampen prospects for an ATRA-based therapy.	Tretinoin	37-41	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	63-70
33724958-5	2021	Specifically, high expression of the ATRA-catabolizing enzyme, CYP26A1, in human IDCM could dampen prospects for an ATRA-based therapy.	Tretinoin	116-120	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	63-70
33472949-3	2021	Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs).	Fluorouracil	50-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	229-236
33472949-3	2021	Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs).	Fluorouracil	68-71	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	229-236
34122632-4	2021	The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1).	Tretinoin	88-92	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	297-317
34122632-4	2021	The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1).	Tretinoin	88-92	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	319-326
34122632-4	2021	The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1).	Tretinoin	275-279	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	297-317
34122632-4	2021	The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1).	Tretinoin	275-279	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	319-326
35565751-7	2022	In addition, increasing concentrations in apo-CRABPs decreased the 4-OH-atRA formation rates by CYP26A1.	4-oh-atra	67-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	96-103
33472949-3	2021	Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs).	Tretinoin	179-181	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	229-236
32151018-0	2020	Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.	Tretinoin	11-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	91-96
31903789-3	2020	In vivo, retinoids induce CYP26 enzyme production in the liver, enhancing their own rapid metabolic clearance, while retinoid resistance in tumour cells themselves is considered to be due in part to increased CYP26 production.	Retinoids	9-18	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-31
31903789-3	2020	In vivo, retinoids induce CYP26 enzyme production in the liver, enhancing their own rapid metabolic clearance, while retinoid resistance in tumour cells themselves is considered to be due in part to increased CYP26 production.	Retinoids	9-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-31
31903789-4	2020	Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models.	Tretinoin	0-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-70
31903789-4	2020	Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models.	Tretinoin	92-105	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-70
31903789-4	2020	Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models.	Tretinoin	42-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-70
32251704-2	2020	The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects.	Azoles	21-26	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	41-46
32251704-2	2020	The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects.	Tretinoin	63-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	41-46
32251704-2	2020	The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects.	Tretinoin	78-80	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	41-46
32251704-9	2020	In silico results confirmed azole-related CYP26 inhibition and a weak general VPA inhibition on the tested HDACs.	Azoles	28-33	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-47
32251704-10	2020	Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE.	Valproic Acid	14-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-88
32251704-10	2020	Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE.	Valproic Acid	149-152	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-88
32251704-10	2020	Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE.	Tretinoin	167-169	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-88
32251704-13	2020	VPA MIEs (HDAC and CYP26 inhibition) impinge on the two converging AOPs.	Valproic Acid	0-3	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	19-24
33294638-0	2020	New luciferin-based probe substrates for human CYP26A1.	D-luciferin	4-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-54
33294638-1	2020	Activity of human CYP26A1 towards six proluciferin probe substrates and their ester derivatives was monitored.	proluciferin	38-50	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-25
33294638-1	2020	Activity of human CYP26A1 towards six proluciferin probe substrates and their ester derivatives was monitored.	Esters	78-83	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-25
33294638-6	2020	Taken together, we describe eleven new probe substrates for CYP26A1 and demonstrate for the first time that CYP26A1 does not only accept acid substrates but can also metabolize esters.	Esters	177-183	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	60-67
33294638-6	2020	Taken together, we describe eleven new probe substrates for CYP26A1 and demonstrate for the first time that CYP26A1 does not only accept acid substrates but can also metabolize esters.	Esters	177-183	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	108-115
32258025-1	2020	Organogenesis, including renal development, requires an appropriate retinoic acid concentration, which is established by differential expression of aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and cytochrome P450 family 26 subfamily A/B/C member 1 (CYP26A1/B1/C1).	Tretinoin	68-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	256-263
32151018-1	2020	This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration.	Tretinoin	76-89	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-67
32151018-1	2020	This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration.	Tretinoin	76-89	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	69-74
32151018-1	2020	This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration.	Tretinoin	91-93	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-67
32151018-1	2020	This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration.	Tretinoin	91-93	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	69-74
32151018-2	2020	Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling.	Tretinoin	26-39	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
32151018-2	2020	Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling.	Tretinoin	90-92	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
32151018-2	2020	Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling.	Tretinoin	154-156	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
32151018-3	2020	Cyp26 enzymes are necessary to generate RA gradients and to protect specific tissues from RA signalling.	Tretinoin	40-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
32151018-3	2020	Cyp26 enzymes are necessary to generate RA gradients and to protect specific tissues from RA signalling.	Tretinoin	90-92	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
32151018-5	2020	Here, the function of CYP26 enzymes is discussed in the context of the RA signalling pathway, enzymatic structure and biochemistry, human genetic disease, and function in development and regeneration as elucidated from animal model studies.	Tretinoin	71-73	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-27
32359660-0	2020	Using the human CYP26A1 gene promoter as a suitable tool for the determination of RAR-mediated retinoid activity.	Retinoids	95-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	16-23
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Tretinoin	99-118	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31744925-0	2020	Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids".	Tretinoin	54-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	28-35
31744925-0	2020	Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids".	Tretinoin	54-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-90
31744925-0	2020	Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids".	Retinoids	143-152	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	28-35
31744925-0	2020	Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids".	Retinoids	143-152	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-90
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Tretinoin	99-118	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Tretinoin	120-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Tretinoin	120-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Isotretinoin	133-138	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Isotretinoin	133-138	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Isotretinoin	146-151	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	Isotretinoin	146-151	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	4-oh-ra	184-191	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	4-oh-ra	184-191	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	4-oxoretinoic acid	196-204	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-2	2019	The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency.	4-oxoretinoic acid	196-204	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	32-39
31419517-4	2019	All three CYP26 enzymes are inducible by treatment with atRA in various prenatal and postnatal tissues and cell types.	Tretinoin	56-60	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-15
31419517-6	2019	In humans and in animal models the expression patterns of CYP26 enzymes have been shown to be tissue and cell type specific, and the expression of the CYP26 enzymes is believed to regulate the formation of critical atRA concentration gradients in various tissue types.	Tretinoin	215-219	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-63
31419517-6	2019	In humans and in animal models the expression patterns of CYP26 enzymes have been shown to be tissue and cell type specific, and the expression of the CYP26 enzymes is believed to regulate the formation of critical atRA concentration gradients in various tissue types.	Tretinoin	215-219	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	151-156
31419517-9	2019	Interestingly, some of these genetic variants result in increased activity of the CYP26 enzymes potentially leading to complex gene-environment interactions due to variability in dietary intake of retinoids.	Retinoids	197-206	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-87
31419517-10	2019	This review highlights the current knowledge of structure-function of CYP26 enzymes and focuses on their role in human retinoid metabolism in different tissues.	Retinoids	119-127	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	70-75
31039331-0	2019	CYP26A1 gene promoter is a useful tool for reporting RAR-mediated retinoid activity.	Retinoids	66-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
31283017-6	2019	We found increases in mRNAs of differentiation-associated genes (Hoxa1, Cyp26a1, and RARbeta2) upon EtOH treatment of WT and Acss2-/- ESCs, but not Aldh2-/- ESCs.	Ethanol	100-104	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	72-79
31039331-1	2019	Of numerous genes regulated by retinoic acid (RA), CYP26A1 is the most inducible gene by RA.	Tretinoin	31-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-58
31039331-2	2019	In this study, we have used a shortened construct form, E4, of the CYP26A1 gene promoter, in a promoter-less vector with either luciferase or red fluorescent protein (RFP) as the reporter gene and have tested its responses to retinoids in transfected HepG2 and HEK293T cells.	Retinoids	226-235	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-74
30250298-5	2019	Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice.	Tretinoin	147-151	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
30885956-4	2019	In this study, we demonstrate that enhancing RA degradation in the host and to a lesser extent donor hematopoietic cells by overexpressing the RA-catabolizing enzyme CYP26A1 reduced GVHD.	Tretinoin	45-47	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	166-173
30885956-4	2019	In this study, we demonstrate that enhancing RA degradation in the host and to a lesser extent donor hematopoietic cells by overexpressing the RA-catabolizing enzyme CYP26A1 reduced GVHD.	Tretinoin	143-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	166-173
30737277-6	2019	As shown with CRISPR/Cas9 knockout lines, the retinol dehydrogenase gene Rdh10 and a functional RARE in the ROL transporter stimulated by retinoic acid 6 (Stra6) gene are required for EtOH induction of Hoxa1 and Cyp26a1 We conclude that EtOH stimulates stem cell differentiation by increasing the influx and metabolism of ROL for downstream RARgamma-dependent transcription.	Ethanol	184-188	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	212-219
30250298-5	2019	Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice.	Tretinoin	132-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
31288815-12	2019	Our studies demonstrated that five PRGs including Bcl2, FOXO1A, SCGB2A2, CYP26a1 and MMP11 exhibited significant progesterone-hyper-responsiveness in human PrMyoF cells as compared to PrMyoN cells (P < 0.05).	Progesterone	113-125	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	73-80
30737277-5	2019	We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum.	Ethanol	20-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	71-117
30737277-5	2019	We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum.	Ethanol	20-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	119-126
30737277-5	2019	We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum.	Ethanol	20-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	325-332
30737277-5	2019	We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum.	Tretinoin	148-150	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	71-117
30737277-5	2019	We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum.	Tretinoin	148-150	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	119-126
29984664-6	2018	RESULTS: RT-qPCR data analysis showed that after 12 h of exposure of HepG2/C3A cells to genistein (5 and 50 microM) there was an upregulation of CYP1A1 and CYP1B1 and downregulation of CYP2D6, CYP26A1 and CYP26B1 mRNA levels.	Genistein	88-97	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	193-200
29337257-5	2018	Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51.	Tretinoin	57-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	330-337
29337257-5	2018	Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51.	Sterols	75-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	330-337
29337257-5	2018	Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51.	Azoles	172-178	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	330-337
29990529-4	2018	Trans-resveratrol also altered expression levels of developmental regulator genes involved in embryonic patterning, such as Wnt3a, Tbx6, and Cyp26a1.	Resveratrol	0-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	141-148
29990529-7	2018	By contrast, a reduction in the DNA replication rate with aphidicolin (0.4 muM) or hydroxyurea (40 muM) created smaller and rounder EBs and altered the expression levels of Wnt3a, Tbx6, and Cyp26a1 in a manner similar to trans-resveratrol.	Aphidicolin	58-69	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	190-197
29990529-7	2018	By contrast, a reduction in the DNA replication rate with aphidicolin (0.4 muM) or hydroxyurea (40 muM) created smaller and rounder EBs and altered the expression levels of Wnt3a, Tbx6, and Cyp26a1 in a manner similar to trans-resveratrol.	Hydroxyurea	83-94	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	190-197
29476041-1	2018	The clearance of retinoic acid (RA) and its metabolites is believed to be regulated by the CYP26 enzymes, but the specific roles of CYP26A1, CYP26B1, and CYP26C1 in clearing active vitamin A metabolites have not been defined.	Vitamin A	181-190	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	132-139
29330906-4	2018	The developing embryo contains regions that produce RA, and specific intracellular concentrations of RA are created through local degradation mediated by Cyp26 enzymes.	Tretinoin	101-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	154-159
29177441-7	2018	These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme.	Tretinoin	90-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	41-48
29177441-7	2018	These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	41-48
28754309-6	2017	Here, we discuss accumulating evidence suggesting that cytochrome P450 (CYP26), the primary retinoid-inactivating enzyme, plays a critical role in the integration of two of these molecular programs: the retinoid and Hedgehog pathways.	Retinoids	92-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	72-77
28735443-8	2017	In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels.	Tretinoin	43-45	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	63-70
29066753-4	2017	Exploration of the orientational phase-space revealed that the placement of central carotenoids minimizes their interaction with the nearest chlorophylls in the plant antenna complexes LHCII, CP26, CP29 and LHCI.	Carotenoids	84-95	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	192-196
28754309-6	2017	Here, we discuss accumulating evidence suggesting that cytochrome P450 (CYP26), the primary retinoid-inactivating enzyme, plays a critical role in the integration of two of these molecular programs: the retinoid and Hedgehog pathways.	Retinoids	203-211	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	72-77
28754309-7	2017	Induction of stromal CYP26 by either one of these pathways limits retinoic acid concentration in the stem cell niche, with profound effects on tissue homeostasis and drug resistance.	Tretinoin	66-79	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	21-26
28087752-6	2017	Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence.	Tretinoin	16-18	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-85
28643469-5	2017	In antler chondrocytes, CYP26A1 and CYP26B1 weakened the sensitivity of ATRA to COL9A1.	Tretinoin	72-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	24-31
28087752-13	2017	CONCLUSIONS: RA regulates lung microvascular angiogenesis; the endothelium produces CYP26A1 which is increased in emphysema, possibly leading to reduced RA availability.	Tretinoin	153-155	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	84-91
28087752-6	2017	Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence.	Tretinoin	16-18	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	87-94
28275201-6	2017	Of these, ketoconazole and liarozole have shown some benefits, but their usage is limited by side effects and low potency toward the cytochrome P450 26A1 isoform (CYP26A1), the main atRA hydroxylase.	Ketoconazole	10-22	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	133-153
28275201-6	2017	Of these, ketoconazole and liarozole have shown some benefits, but their usage is limited by side effects and low potency toward the cytochrome P450 26A1 isoform (CYP26A1), the main atRA hydroxylase.	Ketoconazole	10-22	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	163-170
28275201-9	2017	The population-based PBPK model of atRA disposition incorporated saturable metabolic clearance of atRA, induction of CYP26A1 by atRA, and the absorption and distribution kinetics of atRA.	Tretinoin	35-39	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	117-124
28087565-5	2017	Embryonic tissues expressing Cyp26a1 show reduced efficiency of RA clearance.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-36
27589347-7	2016	The 79 deleted genes included CYP26A1 and C1, both major RA-metabolizing enzymes.	Tretinoin	57-59	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	30-37
28361034-10	2017	Two genes comprising OGS (CYP26A1 and RDH10) are strongly associated with ALDH1A2 in the retinoic acid (RA) pathways, suggesting a major role of RA signaling in early PCa progression.	Tretinoin	89-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-33
27775549-3	2016	We previously showed that expression of CYP26 in BM stromal cells maintains a retinoic acid-low (RA-low) microenvironment that prevents the differentiation of normal and malignant hematopoietic cells.	Tretinoin	78-91	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
27775549-3	2016	We previously showed that expression of CYP26 in BM stromal cells maintains a retinoic acid-low (RA-low) microenvironment that prevents the differentiation of normal and malignant hematopoietic cells.	Radium	97-99	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
27775549-5	2016	CYP26-mediated inactivation of RA within the BM microenvironment prevented plasma cell differentiation and promoted a B cell-like, BTZ-resistant phenotype in human MM cells that were cocultured on BM stroma.	Radium	31-33	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
27775549-5	2016	CYP26-mediated inactivation of RA within the BM microenvironment prevented plasma cell differentiation and promoted a B cell-like, BTZ-resistant phenotype in human MM cells that were cocultured on BM stroma.	Bortezomib	131-134	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
27589347-11	2016	CYP26A1 and C1 haploinsufficiency may contribute to the elevated retinoic acid concentrations and clinical findings of the patient, although this phenotype has not been reported in other patients with similar deletions, suggesting that other unknown genetic or environmental factors may also contribute.	Tretinoin	65-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
27193728-7	2016	PAMAM-50% C12 at 1 mug/mL altered the expression level of the oxidative stress-related genes, ROR1, CYP26A1, and TGFB1, which is a DNA damage response gene.	(Z)-14-methylpentadec-2-enoic acid	10-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
27242163-3	2016	Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARalpha, beta and gamma, and finally the catabolic enzyme CYP26A1.	Tretinoin	65-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	318-325
27366899-2	2016	Cytochrome P450 oxidoreductase (POR) is the only obligate electron donor for all of the microsomal cytochrome P450 enzymes including CYP26A1 which is highly specific for ATRA metabolism and efficacy in human myeloid leukaemia cells.	Tretinoin	170-174	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	133-140
26937021-0	2016	Identification of Tazarotenic Acid as the First Xenobiotic Substrate of Human Retinoic Acid Hydroxylase CYP26A1 and CYP26B1.	tazarotenic acid	18-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	104-111
26937021-1	2016	Cytochrome P450 (CYP) 26A1 and 26B1 are heme-containing enzymes responsible for metabolizing all-trans retinoic acid (at-RA).	Heme	40-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-35
26747727-6	2016	Additionally, Wnt3A attenuated ATRA-induced Cyp26a1 expression, inhibiting the degradation of ATRA into its oxidative forms.	Tretinoin	31-35	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	44-51
27193728-7	2016	PAMAM-50% C12 at 1 mug/mL altered the expression level of the oxidative stress-related genes, ROR1, CYP26A1, and TGFB1, which is a DNA damage response gene.	Poly(amidoamine)	0-5	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
27590114-6	2016	Consistent with these findings, increased colonic expression of the atRA-catabolizing enzyme, CYP26A1, correlated with reduced frequencies of tumoral cytotoxic CD8(+) T cells and with worse disease prognosis in human CRC.	Tretinoin	68-72	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-101
27366899-7	2016	KEY FINDINGS: All-trans-retinoic acid treatment caused the expression of POR upregulation and CYP26A1 downregulation in dose- and time-dependent manners.	Tretinoin	14-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-101
26374207-3	2016	The catabolic enzymes Cyp26a1 and Cyp26b1 have been studied in detail in the embryo, where they limit gradients of RA that form patterns of gene expression, crucial for morphogenesis.	Tretinoin	115-117	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
26374207-7	2016	In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone.	Serine	64-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
26374207-7	2016	In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone.	Serine	64-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	112-117
26374207-7	2016	In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone.	Tretinoin	152-154	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
26374207-7	2016	In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone.	Serine	179-182	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
26374207-7	2016	In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone.	Tretinoin	211-213	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
26937021-1	2016	Cytochrome P450 (CYP) 26A1 and 26B1 are heme-containing enzymes responsible for metabolizing all-trans retinoic acid (at-RA).	Tretinoin	103-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-35
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	tazarotenic acid	86-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-11
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	tazarotenic acid	86-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	212-219
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	Heme	132-136	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-11
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	Heme	132-136	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	212-219
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	tazarotenic acid	171-187	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-11
26937021-6	2016	The CYP26A1 and CYP26B1 homology models predicted that the benzothiopyranyl moiety of tazarotenic acid would be oriented toward the heme of each enzyme and suggested that tazarotenic acid would be a substrate of CYP26A1 and CYP26B1.	tazarotenic acid	171-187	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	212-219
26937021-7	2016	Metabolite identification experiments indicated that CYP26A1 and CYP26B1 oxidatively metabolized tazarotenic acid on the predicted moiety, with in vitro rates of metabolite formation by CYP26A1 and CYP26B1 being the highest across a panel of enzymes.	tazarotenic acid	97-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-60
26937021-7	2016	Metabolite identification experiments indicated that CYP26A1 and CYP26B1 oxidatively metabolized tazarotenic acid on the predicted moiety, with in vitro rates of metabolite formation by CYP26A1 and CYP26B1 being the highest across a panel of enzymes.	tazarotenic acid	97-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	186-193
26937021-9	2016	Overall, the homology models presented herein describe the enzyme characteristics leading to the metabolism of tazarotenic acid by CYP26A1 and CYP26B1 and support a potential role for the CYP26 enzymes in the metabolism of xenobiotics.	tazarotenic acid	111-127	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-138
26937021-9	2016	Overall, the homology models presented herein describe the enzyme characteristics leading to the metabolism of tazarotenic acid by CYP26A1 and CYP26B1 and support a potential role for the CYP26 enzymes in the metabolism of xenobiotics.	tazarotenic acid	111-127	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-136
26918322-1	2016	Cytochrome P450 CYP26 enzymes are responsible for all-trans-retinoic acid (atRA) clearance.	Tretinoin	50-73	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	16-21
26918322-1	2016	Cytochrome P450 CYP26 enzymes are responsible for all-trans-retinoic acid (atRA) clearance.	Tretinoin	75-79	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	16-21
26918322-2	2016	Inhibition of CYP26 enzymes will increase endogenous atRA concentrations and is an attractive therapeutic target.	Tretinoin	53-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-19
26918322-3	2016	However, the selectivity and potency of the existing atRA metabolism inhibitors toward CYP26A1 and CYP26B1 is unknown, and no selective CYP26A1 or CYP26B1 inhibitors have been developed.	Tretinoin	53-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	87-94
26918322-5	2016	A series of nonazole CYP26A1 selective inhibitors was identified with low nM potency.	nonazole	12-20	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	21-28
26999080-3	2016	Furthermore, the docking capabilities of the model were assessed by docking of the natural substrate all-trans-retinoic acid (atRA), and a group of known azole- and tetralone-based CYP26A1 inhibitors.	Tretinoin	126-130	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	181-188
26999080-3	2016	Furthermore, the docking capabilities of the model were assessed by docking of the natural substrate all-trans-retinoic acid (atRA), and a group of known azole- and tetralone-based CYP26A1 inhibitors.	Azoles	154-159	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	181-188
26999080-3	2016	Furthermore, the docking capabilities of the model were assessed by docking of the natural substrate all-trans-retinoic acid (atRA), and a group of known azole- and tetralone-based CYP26A1 inhibitors.	Tetralones	165-174	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	181-188
26009309-1	2016	Retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to have increased expression levels in breast cancers and to effectively promote the survival of breast carcinoma cells, implying a potential oncogenic function.	Tretinoin	0-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-46
26009309-1	2016	Retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to have increased expression levels in breast cancers and to effectively promote the survival of breast carcinoma cells, implying a potential oncogenic function.	Tretinoin	15-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-46
26058854-0	2015	The retinoic acid-metabolizing enzyme CYP26A1 upregulates fascin and promotes the malignant behavior of breast carcinoma cells.	Tretinoin	4-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	38-45
26365710-0	2015	Design, synthesis, and biological evaluation of amide imidazole derivatives as novel metabolic enzyme CYP26A1 inhibitors.	amide imidazole	48-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	102-109
26365710-2	2015	CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA.	Tretinoin	27-31	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
26365710-2	2015	CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA.	Tretinoin	73-77	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
26365710-2	2015	CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA.	4-hydroxyl-ra	83-96	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
26365710-4	2015	Herein, we describe the design, synthesis and biological evaluation of a series of new amide imidazole derivatives as retinoic acid metabolism blocking agents (RAMBAs) toward CYP26A1 enzyme.	amide imidazole	87-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	175-182
26365710-4	2015	Herein, we describe the design, synthesis and biological evaluation of a series of new amide imidazole derivatives as retinoic acid metabolism blocking agents (RAMBAs) toward CYP26A1 enzyme.	Tretinoin	118-131	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	175-182
26365710-11	2015	Both compounds 20 and 23 showed higher selectivity for CYP26A1 over other CYPs (CYP2D6, CYP3A4) when compared to liarozole.	liarozole	113-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
30695588-3	2016	We showed that ALDHA1 and RDH10 expression were inversely related with expression of a key gene for all-trans-retinoic acid catabolism, CYP26A1, and correlated with expression of RARalpha and PPARbeta/ genes.	retinoic	110-118	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	136-143
26058854-1	2015	The retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to efficiently enhance the oncogenic potential of breast cancer, suggesting a potential oncogenic function.	Tretinoin	4-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	43-50
26058854-1	2015	The retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to efficiently enhance the oncogenic potential of breast cancer, suggesting a potential oncogenic function.	Tretinoin	19-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	43-50
26058854-9	2015	These data suggest that fascin expression is modulated by the intracellular RA status regulated by the expression of CYP26A1 and plays a significant role in the malignant behavior of CYP26A1-expressing breast carcinoma cells.	Tretinoin	76-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	117-124
25684424-0	2015	Synthesis and biological evaluation of 3-phenyl-3-aryl carboxamido propanoic acid derivatives as small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26A1).	3-phenyl-3-aryl carboxamido propanoic acid	39-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	155-162
25915157-3	2015	We showed that bone marrow (BM) stromal cytochrome P450 (CYP)26 enzymes protect normal hematopoietic stem cells (HSCs) from the pro-differentiation effects of retinoic acid.	Tretinoin	159-172	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-63
26047326-4	2015	The microenvironment expression of cytochrome P450 (CYP)26, a retinoid-metabolizing enzyme was shown to determine normal hematopoietic stem cell fate.	Retinoids	62-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-58
26047326-8	2015	Inhibition of CYP26 rescued atRA levels and AML cell sensitivity in the presence of stroma.	Tretinoin	28-32	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-19
26047326-9	2015	Our data suggest that stromal CYP26 activity creates retinoid low sanctuaries in the BM that protect AML cells from systemic atRA therapy.	Retinoids	53-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	30-35
26047326-9	2015	Our data suggest that stromal CYP26 activity creates retinoid low sanctuaries in the BM that protect AML cells from systemic atRA therapy.	Tretinoin	125-129	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	30-35
26047326-10	2015	Inhibition of CYP26 provides new opportunities to expand the clinical activity of atRA in both APL and non-APL AML.	Tretinoin	82-86	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-19
25684424-6	2015	The most promising compound 32, with a CYP26A1 IC50 value of 1.36muM (compared to liarozole (IC50=2.45muM) and S8 (IC50=3.21muM)) displayed strong inhibitory and differentiation activity against HL60 cells.	liarozole	82-91	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-46
25684424-7	2015	In addition, the study focused on the effect of beta-phenylalanine, which forms the coordination bond with the heme of CYP26A1.	beta-phenylalanine	48-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	119-126
25684424-7	2015	In addition, the study focused on the effect of beta-phenylalanine, which forms the coordination bond with the heme of CYP26A1.	Heme	111-115	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	119-126
25541526-0	2015	Molecular recognition of CYP26A1 binding pockets and structure-activity relationship studies for design of potent and selective retinoic acid metabolism blocking agents.	Tretinoin	128-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	25-32
25541526-2	2015	However, ATRA is very easy to be metabolized into 4-hydroxyl-RA in vivo by CYP26A1, an inducible cytochrome P450 enzyme, eventually into more polar metabolites.	Tretinoin	9-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	75-82
25541526-2	2015	However, ATRA is very easy to be metabolized into 4-hydroxyl-RA in vivo by CYP26A1, an inducible cytochrome P450 enzyme, eventually into more polar metabolites.	4-hydroxyl-ra	50-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	75-82
25541526-3	2015	Therefore, it is vital to develop specific retinoic acid metabolism blocking agents (RAMBAs) to inhibit the metabolic enzyme CYP26A1 in the treatment of relevant diseases aforementioned.	Tretinoin	43-56	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	125-132
25541526-4	2015	In this study, CYP26A1 and its interactions with retinoic acid-competitive metabolism blocking agents were investigated by a combined ligand- and structure-based approach.	Tretinoin	49-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-22
25492813-12	2015	These data support the role of CYP26A1 to clear bioactive retinoids, and suggest that the enzyme forming active 4-oxo-atRA may be important in modulating retinoid action.	Retinoids	58-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	31-38
26233912-0	2015	Role of Retinoic Acid-Metabolizing Cytochrome P450s, CYP26, in Inflammation and Cancer.	Tretinoin	8-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-58
26233912-3	2015	Concentrations of atRA are tightly regulated in tissues, predominantly by the availability of retinol, synthesis of atRA by ALDH1A enzymes and metabolism and clearance of atRA by CYP26 enzymes.	Tretinoin	18-22	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	179-184
26233912-5	2015	In the immune system, the ALDH1A and CYP26 enzymes appear to modulate RA concentrations.	Radium	70-72	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	37-42
26233912-10	2015	Inhibition of the CYP26 enzymes to increase atRA concentrations and combat therapy resistance has been pursued as a drug target in these cancers.	Tretinoin	44-48	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-23
25492813-0	2015	Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids.	Tretinoin	39-52	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	13-20
25492813-12	2015	These data support the role of CYP26A1 to clear bioactive retinoids, and suggest that the enzyme forming active 4-oxo-atRA may be important in modulating retinoid action.	4-oxoretinoic acid	112-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	31-38
25492813-0	2015	Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids.	Tretinoin	39-52	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-75
25492813-0	2015	Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids.	Retinoids	128-137	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	13-20
25492813-12	2015	These data support the role of CYP26A1 to clear bioactive retinoids, and suggest that the enzyme forming active 4-oxo-atRA may be important in modulating retinoid action.	Retinoids	58-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	31-38
25492813-0	2015	Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids.	Retinoids	128-137	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-75
24667328-2	2014	RA levels in embryos are dampened by Cyp26 enzymes, which metabolize RA into easily degraded derivatives.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	37-42
25492813-2	2015	The primary hydroxylated metabolites formed from atRA by CYP26A1, and the subsequent metabolite 4-oxo-atRA, bind to RARs and potentially have biologic activity.	4-oxoretinoic acid	96-106	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	57-64
25492813-3	2015	Hence, CYP26A1, the main atRA hydroxylase, may function either to deplete bioactive retinoids or to form active metabolites.	Retinoids	84-93	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	7-14
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	Tretinoin	36-40	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	(4S)-OH-atRA	42-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	(4r)-oh-atra	56-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	4-oxoretinoic acid	70-80	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	4-oxoretinoic acid	166-176	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-5	2015	After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers.	Tretinoin	50-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-114
25492813-7	2015	In human hepatocytes, atRA, 4-OH-atRA, and 4-oxo-atRA induced CYP26A1 and 4-oxo-atRA formation was observed from 4-OH-atRA.	Tretinoin	22-26	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-69
25492813-7	2015	In human hepatocytes, atRA, 4-OH-atRA, and 4-oxo-atRA induced CYP26A1 and 4-oxo-atRA formation was observed from 4-OH-atRA.	4-oh-atra	28-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-69
25492813-7	2015	In human hepatocytes, atRA, 4-OH-atRA, and 4-oxo-atRA induced CYP26A1 and 4-oxo-atRA formation was observed from 4-OH-atRA.	4-oxoretinoic acid	43-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-69
25492813-10	2015	Although 4-oxo-atRA was not formed by CYP26A1, it was depleted by CYP26A1 (Km = 63 nM and intrinsic clearance = 90 mul/min per pmol).	4-oxoretinoic acid	9-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-73
25492813-11	2015	Similarly, CYP26A1 depleted 18-OH-atRA and the 4-OH-atRA enantiomers.	18-oh-atra	28-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	11-18
25492813-11	2015	Similarly, CYP26A1 depleted 18-OH-atRA and the 4-OH-atRA enantiomers.	4-oh-atra	47-56	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	11-18
25839051-1	2015	BQ chewing may produce significant amounts of reactive oxygen species (ROS), resulting in oral mucosa damage, and ROS may be metabolized by CYP26 families.	bulaquine	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	140-145
24819304-1	2014	CYP26A1 expression is very highly induced by retinoic acid (RA) in the liver, compared to most other tissues, suggesting that a liver-enriched factor may be required for its physiological transcriptional response.	Tretinoin	45-58	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
24819304-1	2014	CYP26A1 expression is very highly induced by retinoic acid (RA) in the liver, compared to most other tissues, suggesting that a liver-enriched factor may be required for its physiological transcriptional response.	Tretinoin	60-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
24819304-3	2014	In this study, we hypothesized that HNF4alpha and RARs may cooperate in an RA-dependent manner to induce a high level of CYP26A1 expression in liver cells.	Tretinoin	50-52	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	121-128
24819304-4	2014	Partial inhibition of endogenous HNF4alpha by siRNA reduced the level of RA-induced CYP26A1 mRNA in HepG2 cells.	Tretinoin	73-75	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	84-91
24819304-5	2014	Cotransfection of HNF4alpha, with or without RARs, demonstrated RA-dependent activation of a human CYP26A1 promoter-luciferase construct.	Tretinoin	45-47	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	99-106
24819304-7	2014	In EMSA and ChIP analyses HNF4alpha and RARs binding in the proximal and distal CYP26A1 promoter regions was significantly higher in RA-treated cells.	Tretinoin	40-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-87
24819304-9	2014	Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo.	Tretinoin	53-55	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	103-110
24819304-9	2014	Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	103-110
24799257-5	2014	These three natural RAR agonists with diterpene structures, while structurally different from ATRA, were able to increase the mRNA levels of the constitutive androstane receptor in HepG2 cells, induce F9 cell differentiation followed by Cyp26a1 mRNA expression, and differentiate HL-60 cells via RAR activation in a different manner from ATRA.	Diterpenes	38-47	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	237-244
24667328-9	2014	Our results suggest that localized expression of Cyp26 enzymes cell non-autonomously defines the boundaries between the cardiac and VP fields within the ALPM through regulating RA levels, which ensures a proper balance of myocardial and endothelial lineages.	Tretinoin	177-179	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
25839051-1	2015	BQ chewing may produce significant amounts of reactive oxygen species (ROS), resulting in oral mucosa damage, and ROS may be metabolized by CYP26 families.	Reactive Oxygen Species	114-117	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	140-145
25236354-6	2014	PCR analysis revealed a significant upregulation of retinoid-regulated genes such as CYP26A1 and STRA6 in LRAT KD cells, suggesting their possible involvement in mediating retinoid resistance in melanoma cells.	Retinoids	52-60	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	85-92
25236354-6	2014	PCR analysis revealed a significant upregulation of retinoid-regulated genes such as CYP26A1 and STRA6 in LRAT KD cells, suggesting their possible involvement in mediating retinoid resistance in melanoma cells.	Retinoids	172-180	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	85-92
25294402-0	2014	Increased expression of the retinoic acid-metabolizing enzyme CYP26A1 during the progression of cervical squamous neoplasia and head and neck cancer.	Tretinoin	28-41	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-69
24821725-6	2014	Importantly, RA treatment differentially mediates the removal of HDACs from the Hoxa1, Cyp26a1, and RARbeta2 genes and promotes the deposition of the H3K27ac mark at these genes.	Tretinoin	13-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	87-94
24667328-2	2014	RA levels in embryos are dampened by Cyp26 enzymes, which metabolize RA into easily degraded derivatives.	Tretinoin	69-71	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	37-42
24642534-3	2014	Inside the cells 1,25D is degraded to calcitrioic acid by a mitochondrial enzyme CYP24A1, while ATRA is degraded to several polar metabolites by CYP26.	Tretinoin	96-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	145-150
24608339-4	2014	Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression.	Tretinoin	119-132	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	154-161
24608339-12	2014	This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient.	Tretinoin	30-43	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-72
23601821-0	2013	2-(2-Methylfuran-3-carboxamido)-3-phenylpropanoic acid, a potential CYP26A1 inhibitor to enhance all-trans retinoic acid-induced leukemia cell differentiation based on virtual screening and biological evaluation.	2-(2-methylfuran-3-carboxamido)-3-phenylpropanoic acid	0-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-75
25217584-2	2014	We have studied the effect of activation of the retinoic A receptor, at the RARE-promoter chromatin of CASP9 and CYP26A1 genes, 15 and 45 min following RA exposure, and we found that histone H3 lysines 4 and 9 are demethylated by the lysine-specific demethylase, LSD1 and by the JMJ-domain containing demethylase, D2A.	Radium	76-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	113-120
23946489-3	2013	We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes.	Tretinoin	72-95	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
23946489-3	2013	We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes.	Tretinoin	97-99	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
23946489-3	2013	We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes.	Tretinoin	121-123	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
24043786-9	2013	Accordingly, we found that bone marrow stromal cell CYP26 was also able to inactivate retinoids in serum, preventing RA signaling.	Retinoids	86-95	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	52-57
24043786-9	2013	Accordingly, we found that bone marrow stromal cell CYP26 was also able to inactivate retinoids in serum, preventing RA signaling.	Tretinoin	117-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	52-57
23601821-0	2013	2-(2-Methylfuran-3-carboxamido)-3-phenylpropanoic acid, a potential CYP26A1 inhibitor to enhance all-trans retinoic acid-induced leukemia cell differentiation based on virtual screening and biological evaluation.	Tretinoin	107-120	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-75
23053054-2	2012	Cytochrome P450 26A1 (Cyp26a1), an RA-metabolizing enzyme, is involved in mammalian early pregnancy.	Tretinoin	35-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-20
23441061-6	2013	Finally, overexpression of SKI in human cells results in reduced levels of CYP26A1 mRNA, a known target of retinoic acid signaling.	Tretinoin	107-120	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	75-82
23688132-6	2013	Since the initial identification of inhibitors of RA metabolism, CYP26 enzymes have been characterized as the main enzymes responsible for RA clearance.	Tretinoin	50-52	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-70
23688132-6	2013	Since the initial identification of inhibitors of RA metabolism, CYP26 enzymes have been characterized as the main enzymes responsible for RA clearance.	Tretinoin	139-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	65-70
23688132-8	2013	The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner.	Tretinoin	74-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	38-43
23688132-8	2013	The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner.	Tretinoin	74-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-136
23688132-8	2013	The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner.	Tretinoin	194-196	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	38-43
23688132-8	2013	The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner.	Tretinoin	194-196	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-136
23071109-2	2012	atRA is metabolized mainly by CYP26A1, but other P450 enzymes such as CYP2C8 and CYP3As also contribute to atRA 4-hydroxylation.	Tretinoin	0-4	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	30-37
23071109-5	2012	CYP26A1 was found to form predominantly (4S)-OH-RA.	(4s)-oh-ra	40-50	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
23071109-6	2012	This stereoselectivity was rationalized via docking of atRA in the active site of a CYP26A1 homology model.	Tretinoin	55-59	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	84-91
23071109-10	2012	Both (4S)- and (4R)-OH-RA were substrates of CYP26A1 but (4S)-OH-RA was cleared 3-fold faster than (4R)-OH-RA.	(4s)- and	5-14	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
23071109-10	2012	Both (4S)- and (4R)-OH-RA were substrates of CYP26A1 but (4S)-OH-RA was cleared 3-fold faster than (4R)-OH-RA.	(4r)-oh-ra	15-25	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
23071109-13	2012	The stereoselectivity observed in CYP26A1 function will aid in better understanding of the active site features of the enzyme and the disposition of biologically active retinoids.	Retinoids	169-178	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	34-41
23053054-2	2012	Cytochrome P450 26A1 (Cyp26a1), an RA-metabolizing enzyme, is involved in mammalian early pregnancy.	Tretinoin	35-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
21428449-0	2011	Small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26): synthesis and biological evaluation of imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates.	imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates	105-161	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-56
22542753-5	2012	Functionality of the co-cultures was assayed using as endpoints the retinol-dependent secretion of RBP4 and the retinoic acid-dependent induction of CYP26A1 in hepatocytes.	Tretinoin	112-125	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	149-156
22542753-7	2012	HepaRG hepatocytes were also shown to up-regulate the expression of CYP26A1 mRNA in response to retinoid treatment.	Retinoids	96-104	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-75
22727372-0	2012	Novel retinoic acid 4-hydroxylase (CYP26) inhibitors based on a 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl scaffold.	3-(1h-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl scaffold	64-151	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	6-33
22727372-0	2012	Novel retinoic acid 4-hydroxylase (CYP26) inhibitors based on a 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl scaffold.	3-(1h-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl scaffold	64-151	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-40
22727372-3	2012	RA metabolism inhibitors (RAMBAs or CYP26 inhibitors) are attracting increasing interest as an alternative method for enhancing endogenous levels of retinoic acid in the treatment of hyperproliferative disease.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	36-41
22727372-3	2012	RA metabolism inhibitors (RAMBAs or CYP26 inhibitors) are attracting increasing interest as an alternative method for enhancing endogenous levels of retinoic acid in the treatment of hyperproliferative disease.	Tretinoin	149-162	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	36-41
22727372-4	2012	Here the synthesis and inhibitory activity of novel 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl derivatives in a MCF-7 CYP26A1 microsomal assay are described.	3-(1h-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(phenylamino)phenyl)propyl derivatives	52-142	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	154-161
22640768-10	2012	A few well-validated, specific predictors such as OPRM1, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol-related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).	Alcohols	177-184	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-88
22640768-10	2012	A few well-validated, specific predictors such as OPRM1, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol-related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).	Alcohols	177-184	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	281-286
22640768-10	2012	A few well-validated, specific predictors such as OPRM1, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol-related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).	Nicotine	260-268	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-88
22640768-10	2012	A few well-validated, specific predictors such as OPRM1, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol-related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).	Naltrexone	307-317	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-88
22179182-0	2011	Enhanced expression of retinoic acid-metabolizing enzyme CYP26A1 in sunlight-damaged human skin.	Tretinoin	23-36	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	57-64
22179182-2	2011	CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, has been shown to result in a state of functional VAD of the cell.	Tretinoin	103-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
22179182-2	2011	CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, has been shown to result in a state of functional VAD of the cell.	Tretinoin	118-120	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
22179182-2	2011	CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, has been shown to result in a state of functional VAD of the cell.	Vitamin A	139-148	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
21906690-9	2011	DISCUSSION: CYP26 enzymes are functionally expressed in microsomal fractions of insect cells and stably bind radiolabeled RA isomers with affinities respecting their substrate specificities.	Tretinoin	122-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	12-17
21838328-0	2011	Synthesis and biological evaluation of 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives as small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26).	3-(1h-imidazol	39-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	171-198
21838328-0	2011	Synthesis and biological evaluation of 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives as small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26).	3-(1h-imidazol	39-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	200-205
21838328-0	2011	Synthesis and biological evaluation of 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives as small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26).	triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives	59-138	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	171-198
21838328-0	2011	Synthesis and biological evaluation of 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives as small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26).	triazol-1-yl)-2,2-dimethyl-3-[4-(naphthalen-2-ylamino)phenyl]propyl derivatives	59-138	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	200-205
21838328-1	2011	The synthesis and potent inhibitory activity of novel 3-(1H-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(naphthalen-2-ylamino)phenyl)propyl derivatives vs a MCF-7 CYP26A1 microsomal assay is described.	3-(1h-imidazol- and triazol-1-yl)-2,2-dimethyl-3-(4-(naphthalen-2-ylamino)phenyl)propyl derivatives	54-153	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	165-172
21838328-4	2011	Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone.	Tretinoin	103-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
21838328-4	2011	Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone.	Tretinoin	103-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	152-159
21838328-4	2011	Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone.	Tretinoin	213-217	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
21521770-2	2011	The hepatic clearance of atRA is mediated primarily by CYP26A1, but design of CYP26A1 inhibitors is hindered by lack of information on CYP26A1 structure and structure-activity relationships of its ligands.	Tretinoin	25-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
21521770-3	2011	The aim of this study was to identify the primary metabolites of atRA formed by CYP26A1 and to characterize the ligand selectivity and ligand interactions of CYP26A1.	Tretinoin	65-69	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-87
21521770-3	2011	The aim of this study was to identify the primary metabolites of atRA formed by CYP26A1 and to characterize the ligand selectivity and ligand interactions of CYP26A1.	Tretinoin	65-69	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	158-165
21521770-4	2011	On the basis of high-resolution tandem mass spectrometry data, four metabolites formed from atRA by CYP26A1 were identified as 4-OH-RA, 4-oxo-RA, 16-OH-RA and 18-OH-RA.	4-oh-ra	127-134	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
21521770-4	2011	On the basis of high-resolution tandem mass spectrometry data, four metabolites formed from atRA by CYP26A1 were identified as 4-OH-RA, 4-oxo-RA, 16-OH-RA and 18-OH-RA.	4-oxoretinoic acid	136-144	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
21521770-4	2011	On the basis of high-resolution tandem mass spectrometry data, four metabolites formed from atRA by CYP26A1 were identified as 4-OH-RA, 4-oxo-RA, 16-OH-RA and 18-OH-RA.	16-oh-ra	146-154	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
21521770-4	2011	On the basis of high-resolution tandem mass spectrometry data, four metabolites formed from atRA by CYP26A1 were identified as 4-OH-RA, 4-oxo-RA, 16-OH-RA and 18-OH-RA.	18-oh-ra	159-167	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	100-107
21521770-5	2011	9-cis-RA and 13-cis-RA were also substrates of CYP26A1.	Alitretinoin	0-8	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-54
21521770-5	2011	9-cis-RA and 13-cis-RA were also substrates of CYP26A1.	Isotretinoin	13-22	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-54
22989911-0	2012	Synthesis and CYP26A1 inhibitory activity of novel methyl 3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates.	methyl 3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates	51-115	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-21
22989911-2	2012	The use of ATRA or prodrugs as pharmacological agents is limited by a short half-life in vivo resulting from the activity of specific ATRA hydroxylases, CYP26 enzymes, induced by ATRA in liver and target tissues.	Tretinoin	11-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	153-158
22989911-4	2012	The synthesis, CYP26A1 inhibitory activity and molecular modeling studies of novel methyl 3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates are presented.	3-[4-(arylamino)phenyl]-3-(azole)-2,2-dimethylpropanoates	90-147	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-22
22989911-6	2012	Both the methylenedioxyphenyl imidazole (17, IC(50) = 8 nM) and triazole (18, IC(50) = 6.7 nM) derivatives were potent inhibitors with additional binding interactions between the methylenedioxy moiety and the CYP26 active site likely to be the main factor.	methylenedioxyphenyl imidazole	9-39	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	209-214
22989911-6	2012	Both the methylenedioxyphenyl imidazole (17, IC(50) = 8 nM) and triazole (18, IC(50) = 6.7 nM) derivatives were potent inhibitors with additional binding interactions between the methylenedioxy moiety and the CYP26 active site likely to be the main factor.	Triazoles	64-72	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	209-214
22415012-1	2012	All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment.	Tretinoin	10-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-65
22415012-1	2012	All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment.	Tretinoin	10-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-72
22020119-2	2012	The cytochrome P450 enzymes CYP26 are believed to partially regulate cellular concentrations of atRA via oxidative metabolism and hence affect retinoid homeostasis and signaling.	Tretinoin	96-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	28-33
22020119-8	2012	Qualitatively, recombinant CYP26A1 and CYP26B1 formed the same primary and sequential metabolites from atRA.	Tretinoin	103-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	27-34
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	Tretinoin	10-14	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	81-88
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	Tretinoin	10-14	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	106-113
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	4-oh-ra	27-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	81-88
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	4-oh-ra	27-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	106-113
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	18-oh-ra	36-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	81-88
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	18-oh-ra	36-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	106-113
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	4-oxo-ra	49-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	81-88
22020119-10	2012	The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested.	4-oxo-ra	49-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	106-113
22020119-12	2012	CYP26A1 has higher catalytic activity than CYP26B1 and seems to be responsible for metabolism of atRA in tissues that function as a barrier for atRA exposure.	Tretinoin	97-101	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	50-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	34-39
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	50-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	102-109
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	65-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	34-39
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	65-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	102-109
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	173-175	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	34-39
21906690-1	2011	INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult.	Tretinoin	173-175	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	102-109
21529158-5	2011	The CYP26A1 gene is regulated by multiple RA response elements.	Tretinoin	42-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-11
21529158-7	2011	Enzyme kinetic studies have demonstrated that several CYP proteins are capable of metabolizing at-RA; however, it is likely that CYP26A1 plays a major role in RA clearance.	Tretinoin	98-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	129-136
21521770-9	2011	The retinoic acid receptor (RAR) gamma agonist CD1530 was as potent an inhibitor of CYP26A1 as ketoconazole with an IC(50) of 530 nM, whereas the RARalpha and RARbeta agonists tested did not significantly inhibit CYP26A1.	4-(6-hydroxy-7-tricyclo(3.3.1.13,7)dec-1-yl-2-naphthalenyl)benzoic acid	47-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	84-91
21521770-9	2011	The retinoic acid receptor (RAR) gamma agonist CD1530 was as potent an inhibitor of CYP26A1 as ketoconazole with an IC(50) of 530 nM, whereas the RARalpha and RARbeta agonists tested did not significantly inhibit CYP26A1.	4-(6-hydroxy-7-tricyclo(3.3.1.13,7)dec-1-yl-2-naphthalenyl)benzoic acid	47-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	213-220
21641329-0	2011	Minor complexes at work: light-harvesting by carotenoids in the photosystem II antenna complexes CP24 and CP26.	Carotenoids	45-56	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	106-110
21641329-5	2011	In CP26 fast transfer (80 fs) occurs from the carotenoid S(2) state to chlorophylls a absorbing at 675 and 678 nm, whereas transfer from the hot S(1) state to the lowest energy chlorophylls is observed in <1 ps.	Carotenoids	46-56	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	3-7
21641329-5	2011	In CP26 fast transfer (80 fs) occurs from the carotenoid S(2) state to chlorophylls a absorbing at 675 and 678 nm, whereas transfer from the hot S(1) state to the lowest energy chlorophylls is observed in <1 ps.	chlorophylls a	71-85	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	3-7
21428449-0	2011	Small molecule inhibitors of retinoic acid 4-hydroxylase (CYP26): synthesis and biological evaluation of imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates.	imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates	105-161	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-63
21428449-1	2011	The synthesis and potent inhibitory activity of novel imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates in a MCF-7 CYP26A1 microsomal assay is described.	imidazole	54-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	122-129
21428449-1	2011	The synthesis and potent inhibitory activity of novel imidazole methyl 3-(4-(aryl-2-ylamino)phenyl)propanoates in a MCF-7 CYP26A1 microsomal assay is described.	3-(4-(aryl-2-ylamino)phenyl)propanoates	71-110	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	122-129
21428449-2	2011	The induction of CYP26A1 mRNA was used to evaluate the ability of the compounds to enhance the biological effects of all-trans retinoic acid (ATRA) in a retinoid-responsive neuroblastoma cell line.	Tretinoin	142-146	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-24
22347780-0	2011	2 D - QSAR studies on CYP26A1 inhibitory activity of 1-[benzofuran-2-yl-(4-alkyl/aryl-phenyl)-methyl]- 1 H-triazoles.	1-[benzofuran-2-yl-(4-alkyl/aryl-phenyl)-methyl]- 1 h-triazoles	53-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
20513361-0	2010	The relative importance of CYP26A1 in hepatic clearance of all-trans retinoic acid.	Tretinoin	69-82	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	27-34
20606468-1	2011	AIM: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA).	Retinoids	111-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
20606468-1	2011	AIM: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA).	Tretinoin	120-143	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
20606468-1	2011	AIM: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA).	Tretinoin	145-149	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
20606468-2	2011	Since it is possible that an increased local CYP26 activity would reduce the effects of retinoids in vascular injury, we investigated the role of CYP26 in the regulation of atRA levels in human aortic smooth muscle cells (AOSMCs).	Tretinoin	173-177	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	146-151
20606468-7	2011	The CYP26 inhibitor also induced expression of atRA-responsive genes.	Tretinoin	47-51	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
20606468-8	2011	Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop.	Tretinoin	11-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	24-29
20606468-8	2011	Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop.	Tretinoin	11-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	105-110
20606468-8	2011	Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop.	Tretinoin	53-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	24-29
20606468-8	2011	Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop.	Tretinoin	53-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	105-110
20606468-9	2011	Inhibition of this loop with a CYP26 inhibitor increased retinoid signaling.	Retinoids	57-65	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	31-36
20513361-2	2010	Several P450 enzymes including CYP26A1, CYP2C8, and CYP3A4 have been proposed to be responsible for RA clearance in the liver but their quantitative importance has not been demonstrated.	Tretinoin	100-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	31-38
20513361-6	2010	CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA.	Tretinoin	46-48	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	168-175
20513361-7	2010	Simulations performed for livers with varying P450 expression levels over a range of RA concentrations demonstrated that at both endogenous and therapeutic concentrations of RA, CYP26A1 is the primary enzyme responsible for 4-OH RA formation clearance.	Tretinoin	85-87	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
20513361-7	2010	Simulations performed for livers with varying P450 expression levels over a range of RA concentrations demonstrated that at both endogenous and therapeutic concentrations of RA, CYP26A1 is the primary enzyme responsible for 4-OH RA formation clearance.	Tretinoin	174-176	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
20513361-7	2010	Simulations performed for livers with varying P450 expression levels over a range of RA concentrations demonstrated that at both endogenous and therapeutic concentrations of RA, CYP26A1 is the primary enzyme responsible for 4-OH RA formation clearance.	4-oh ra	224-231	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
20513361-8	2010	HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8.	4-oh	32-36	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
20682464-0	2010	Multiple retinoic acid response elements cooperate to enhance the inducibility of CYP26A1 gene expression in liver.	Tretinoin	9-22	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-89
20682464-1	2010	CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver.	Tretinoin	52-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
20682464-1	2010	CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver.	Tretinoin	72-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
20682464-5	2010	In DNA binding and chromatin immunoprecipitation assays, the binding of RARs to the proximal RARE1 and distal RARE2, -3, and -4 regions of the CYP26A1 promoter was increased in RA-treated HepG2 cells, and greater in VA-sufficient than VA-deficient liver.	Vitamin A	216-218	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	143-150
20682464-7	2010	The results support a cooperative model in which the functioning of multiple RAREs may account for the strong inducibility of CYP26A1 in liver, which, in turn, may be important physiologically for restoring retinoid homeostasis when the concentration of RA rises.	Retinoids	207-215	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-133
20682464-7	2010	The results support a cooperative model in which the functioning of multiple RAREs may account for the strong inducibility of CYP26A1 in liver, which, in turn, may be important physiologically for restoring retinoid homeostasis when the concentration of RA rises.	Tretinoin	77-79	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-133
20682464-1	2010	CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver.	Tretinoin	102-104	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
20513361-8	2010	HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8.	Tretinoin	37-39	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	178-185
20513361-10	2010	These findings suggest that CYP26A1 is the P450 isoform that should be targeted when designing RA metabolism blocking agents.	Tretinoin	95-97	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	28-35
20409737-1	2010	CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA).	Tretinoin	153-166	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	109-114
20658618-6	2010	RESULTS: Treatment of NB cells with retinoids induced expression of several genes including the retinoid metabolizing enzymes CYP26A1 and CYP26B1.	Retinoids	36-45	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-133
20658618-6	2010	RESULTS: Treatment of NB cells with retinoids induced expression of several genes including the retinoid metabolizing enzymes CYP26A1 and CYP26B1.	Retinoids	36-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-133
20409737-1	2010	CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA).	Tretinoin	168-172	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	109-114
19884280-7	2010	Classic cytochrome P450 inducers did not affect CYP26 transcription, whereas the peroxisome proliferator-activated receptor (PPAR) gamma agonists pioglitazone and rosiglitazone up-regulated CYP26B1 transcription by as much as 209- +/- 80-fold and CYP26A1 by 10-fold.	Pioglitazone	146-158	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	247-254
19935721-2	2010	Here, we found that CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, is highly expressed in 42% (27/65) of primary breast cancers.	Tretinoin	123-136	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-27
19935721-2	2010	Here, we found that CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, is highly expressed in 42% (27/65) of primary breast cancers.	Tretinoin	138-140	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-27
19935721-2	2010	Here, we found that CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, is highly expressed in 42% (27/65) of primary breast cancers.	Vitamin A	159-168	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-27
19935721-5	2010	Suppression of CYP26A1 significantly reversed the CYP26A1-mediated oncogenic characteristics, suggesting a direct link between intracellular RA status and tumorigenicity.	Tretinoin	141-143	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-22
19935721-5	2010	Suppression of CYP26A1 significantly reversed the CYP26A1-mediated oncogenic characteristics, suggesting a direct link between intracellular RA status and tumorigenicity.	Tretinoin	141-143	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	50-57
20200558-6	2010	Co-treatment with a pharmacologic inhibitor of PRKCD and RA resulted in the induction of an RA responsive reporter construct, as well as the endogenous RA target genes, CEBPE, CYP26A1 and RIG-I.	Tretinoin	57-59	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	176-183
19884280-7	2010	Classic cytochrome P450 inducers did not affect CYP26 transcription, whereas the peroxisome proliferator-activated receptor (PPAR) gamma agonists pioglitazone and rosiglitazone up-regulated CYP26B1 transcription by as much as 209- +/- 80-fold and CYP26A1 by 10-fold.	Rosiglitazone	163-176	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	247-254
19294396-1	2009	The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes.	Vitamin A	44-51	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	202-207
19853565-8	2009	Concomitant regulation of Cyp26a1 expression, restraining retinoic acid signaling away from the posterior growth zone, may likewise play a role in timing the trunk-tail transition.	Tretinoin	58-71	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-33
19294396-0	2009	Both all-trans retinoic acid and cytochrome P450 (CYP26) inhibitors affect the expression of vitamin A metabolizing enzymes and retinoid biomarkers in organotypic epidermis.	Vitamin A	93-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	50-55
19294396-0	2009	Both all-trans retinoic acid and cytochrome P450 (CYP26) inhibitors affect the expression of vitamin A metabolizing enzymes and retinoid biomarkers in organotypic epidermis.	Retinoids	128-136	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	50-55
19294396-1	2009	The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes.	Tretinoin	20-33	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	202-207
19294396-1	2009	The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes.	Tretinoin	35-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	202-207
19294396-3	2009	Here, we examined the effects of RA and the CYP26 inhibitors, liarozole and talarozole, on retinoid metabolism and RA-regulated genes in organotypic epidermis.	Retinoids	91-99	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	44-49
19294396-4	2009	RA induced the expression of CYP26 enzymes already after 8 h, whereas LRAT exhibited a later response and peaked at 48 h, indicating a feedback induction of retinol esterification.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-34
19294396-8	2009	Cellular accumulation of exogenous [3H]RA was higher after talarozole than after liarozole, probably indicating a greater CYP26-inhibitory potency of the former drug.	Tritium	36-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	122-127
19294396-8	2009	Cellular accumulation of exogenous [3H]RA was higher after talarozole than after liarozole, probably indicating a greater CYP26-inhibitory potency of the former drug.	Tretinoin	39-41	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	122-127
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Tretinoin	89-91	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-36
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Tretinoin	89-91	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-34
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Tretinoin	117-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-36
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Tretinoin	117-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-34
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Retinoids	194-202	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-36
19294396-9	2009	The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis.	Retinoids	194-202	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-34
19519282-4	2009	The CYP26 enzymes have been shown to metabolize RA efficiently and they are also inducible by RA in selected systems.	Tretinoin	94-96	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19519282-4	2009	The CYP26 enzymes have been shown to metabolize RA efficiently and they are also inducible by RA in selected systems.	Tretinoin	48-50	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19519282-0	2009	The role of CYP26 enzymes in retinoic acid clearance.	Tretinoin	29-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	12-17
19519282-8	2009	To further the understanding of how CYP26 enzymes contribute to the regulation of RA homeostasis, structural information of the CYP26s, commercially available recombinant enzymes and good specific and sensitive antibodies are needed.	Tretinoin	82-84	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	36-41
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	120-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-51
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	120-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-58
19147277-8	2009	The effect of EBBP on retinoid-responsive transcription appeared to be limited to genes with the retinoic acid response element (betaRARE) regulatory sequence, such as CYP26A1.	Retinoids	22-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	168-175
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	139-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-51
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	139-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-58
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	139-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-51
19519282-3	2009	It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA.	Tretinoin	139-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-58
19147277-8	2009	The effect of EBBP on retinoid-responsive transcription appeared to be limited to genes with the retinoic acid response element (betaRARE) regulatory sequence, such as CYP26A1.	Tretinoin	97-110	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	168-175
19171200-1	2009	All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1).	2-octenal	4-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	135-140
18608743-4	2009	The benzooxazol-2-yl-[phenyl-imidazol-1-yl-methyl)phenyl]amines with small substituents in the phenyl ring were moderately potent CYP26A1 inhibitors (IC(50) 8 and 12 microM) and comparable with liarozole (IC(50) 7 microM).	benzooxazol-2-yl-[phenyl-imidazol-1-yl-methyl)phenyl]amines	4-63	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	130-137
18608743-1	2009	The design of N-phenylbenzo[d]oxazolamines as CYP26A1 inhibitors involved ligand docking experiments using molecular modeling (FlexX) and analysis of ligand interactions at the binding domain.	n-phenylbenzo[d]oxazolamines	14-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	46-53
19171200-7	2009	Thus CYP26B1 appears essential for RA catabolism under physiological conditions, whereas CYP26A1 might play a greater role during RA excess.	Tretinoin	130-132	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	89-96
19171200-1	2009	All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1).	Tretinoin	10-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	135-140
19171200-1	2009	All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1).	Tretinoin	25-27	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	135-140
19171200-4	2009	RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
19171200-5	2009	The CYP26 inhibitor talarozole altered CYP26A1 and LRAT mRNA expression in a similar way as RA, increased the cellular accumulation of [(3)H]RA, and induced a punctate CRABPII staining, also observed after siRNA knock-down of CYP26B1 (but not after RA exposure).	R 115866	20-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19171200-5	2009	The CYP26 inhibitor talarozole altered CYP26A1 and LRAT mRNA expression in a similar way as RA, increased the cellular accumulation of [(3)H]RA, and induced a punctate CRABPII staining, also observed after siRNA knock-down of CYP26B1 (but not after RA exposure).	R 115866	20-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	39-46
19120344-0	2009	The CYP26 inhibitor R115866 potentiates the effects of all-trans retinoic acid on cultured human epidermal keratinocytes.	R 115866	20-27	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19120344-4	2009	R115866 is a specific inhibitor of the cytochrome P450 isoform CYP26, which is involved in the metabolic inactivation pathway of RA.	Tretinoin	129-131	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	63-68
19171200-5	2009	The CYP26 inhibitor talarozole altered CYP26A1 and LRAT mRNA expression in a similar way as RA, increased the cellular accumulation of [(3)H]RA, and induced a punctate CRABPII staining, also observed after siRNA knock-down of CYP26B1 (but not after RA exposure).	Tretinoin	52-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
18992717-3	2009	Enzymes in the CYP26 family are thought to be responsible for the elimination of RA, and CYP26A1 appears to serve the most critical functions in this family.	Tretinoin	81-83	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	89-96
19120344-0	2009	The CYP26 inhibitor R115866 potentiates the effects of all-trans retinoic acid on cultured human epidermal keratinocytes.	all-trans	55-64	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19120344-0	2009	The CYP26 inhibitor R115866 potentiates the effects of all-trans retinoic acid on cultured human epidermal keratinocytes.	Tretinoin	65-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
19100254-6	2009	We further show that fibroblast growth factor (FGF) signalling, induces the expression of the retinoic acid degrading enzyme cytochrome P450 (cyp) 26a1, and that one of its products, 4-oxo-RA, mimics the action of the RARalpha agonist in the differentiation of the NPCs into cholinergic neurons.	Tretinoin	94-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	125-151
18992717-6	2009	Heme incorporation was determined by carbon monoxide difference spectrum and a type 1 spectrum was observed with RA binding to CYP26A1.	Heme	0-4	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	127-134
18992717-6	2009	Heme incorporation was determined by carbon monoxide difference spectrum and a type 1 spectrum was observed with RA binding to CYP26A1.	Tretinoin	113-115	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	127-134
18992717-7	2009	We found that RA is a tight binding ligand of CYP26A1 with low nM binding affinity.	Tretinoin	14-16	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	46-53
18992717-8	2009	CYP26A1 oxidized RA efficiently (depletion K(m) 9.4+/-3.3nM and V(max) 11.3+/-4.3pmolesmin(-1)pmoleP450(-1)) when supplemented with P450 oxidoreductase and NADPH but was independent of cytochrome b5.	Tretinoin	17-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18992717-8	2009	CYP26A1 oxidized RA efficiently (depletion K(m) 9.4+/-3.3nM and V(max) 11.3+/-4.3pmolesmin(-1)pmoleP450(-1)) when supplemented with P450 oxidoreductase and NADPH but was independent of cytochrome b5.	NADP	156-161	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18990705-7	2009	We also show that lutein radical cation formation in CP26 is dependent on binding of zeaxanthin to the L2 domain, implying that zeaxanthin acts as an allosteric effector of charge transfer quenching involving lutein in the L1 domain.	Zeaxanthins	85-95	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-57
18992717-10	2009	4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1.	4-oh-ra	0-7	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-42
18992717-10	2009	4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1.	4-oh-ra	0-7	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	166-173
18992717-10	2009	4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1.	Tretinoin	5-7	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-42
18992717-10	2009	4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1.	Tretinoin	5-7	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	166-173
18992717-11	2009	The high efficiency of CYP26A1 in eliminating both RA and its potentially active metabolites supports the major role of this enzyme in regulating RA clearance in vivo.	Tretinoin	51-53	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	23-30
18992717-11	2009	The high efficiency of CYP26A1 in eliminating both RA and its potentially active metabolites supports the major role of this enzyme in regulating RA clearance in vivo.	Tretinoin	146-148	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	23-30
19016711-0	2009	Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis.	Retinoids	102-110	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	23-28
19197536-6	2009	A significant decrease in the mRNA expression of KRT2 and TNF-alpha, and trends toward increased expression of KRT4 and CYP26A1 were observed in liarozole-treated patients, consistent with an increased retinoid stimulation of epidermis.	liarozole	145-154	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	120-127
19016711-6	2009	RESULTS: Talarozole treatment increased the mRNA expression of CRABP2, KRT4, CYP26A1 and CYP26B1 dose dependently, and decreased the expression of KRT2 and IL-1alpha compared with vehicle-treated skin.	R 115866	9-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	77-84
19016711-0	2009	Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis.	R 115866	39-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	23-28
18927157-8	2008	Together with data on the expression of osteoblast markers, our results indicate that temporal and spatial restriction of RA signaling by Cyp26 enzymes is required to attenuate osteoblast maturation and/or activity in vivo.	Tretinoin	122-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	138-143
18722776-0	2008	Novel azolyl-(phenylmethyl)]aryl/heteroarylamines: potent CYP26 inhibitors and enhancers of all-trans retinoic acid activity in neuroblastoma cells.	azolyl-(phenylmethyl)]aryl/heteroarylamines	6-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-63
18769122-8	2008	Several retinoid-regulated genes exhibited much higher mRNA levels in SKRC06 than in SKRC39, even in the absence of drugs; these included crabp2, rargamma and cyp26A1.	Retinoids	8-16	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	159-166
18816852-3	2008	These have shown local control of synthesis and degradation, and computational models suggest that degradation by the Cyp26 enzymes plays a critical role in the formation of a morphogen gradient as well as its ability to compensate for fluctuations in RA levels.	Radium	252-254	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	118-123
18722776-1	2008	The synthesis and potent inhibitory activity of novel 4-[(imidazol-1-yl and triazol-1-yl)(phenyl)methyl]aryl-and heteroaryl amines versus a MCF-7 CYP26A1 cell assay is described.	4-[(imidazol-1-yl and triazol-1-yl)(phenyl)methyl]aryl-and heteroaryl amines	54-130	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	146-153
18606996-8	2008	These extracts contained retinoids (5.4 nM) as assessed by RA-inducible Cyp26A1-promoter luciferase reporter cell lines.	Retinoids	25-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	72-79
18606996-8	2008	These extracts contained retinoids (5.4 nM) as assessed by RA-inducible Cyp26A1-promoter luciferase reporter cell lines.	Radium	59-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	72-79
18502188-6	2008	And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction.	Tretinoin	58-77	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-138
18502188-6	2008	And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction.	Tretinoin	184-188	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-138
18059332-9	2008	CYP26A1 expression was increased synergistically by RA and lithocholic acid (P<0.05).	Tretinoin	52-54	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
26621242-0	2008	Homology Models and Molecular Modeling of Human Retinoic Acid Metabolizing Enzymes Cytochrome P450 26A1 (CYP26A1) and P450 26B1 (CYP26B1).	Tretinoin	48-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	83-103
26621242-0	2008	Homology Models and Molecular Modeling of Human Retinoic Acid Metabolizing Enzymes Cytochrome P450 26A1 (CYP26A1) and P450 26B1 (CYP26B1).	Tretinoin	48-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	105-112
26621242-6	2008	Residues involved in hydrophobic interactions with atRA were Pro113, Phe222, Phe299, Val370, Pro371, and Phe374 in CYP26A1 and Leu88, Pro118, Phe222, Phe295, Ile368, and Tyr272 in CYP26B1.	Tretinoin	51-55	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	115-122
26621242-7	2008	Hydrogen bonding interactions were observed between the atRA carboxylate group and Arg 90 in CYP26A1 and with Arg76, Arg95, and Ser369 in CYP26B1.	Hydrogen	0-8	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	93-100
26621242-7	2008	Hydrogen bonding interactions were observed between the atRA carboxylate group and Arg 90 in CYP26A1 and with Arg76, Arg95, and Ser369 in CYP26B1.	atra carboxylate	56-72	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	93-100
26621242-7	2008	Hydrogen bonding interactions were observed between the atRA carboxylate group and Arg 90 in CYP26A1 and with Arg76, Arg95, and Ser369 in CYP26B1.	Arginine	83-86	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	93-100
18059332-0	2008	A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett"s associated adenocarcinoma.	Tretinoin	21-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
18059332-1	2008	Vitamin A deficiency is associated with carcinogenesis, and upregulation of CYP26A1, a major retinoic acid (RA)-catabolizing enzyme, has recently been shown in cancer.	Tretinoin	93-106	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
18059332-1	2008	Vitamin A deficiency is associated with carcinogenesis, and upregulation of CYP26A1, a major retinoic acid (RA)-catabolizing enzyme, has recently been shown in cancer.	Tretinoin	108-110	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
18059332-9	2008	CYP26A1 expression was increased synergistically by RA and lithocholic acid (P<0.05).	Lithocholic Acid	59-75	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18059332-7	2008	CYP26A1 was stably overexpressed in GihTERT cells, which were evaluated for gene-expression changes (pathway array and quantitative RT-PCR), cellular proliferation (cytometric DNA profile and colorimetric assay) and invasion (in vitro matrigel assay) with or without the CYP inhibitor ketaconazole.	ketaconazole	285-297	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18059332-9	2008	CYP26A1 expression was increased synergistically by RA and lithocholic acid (P<0.05).	p&lt	77-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18059332-8	2008	RA levels decreased progressively with the degree of dysplasia (P<0.05) and were inversely correlated with CYP26A1 gene levels and activity (P<0.01).	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	110-117
18059332-11	2008	Functional effects of CYP26A1 overexpression were increased proliferation (P<0.01) and invasion in vitro (P<0.01), which were inhibited by ketaconazole.	ketaconazole	145-157	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
18059332-12	2008	Overexpression of CYP26A1 causes intracellular RA depletion and drives the cell into a highly proliferative and invasive state with induction of other known oncogenes.	Tretinoin	47-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-25
18318834-5	2008	We postulate that nonphotochemical quenching occurs within a structural locus comprising the PsbS subunit and components of the light-harvesting antenna, CP26, CP24, CP29 and LHCIIb (the major trimeric light-harvesting complex), formed in response to protonation and controlled by the xanthophyll cycle carotenoids.	Xanthophylls	285-296	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	154-158
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	139-146
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	139-146
18241852-4	2008	Despite increased intracellular RA levels, CYP26a1(-/-) ES cells were more resistant than Wt ES cells to RA-induced proliferation arrest.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	43-50
18241852-6	2008	Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1).	Tretinoin	34-36	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
18241852-7	2008	In contrast, genes involved in the stress response (e.g. Tlr2, Stk2, Fcgr2b, Bnip3, Pdk1) were expressed at higher levels in CYP26A1(-/-) than in Wt ES cells without RA.	Tretinoin	166-168	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	125-132
18241852-8	2008	Collectively, our results show that CYP26A1 activity regulates intracellular RA levels, cell proliferation, transcriptional regulation of primary RA target genes, and ES cell differentiation to parietal endoderm.	Tretinoin	77-79	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	36-43
18241852-0	2008	CYP26A1 knockout embryonic stem cells exhibit reduced differentiation and growth arrest in response to retinoic acid.	Tretinoin	103-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-1	2008	CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA.	Tretinoin	47-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-1	2008	CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA.	Tretinoin	72-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-1	2008	CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA.	4-oxoretinoic acid	105-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-1	2008	CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA.	4-oh-ra	118-125	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	65-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	65-67	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	139-146
18241852-3	2008	CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
18318834-5	2008	We postulate that nonphotochemical quenching occurs within a structural locus comprising the PsbS subunit and components of the light-harvesting antenna, CP26, CP24, CP29 and LHCIIb (the major trimeric light-harvesting complex), formed in response to protonation and controlled by the xanthophyll cycle carotenoids.	Carotenoids	303-314	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	154-158
17998248-10	2008	The loss of the forebrain-specific RA-degrading enzyme cyp26a1 causes a forebrain phenotype that mimics tgif morphants.	Tretinoin	35-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
18093970-7	2008	Moreover, in the case of excessive maternal dietary vitamin A intake, LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with STRA6, the recently identified cell surface receptor for retinol-RBP, in maintaining adequate levels of retinoids in embryonic and extraembryonic tissues.	Vitamin A	52-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-101
18093970-7	2008	Moreover, in the case of excessive maternal dietary vitamin A intake, LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with STRA6, the recently identified cell surface receptor for retinol-RBP, in maintaining adequate levels of retinoids in embryonic and extraembryonic tissues.	Tretinoin	155-168	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-101
17663992-0	2007	Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells.	Retinoids	0-8	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	168-175
18050373-6	2007	The CYP26 gene, which plays a key role in retinol metabolism, was examined to define any single-nucleotide polymorphisms (SNP) associations with AS.	Vitamin A	42-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
17850797-0	2007	A specific binding site for neoxanthin in the monomeric antenna proteins CP26 and CP29 of Photosystem II.	neoxanthin	28-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	73-77
17850797-1	2007	The location of the neoxanthin binding site in CP26 and CP29 was investigated by site-directed mutagenesis.	neoxanthin	20-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-51
17663992-0	2007	Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells.	Tretinoin	110-123	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	168-175
17714122-1	2007	BACKGROUND: R115866 (Rambazole) is a new generation all-trans retinoic acid metabolism blocking agent, highly specific against the retinoic acid 4-hydroxylase.	R 115866	21-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-158
17714122-1	2007	BACKGROUND: R115866 (Rambazole) is a new generation all-trans retinoic acid metabolism blocking agent, highly specific against the retinoic acid 4-hydroxylase.	Tretinoin	62-75	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	131-158
17526768-8	2007	Lastly, treatment of LNCaP with all-trans retinal (RAL) in the presence of DHT resulted in significant up-regulation of the RA-inducible, RA-metabolizing enzyme CYP26A1 mRNA compared with RAL treatment alone.	Dihydrotestosterone	75-78	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	161-168
17510468-0	2007	CYP26 inhibitor R115866 increases retinoid signaling in intimal smooth muscle cells.	R 115866	16-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
17510468-0	2007	CYP26 inhibitor R115866 increases retinoid signaling in intimal smooth muscle cells.	Retinoids	34-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
17510468-5	2007	A key enzyme is the all-trans retinoic acid-degrading enzyme cytochrome p450 isoform 26 (CYP26).	Tretinoin	20-43	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	61-87
17510468-5	2007	A key enzyme is the all-trans retinoic acid-degrading enzyme cytochrome p450 isoform 26 (CYP26).	Tretinoin	20-43	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	89-94
17510468-6	2007	Thus, an alternative approach to exogenous retinoid administration could be to increase the intracellular level of all-trans retinoic acid by blocking CYP26-mediated degradation of retinoids.	Retinoids	43-51	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	151-156
17510468-6	2007	Thus, an alternative approach to exogenous retinoid administration could be to increase the intracellular level of all-trans retinoic acid by blocking CYP26-mediated degradation of retinoids.	2-octenal	119-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	151-156
17510468-6	2007	Thus, an alternative approach to exogenous retinoid administration could be to increase the intracellular level of all-trans retinoic acid by blocking CYP26-mediated degradation of retinoids.	Tretinoin	125-138	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	151-156
17510468-6	2007	Thus, an alternative approach to exogenous retinoid administration could be to increase the intracellular level of all-trans retinoic acid by blocking CYP26-mediated degradation of retinoids.	Retinoids	181-190	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	151-156
17510468-8	2007	Although medial cells remained unaffected, treatment with the CYP26-inhibitor R115866 significantly increased cellular levels of all-trans retinoic acid in intimal SMCs.	R 115866	78-85	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-67
17510468-8	2007	Although medial cells remained unaffected, treatment with the CYP26-inhibitor R115866 significantly increased cellular levels of all-trans retinoic acid in intimal SMCs.	Tretinoin	139-152	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	62-67
17510468-10	2007	CONCLUSIONS: Blocking of the CYP26-mediated catabolism mimics the effects of exogenously administrated active retinoids on intimal SMCs.	Retinoids	110-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	29-34
17070795-7	2007	It is proposed that heterogeneous local distribution of retinoids controlled through Raldh2 and Cyp26A1 is responsible for matching the fleshy and the tendinous components of each muscle belly.	Retinoids	56-65	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	96-103
17276435-7	2007	Cytochrome P450 (CYP 26A1), which is responsible for retinoic acid metabolism, was highly up-regulated in leiomyomas (+5.4- +/- 0.53-fold).	Tretinoin	53-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-25
17218384-0	2007	Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity.	Tretinoin	128-141	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	74-79
17218384-5	2007	In opposition, only high-sensitive blasts expressed the CYP26A1 gene, encoding the p450 cytochrome which is known to be involved in retinoic acid catabolism.	Tretinoin	132-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	56-63
17218384-6	2007	In NB4 cells, ATRA treatment activates a novel signaling pathway, whereby interleukin-8 stimulates the expression of the homeobox transcription factor HOXA10v2, an effective enhancer of CYP26A1 transcription.	Tretinoin	14-18	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	186-193
17244623-7	2007	Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and increases the ability of retinol to induce the RA-responsive gene, CYP26A1.	Vitamin A	120-127	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	162-169
17244623-7	2007	Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and increases the ability of retinol to induce the RA-responsive gene, CYP26A1.	Tretinoin	142-144	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	162-169
17460545-0	2007	The discovery of new coding alleles of human CYP26A1 that are potentially defective in the metabolism of all-trans retinoic acid and their assessment in a recombinant cDNA expression system.	Tretinoin	115-128	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	45-52
17460545-3	2007	We sequenced CYP26A1 in racially diverse individuals and assessed the metabolism of retinoic acid by newly identified coding alleles of CYP26A1 in a recombinant system.	Tretinoin	84-97	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	136-143
17460545-10	2007	Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites.	Tretinoin	42-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-17
17460545-10	2007	Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites.	Tretinoin	63-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-17
17460545-10	2007	Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites.	4-oxoretinoic acid	73-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-17
17460545-10	2007	Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites.	4-oh-ra	83-90	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-17
17460545-10	2007	Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites.	Water	102-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	10-17
17059167-0	2006	Homology model of human retinoic acid metabolising enzyme cytochrome P450 26A1 (CYP26A1): active site architecture and ligand binding.	Tretinoin	24-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-78
17164423-0	2007	Cyp26 enzymes generate the retinoic acid response pattern necessary for hindbrain development.	Tretinoin	27-40	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
17164423-4	2007	Here, we show that the cytochrome p450 enzymes of the Cyp26 class, which metabolize RA into polar derivatives, function redundantly to shape RA-dependent gene-expression domains during hindbrain development.	Tretinoin	84-86	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-59
17164423-4	2007	Here, we show that the cytochrome p450 enzymes of the Cyp26 class, which metabolize RA into polar derivatives, function redundantly to shape RA-dependent gene-expression domains during hindbrain development.	Tretinoin	141-143	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-59
17164423-5	2007	In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain.	Tretinoin	143-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	70-75
17164423-5	2007	In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain.	Tretinoin	143-145	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-89
17164423-6	2007	Furthermore, we show that Cyp26 enzymes are essential for exogenous RA to rescue hindbrain patterning in RA-depleted embryos.	Tretinoin	68-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-31
17164423-6	2007	Furthermore, we show that Cyp26 enzymes are essential for exogenous RA to rescue hindbrain patterning in RA-depleted embryos.	Tretinoin	105-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	26-31
16778795-0	2006	Skin retinoid concentrations are modulated by CYP26AI expression restricted to basal keratinocytes in normal human skin and differentiated 3D skin models.	Retinoids	5-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	46-51
16778795-9	2006	In light of our prior studies documenting the functional activity of RA metabolites, expression of CYP26 in the sebaceous gland epithelium supports the suggestion that altered RA metabolism may be involved in the pathogenesis of acne.	Tretinoin	176-178	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	99-104
17059167-0	2006	Homology model of human retinoic acid metabolising enzyme cytochrome P450 26A1 (CYP26A1): active site architecture and ligand binding.	Tretinoin	24-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	80-87
16837774-8	2006	Furthermore, the retinoic acid-catabolizing enzyme CYP26A1 is expressed at higher levels in medial SMCs compared to intimal SMCs.	Tretinoin	17-30	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-58
16458519-0	2006	Synthesis and CYP26A1 inhibitory activity of 1-[benzofuran-2-yl-(4-alkyl/aryl-phenyl)-methyl]-1H-triazoles.	1-[benzofuran-2-yl-(4-alkyl/aryl-phenyl)-methyl]-1h-triazoles	45-106	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-21
16458519-3	2006	All the triazole derivatives were evaluated for CYP26A1 inhibitory activity using a MCF-7 cell-based assay.	Triazoles	8-16	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	48-55
16458519-4	2006	The 4-ethyl and 4-phenyl-1,2,4-triazole derivatives displayed inhibitory activity (IC(50) 4.5 and 7 microM, respectively) comparable with that of the CYP26 inhibitor liarozole (IC(50) 7 microM).	liarozole	166-175	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	150-155
16458519-5	2006	Using a CYP26A1 homology model (based on CYP3A4) template, docking experiments were performed with MOE with multiple hydrophobic interactions observed in addition to coordination between the triazole nitrogen and the haem transition metal.	Triazoles	191-199	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	8-15
16458519-5	2006	Using a CYP26A1 homology model (based on CYP3A4) template, docking experiments were performed with MOE with multiple hydrophobic interactions observed in addition to coordination between the triazole nitrogen and the haem transition metal.	Nitrogen	200-208	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	8-15
16933217-1	2006	BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels.	Tretinoin	85-98	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	12-19
16933217-1	2006	BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels.	Tretinoin	100-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	12-19
16933217-1	2006	BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels.	Tretinoin	215-217	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	12-19
16279770-0	2005	Novel tetralone-derived retinoic acid metabolism blocking agents: synthesis and in vitro evaluation with liver microsomal and MCF-7 CYP26A1 cell assays.	Tetralones	6-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	132-139
16279770-0	2005	Novel tetralone-derived retinoic acid metabolism blocking agents: synthesis and in vitro evaluation with liver microsomal and MCF-7 CYP26A1 cell assays.	Tretinoin	24-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	132-139
16279770-1	2005	The potent inhibitory activity of novel 2-benzyltetralone and 2-benzylidenetetralone derivatives vs liver microsomal retinoic acid metabolizing enzymes and a MCF-7 CYP26A1 cell assay is described.	2-benzyltetralone	40-57	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	164-171
16279770-1	2005	The potent inhibitory activity of novel 2-benzyltetralone and 2-benzylidenetetralone derivatives vs liver microsomal retinoic acid metabolizing enzymes and a MCF-7 CYP26A1 cell assay is described.	2-benzylidenetetralone	62-84	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	164-171
16279770-3	2005	In the MCF-7 CYP26A1 cell assay, the 2-(4-hydroxybenzyl)-6-methoxytetralone 5 and unsaturated benzylidene precursor 6 were found to be the most potent (IC50 = 7 and 5 microM, respectively), which was comparable with liarozole (7 microM) but considerably less active than R115866 (IC50 = 5 nM).	2-(4-hydroxybenzyl)-6-methoxytetralone	37-75	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	13-20
16279770-3	2005	In the MCF-7 CYP26A1 cell assay, the 2-(4-hydroxybenzyl)-6-methoxytetralone 5 and unsaturated benzylidene precursor 6 were found to be the most potent (IC50 = 7 and 5 microM, respectively), which was comparable with liarozole (7 microM) but considerably less active than R115866 (IC50 = 5 nM).	unsaturated benzylidene	82-105	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	13-20
16279770-4	2005	With a CYP26A1 homology model, the tetralones were shown to be positioned in a hydrophobic tunnel with additional interactions, e.g., transition metal coordination and hydrogen-bonding interactions with GLY300, observed for the potent 4-hydroxyphenyl substituted inhibitors.	Metals	145-150	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	7-14
16504501-1	2006	3-[6-(2-Dimethylamino-1-imidazol-1-yl-butyl)-naphthalen-2-yloxy]-2,2-dimethyl-propionic acid and analogs were designed and synthesized as highly potent and selective CYP26 inhibitors, serving as retinoic acid metabolic blocking agents (RAMBAs), with demonstrated in vivo efficacy to increase the half-life of exogenous atRA.	3-(6-(2-dimethylamino-1-imidazol-1-yl-butyl)naphthalen-2-yloxy)-2,2-dimethyl-propionic acid	0-92	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	166-171
16463413-1	2006	BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA.	Tretinoin	16-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
16463413-1	2006	BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA.	Tretinoin	31-33	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
16463413-1	2006	BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA.	Tretinoin	148-150	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	55-62
16279770-4	2005	With a CYP26A1 homology model, the tetralones were shown to be positioned in a hydrophobic tunnel with additional interactions, e.g., transition metal coordination and hydrogen-bonding interactions with GLY300, observed for the potent 4-hydroxyphenyl substituted inhibitors.	Tetralones	35-45	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	7-14
16194896-1	2005	The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels.	Tretinoin	24-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
16194896-1	2005	The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels.	Tretinoin	39-41	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
16194896-1	2005	The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels.	Tretinoin	156-179	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
16194896-1	2005	The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels.	Tretinoin	181-185	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	78-85
16194896-3	2005	ATRA rapidly induced upregulation of CYP26A1 mRNA expression in a dose-dependent manner.	Tretinoin	0-4	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	37-44
16194896-4	2005	Other retinoids (retinol, 9-cis-RA, and 13-cis-RA) also induced significant CYP26A1 expression in HepG2 and NB4 cells.	Retinoids	6-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
16194896-4	2005	Other retinoids (retinol, 9-cis-RA, and 13-cis-RA) also induced significant CYP26A1 expression in HepG2 and NB4 cells.	Vitamin A	17-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
16194896-4	2005	Other retinoids (retinol, 9-cis-RA, and 13-cis-RA) also induced significant CYP26A1 expression in HepG2 and NB4 cells.	Alitretinoin	26-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
16194896-4	2005	Other retinoids (retinol, 9-cis-RA, and 13-cis-RA) also induced significant CYP26A1 expression in HepG2 and NB4 cells.	Isotretinoin	40-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-83
16194896-5	2005	CYP26A1 mRNA expression in HepG2 cells returned to baseline in 48 h upon removal of ATRA from the culture medium, suggesting that the expression is reversible and requires the presence of ATRA.	Tretinoin	84-88	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
16194896-5	2005	CYP26A1 mRNA expression in HepG2 cells returned to baseline in 48 h upon removal of ATRA from the culture medium, suggesting that the expression is reversible and requires the presence of ATRA.	Tretinoin	188-192	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-7
16194896-6	2005	In endothelial cells, however, a higher concentration of ATRA (10 microM) was required to induce expression of CYP26A1.	Tretinoin	57-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	111-118
16194896-7	2005	A specific RA receptor-alpha antagonist totally inhibited ATRA-induced expression of CYP26A1, indicating that RA receptor-alpha plays a major role in CYP26A1 expression in HepG2 cells.	Tretinoin	58-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	85-92
16194896-7	2005	A specific RA receptor-alpha antagonist totally inhibited ATRA-induced expression of CYP26A1, indicating that RA receptor-alpha plays a major role in CYP26A1 expression in HepG2 cells.	Tretinoin	58-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	150-157
16194896-10	2005	L-ATRA induced lower CYP26A1 expression and metabolic activity in HepG2 and NB4 cells when compared with free ATRA.	Tretinoin	2-6	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	21-28
16194896-12	2005	Our data suggest that upregulation of CYP26A1 expression in intestinal, endothelial, liver, and APL cells and metabolism of ATRA may play a role in rapid clearance of ATRA after continuous oral administration.	Tretinoin	167-171	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	38-45
15597402-9	2004	In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate.	liarozole	59-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	104-109
15896339-2	2005	Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells.	Tretinoin	46-50	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-102
15896339-2	2005	Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells.	Tretinoin	46-50	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	104-111
15896339-2	2005	Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells.	Tretinoin	67-71	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-102
15896339-2	2005	Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells.	Tretinoin	67-71	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	104-111
15896339-4	2005	CYP26A1 constitutive expression was barely detectable in NB4 cells, but ATRA could induce high levels of CYP26A1 expression, which reached a maximum at 72h.	Tretinoin	72-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	105-112
15714209-7	2005	Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1.	Tretinoin	5-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	61-68
15714209-7	2005	Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1.	Tretinoin	5-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	195-202
15714209-7	2005	Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1.	Isotretinoin	14-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	61-68
15714209-7	2005	Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1.	Isotretinoin	14-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	195-202
16143075-7	2005	CONCLUSION: ATRA has remarkable synergic effect with IFN-alpha on HL-60 cells, probably because IFN-alpha inhibits CYP26 mRNA expression and thus reduces the metabolism of ATRA.	Tretinoin	12-16	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	115-120
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	15-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	77-84
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	140-148	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	77-84
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	140-148	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	77-84
16012519-6	2005	In retinoid-sensitive neuroblastoma, lung and breast cancer cell lines, direct inhibition of retinoid-induced RARbeta2 expression blocked induction of only one of eight retinoid target genes (CYP26A1).	Retinoids	93-101	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	192-199
16012519-6	2005	In retinoid-sensitive neuroblastoma, lung and breast cancer cell lines, direct inhibition of retinoid-induced RARbeta2 expression blocked induction of only one of eight retinoid target genes (CYP26A1).	Retinoids	93-101	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	192-199
16012519-7	2005	DNA demethylation, histone acetylation, and exogenous overexpression of RARbeta2 partially restored retinoid-responsive CYP26A1 expression in RA-resistant MDA-MB-231 breast, but not SK-MES-1 lung, cancer cells.	Retinoids	100-108	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	120-127
15703382-0	2005	Expression of the retinoic acid-metabolizing enzyme CYP26A1 limits programmed cell death.	Tretinoin	18-31	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	52-59
15703382-3	2005	On the other hand, we show here that various cell lines overexpressing CYP26A1, a cytochrome P450 enzyme specifically involved in the catabolic inactivation of RA, exhibit increased resistance to various apoptogenic factors, including death receptor ligands such as tumor necrosis factor-related apoptosis-inducing ligand.	Tretinoin	160-162	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	71-78
15703382-5	2005	In addition, synthetic retinoids Am80 (4[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)carbamoyl]benzoic acid) and Am580 [4(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphtamido)benzoic acid], which are resistant to CYP26A1 metabolism, can restore the sensitivity of these cells to apoptogens.	Retinoids	23-32	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	223-230
15703382-5	2005	In addition, synthetic retinoids Am80 (4[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)carbamoyl]benzoic acid) and Am580 [4(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphtamido)benzoic acid], which are resistant to CYP26A1 metabolism, can restore the sensitivity of these cells to apoptogens.	tamibarotene	33-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	223-230
15745819-1	2005	A series of [2-imidazol-1-yl-2-(6-alkoxy-naphthalen-2-yl)-1-methyl-ethyl]-dimethyl-amines were designed and synthesized as CYP26 inhibitors, serving as retinoic acid metabolic blocking agents (RAMBA"s).	[2-imidazol-1-yl-2-(6-alkoxy-naphthalen-2-yl)-1-methyl-ethyl]-dimethyl-amines	12-89	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	123-128
15745819-1	2005	A series of [2-imidazol-1-yl-2-(6-alkoxy-naphthalen-2-yl)-1-methyl-ethyl]-dimethyl-amines were designed and synthesized as CYP26 inhibitors, serving as retinoic acid metabolic blocking agents (RAMBA"s).	Tretinoin	152-165	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	123-128
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Hydrocarbons, Chlorinated	13-27	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-74
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Hydrocarbons, Chlorinated	13-27	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-84
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Tretinoin	103-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-74
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Tretinoin	103-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-84
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Tretinoin	208-221	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-74
15589975-6	2005	In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid.	Tretinoin	208-221	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	76-84
15597402-9	2004	In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate.	liarozole	59-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	111-138
15281009-0	2004	The effect of cellular retinoic acid binding protein-I expression on the CYP26-mediated catabolism of all-trans retinoic acid and cell proliferation in head and neck squamous cell carcinoma.	Tretinoin	23-36	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	73-78
15451545-1	2004	All trans-retinoic acid (RA) plays a role in regulation of P450RAI gene expression.	Tretinoin	4-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	59-66
15448016-0	2004	Identification of the fenretinide metabolite 4-oxo-fenretinide present in human plasma and formed in human ovarian carcinoma cells through induction of cytochrome P450 26A1.	Fenretinide	22-33	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	152-172
15448016-0	2004	Identification of the fenretinide metabolite 4-oxo-fenretinide present in human plasma and formed in human ovarian carcinoma cells through induction of cytochrome P450 26A1.	4-oxofenretinide	45-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	152-172
14532297-4	2004	We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult.	Tretinoin	165-169	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	52-61
15291358-8	2004	Although ATRA and 4-HPR induced expression of CYP26, an ATRA-inducible gene encoding a cytochrome P450 enzyme, in HL-60 cells, both retinoids failed to induce CYP26 in HL-60R cells.	Tretinoin	9-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	46-51
15291358-8	2004	Although ATRA and 4-HPR induced expression of CYP26, an ATRA-inducible gene encoding a cytochrome P450 enzyme, in HL-60 cells, both retinoids failed to induce CYP26 in HL-60R cells.	Tretinoin	56-60	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	46-51
14532297-4	2004	We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult.	Tretinoin	165-169	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	90-97
14532297-9	2004	Specifically, CYP26C1 can also recognize and metabolize 9-cis-RA and is much less sensitive than the other CYP26 family members to the inhibitory effects of ketoconazole.	Tretinoin	56-64	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-19
14532297-9	2004	Specifically, CYP26C1 can also recognize and metabolize 9-cis-RA and is much less sensitive than the other CYP26 family members to the inhibitory effects of ketoconazole.	Ketoconazole	157-169	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	14-19
14532297-11	2004	This third CYP26 member may play a specific role in catabolizing both all-trans and 9-cis isomers of RA.	Radium	101-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	11-16
14704332-6	2004	Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA.	Tretinoin	17-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-54
14704332-6	2004	Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA.	Tretinoin	17-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-63
14704332-6	2004	Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA.	Vitamin A	99-108	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-54
14704332-7	2004	Based on these results, we propose that LRAT and CYP26 serve as two molecular mechanisms, coordinately regulated by all-trans-RA, to control the availability of retinol and RA, respectively.	Vitamin A	161-168	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	49-54
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	Tretinoin	8-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-62
12870655-6	2003	The same ATRA treatment also resulted in the detection of CYP26A1 but not CYP1A1, CYP2B6, CYP2C8, CY2C9, CYP3A4, or CYP3A5 mRNA.	Tretinoin	9-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-65
12711469-7	2003	We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme.	Tretinoin	25-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	108-113
12711469-7	2003	We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme.	Tretinoin	167-180	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	108-113
12044165-8	2002	We also found that in CP26 three chlorophyll binding sites are selective for Chl a, one of them being essential for the folding of the pigment-protein complex.	Chlorophyll	33-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-26
14704332-6	2004	Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA.	Vitamin A	99-108	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-63
14692511-2	2003	Several of the compounds were weak inhibitors of the non-specific rat liver microsomal P450 enzymes and moderate inhibitors of the RA-induced enzymes in cultured human genital fibroblasts, where the RA-specific enzyme CYP26 is probably expressed.	Radium	131-133	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	218-223
14692511-2	2003	Several of the compounds were weak inhibitors of the non-specific rat liver microsomal P450 enzymes and moderate inhibitors of the RA-induced enzymes in cultured human genital fibroblasts, where the RA-specific enzyme CYP26 is probably expressed.	Radium	199-201	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	218-223
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	Tretinoin	8-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-71
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	Tretinoin	23-25	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-62
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	Tretinoin	23-25	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-71
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	Tretinoin	59-61	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-71
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	4-hydroxyretinoic acid	202-214	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-62
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	4-hydroxyretinoic acid	202-214	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-71
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	4-oxoretinoic acid	219-227	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	54-62
12054474-1	2002	A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA.	4-oxoretinoic acid	219-227	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	66-71
12054474-3	2002	The nucleotide sequence predicts a 497-amino-acid protein whose sequence is 95% identical to mouse and 91% homologous to human CYP26.	amino	39-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	127-132
11994980-0	2002	all-trans-Retinoic acid-induced expression and regulation of retinoic acid 4-hydroxylase (CYP26) in human promyelocytic leukemia.	Tretinoin	0-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	61-88
11994980-0	2002	all-trans-Retinoic acid-induced expression and regulation of retinoic acid 4-hydroxylase (CYP26) in human promyelocytic leukemia.	Tretinoin	0-23	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	90-95
11994980-4	2002	We found that treatment of NB4 cells with a pharmacological concentration of ATRA (1 microM) induced rapid and dose-dependent expression of CYP26 mRNA.	Tretinoin	77-81	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	140-145
11994980-5	2002	The CYP26 expression returned to pretreatment levels in both cells after ATRA was removed from the media.	Tretinoin	73-77	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	4-9
11994980-6	2002	Retinoic acid receptor-alpha (RARalpha) specific antagonist (CD2503) totally abolished the ATRA-induced expression of CYP26 mRNA in HL-60 and NB4 cells.	Tretinoin	91-95	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	118-123
11994980-8	2002	ATRA-induced expression of CYP26 was restored in HL-60R cells retrovirally transduced with RARalpha, but not in those cells transduced with the other retinoid receptors.	Tretinoin	0-4	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	27-32
11994980-9	2002	In conclusion, ATRA induces expression of CYP26 in myeloid and promyelocytic leukemia cells and this expression is modulated by RARalpha.	Tretinoin	15-19	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-47
11994980-10	2002	The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy.	Tretinoin	37-41	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
11994980-10	2002	The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy.	Tretinoin	154-158	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
11994980-10	2002	The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy.	Tretinoin	154-158	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
11606945-2	2001	Presented is a summary of recent research that examines the role of some of the enzymes involved in RA distribution, particularly those involved in RA catabolism (P450RAI).	Tretinoin	100-102	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	163-170
11953746-4	2002	Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development.	Tretinoin	100-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	152-159
11953746-4	2002	Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development.	Tretinoin	192-205	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	152-159
11912557-0	2002	Retinoic acid 4-hydroxylase-mediated catabolism of all-trans retinoic acid and the cell proliferation in head and neck squamous cell carcinoma.	Tretinoin	61-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-27
11912557-2	2002	The aim of this study was to confirm if retinoic acid 4-hydroxylase (CYP26) is a P450 induced by RA and to investigate the role of cellular RA binding proteins (CRABPs), using a slow catabolizer, AMC-HN-4, and a rapid catabolizer, AMC-HN-6.	Tretinoin	97-99	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-67
11912557-2	2002	The aim of this study was to confirm if retinoic acid 4-hydroxylase (CYP26) is a P450 induced by RA and to investigate the role of cellular RA binding proteins (CRABPs), using a slow catabolizer, AMC-HN-4, and a rapid catabolizer, AMC-HN-6.	Tretinoin	97-99	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	69-74
11912557-5	2002	The sensitivity to RA was variable by the amount of CYP26, and the rapid catabolism by CYP26 made AMC-HN-6 resistant to RA in vitro.	Tretinoin	19-21	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	52-57
11912557-5	2002	The sensitivity to RA was variable by the amount of CYP26, and the rapid catabolism by CYP26 made AMC-HN-6 resistant to RA in vitro.	Tretinoin	120-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	87-92
11912557-7	2002	Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism.	Tretinoin	71-73	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-23
11912557-7	2002	Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism.	Tretinoin	132-134	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	121-126
11912557-7	2002	Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism.	Tretinoin	132-134	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	121-126
11766909-4	2001	RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	56-61
11766909-4	2001	RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA.	Tretinoin	98-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	56-61
11766909-4	2001	RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA.	Tretinoin	98-100	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	56-61
11766909-4	2001	RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA.	4-oxoretinoic acid	120-128	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	56-61
11766909-5	2001	CYP26 is downregulated upon vitamin A depletion.	Vitamin A	28-37	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
11302942-0	2001	Effects of receptor-selective retinoids on CYP26 gene expression and metabolism of all-trans-retinoic acid in intestinal cells.	Tretinoin	86-106	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	43-48
11690641-0	2001	Phytanic acid and docosahexaenoic acid increase the metabolism of all-trans-retinoic acid and CYP26 gene expression in intestinal cells.	Phytanic Acid	0-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-99
11690641-0	2001	Phytanic acid and docosahexaenoic acid increase the metabolism of all-trans-retinoic acid and CYP26 gene expression in intestinal cells.	Docosahexaenoic Acids	18-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	94-99
11690641-6	2001	However, in combination with retinoic acid receptor (RAR)-ligands (all-trans-RA or synthetic Am580) phytanic acid enhanced the induction of CYP26 and RA-metabolism in comparison to treatments with all-trans-RA or Am580 alone.	Phytanic Acid	100-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	140-145
11690641-7	2001	Also treatment with DHA did not affect CYP26 gene expression and RA-metabolism but cotreatment of the cells with DHA and all-trans-RA or Am580 enhanced the induction of CYP26, in comparison to the induction caused by all-trans-RA or Am580 alone.	Docosahexaenoic Acids	113-116	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	169-174
11690641-8	2001	This study indicates that food compounds such as phytanic acid and DHA that are RXR-agonists and have an impact on intestinal CYP26 gene expression and metabolism of all-trans-RA in intestinal cells.	Phytanic Acid	49-62	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-131
11690641-8	2001	This study indicates that food compounds such as phytanic acid and DHA that are RXR-agonists and have an impact on intestinal CYP26 gene expression and metabolism of all-trans-RA in intestinal cells.	Docosahexaenoic Acids	67-70	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-131
11690641-8	2001	This study indicates that food compounds such as phytanic acid and DHA that are RXR-agonists and have an impact on intestinal CYP26 gene expression and metabolism of all-trans-RA in intestinal cells.	Tretinoin	176-178	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	126-131
11471143-0	2001	Differential expression of chicken CYP26 in anterior versus posterior limb bud in response to retinoic acid.	Tretinoin	94-107	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-40
11471143-4	2001	Recently, enzymes capable of catabolizing RA were found to constitute a new family, called CYP26, within the cytochrome P450 superfamily.	Tretinoin	42-44	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	91-96
11302942-2	2001	The complex mechanistic pattern of retinoid-induced effects on gene expression of CYP26 and intestinal metabolism of all-trans-retinoic acid (RA) was investigated here by studying the effects of retinoid ligands with relative selectivity for binding and transactivation of the retinoid acid receptors, RARs and RXRs, in human intestinal Caco-2 cells.	Retinoids	35-43	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-87
11302942-2	2001	The complex mechanistic pattern of retinoid-induced effects on gene expression of CYP26 and intestinal metabolism of all-trans-retinoic acid (RA) was investigated here by studying the effects of retinoid ligands with relative selectivity for binding and transactivation of the retinoid acid receptors, RARs and RXRs, in human intestinal Caco-2 cells.	Retinoids	195-203	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	82-87
11302942-10	2001	Receptor-selective retinoids showed enhanced effects on induction of CYP26 gene expression and all-trans-retinoic acid metabolism.	Retinoids	19-28	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	69-74
11309353-5	2001	Furthermore, the mRNA expression of the RA-specific 4-hydroxylase, CYP26A1, was dramatically increased after RA-induction in the two HNSCC cell lines with the highest metabolism, was undetectable in normal keratinocytes, and was not inducible by RA.	Tretinoin	40-42	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-74
11309353-5	2001	Furthermore, the mRNA expression of the RA-specific 4-hydroxylase, CYP26A1, was dramatically increased after RA-induction in the two HNSCC cell lines with the highest metabolism, was undetectable in normal keratinocytes, and was not inducible by RA.	Tretinoin	109-111	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-74
11309353-6	2001	Next, introduction of CYP26A1 cDNA in a low-metabolizing HNSCC cell line resulted in an 11-fold higher turnover rate of RA and a 12-fold increase in the amount of polar metabolites, but it did not change sensitivity to RA.	Tretinoin	120-122	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	22-29
11522124-11	2001	One known morphogen, retinoic acid, has the enzymes retinal dehydrogenase (RALDH) and CYP26 maintaining its actions, the former responsible for its generation and the latter for its elimination.	Tretinoin	21-34	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	86-91
10953040-5	2000	CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302.	Retinoids	47-55	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
11082432-10	2000	The specific retinoic acid metabolizing CYP26 was induced after RA treatment in Caco-2 cells.	Tretinoin	13-26	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
11082432-10	2000	The specific retinoic acid metabolizing CYP26 was induced after RA treatment in Caco-2 cells.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	40-45
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	liarozole	280-289	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-49
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	7-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-49
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	7-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-56
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	7-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	293-300
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	27-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-49
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	27-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-56
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	Tretinoin	27-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	293-300
11025452-8	2000	Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor.	liarozole	280-289	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-56
11041855-6	2000	It is concluded that the extrinsic subunits keep the S-LHCII and CP29 subunits in proper positions at some distance from the central part of the photosystem II core dimer to ensure a directed transfer of excitation energy through the monomeric peripheral antenna proteins CP26 and CP29 and/or to maintain sequestered domains of inorganic cofactors required for oxygen evolution.	Oxygen	361-367	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	272-276
11023996-10	2000	We conclude that CYP26 expression and RA metabolism are regulated in adult liver not only acutely by RA administration, as may be relevant to retinoid therapy, but under chronic dietary conditions relevant to vitamin A nutrition in humans.	Tretinoin	101-103	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
11023996-10	2000	We conclude that CYP26 expression and RA metabolism are regulated in adult liver not only acutely by RA administration, as may be relevant to retinoid therapy, but under chronic dietary conditions relevant to vitamin A nutrition in humans.	Retinoids	142-150	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
11023996-10	2000	We conclude that CYP26 expression and RA metabolism are regulated in adult liver not only acutely by RA administration, as may be relevant to retinoid therapy, but under chronic dietary conditions relevant to vitamin A nutrition in humans.	Vitamin A	209-218	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
10953040-5	2000	CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302.	Retinoids	162-170	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10953040-5	2000	CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302.	SR 11302	230-237	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10953040-6	2000	RARalpha-, beta-, and gamma-selective retinoids are able to induce CYP26; this induction is inhibited by the RARalpha-selective antagonist Ro41-5253.	Retinoids	38-47	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-72
10953040-6	2000	RARalpha-, beta-, and gamma-selective retinoids are able to induce CYP26; this induction is inhibited by the RARalpha-selective antagonist Ro41-5253.	Ro 41-5253	139-148	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	67-72
10953040-7	2000	TTAB is able to induce CYP26 mRNA expression in only a few of the lung carcinoma cell lines tested.	4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)benzoic acid	0-4	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	23-28
10953040-9	2000	The induction of CYP26 correlated with increased metabolism of RA into 18-hydroxy-, 4-oxo-, and 4-hydroxy-RA.	Tretinoin	63-65	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
10953040-9	2000	The induction of CYP26 correlated with increased metabolism of RA into 18-hydroxy-, 4-oxo-, and 4-hydroxy-RA.	18-hydroxy-, 4-oxo-, and 4-hydroxy-ra	71-108	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	17-22
10862743-7	2000	Furthermore, RA upregulates P450RAI expression, suggesting the presence of feedback mechanisms controlling RA availability.	Tretinoin	13-15	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	28-35
9228041-0	1997	CYP26, a novel mammalian cytochrome P450, is induced by retinoic acid and defines a new family.	Tretinoin	56-69	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10702251-9	2000	We also propose that atRA induces its own oxidative metabolism via a cytochrome P450 (CYP26) and is further biotransformed into glucuronides via UGT-mediated pathways.	Tretinoin	21-25	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	86-91
10540859-5	1999	A refined control mechanism for intracellular level of retinoic acid is also discussed with retinal dehydrogenase II and cytochrome P450 RAI (CYP26).	Tretinoin	55-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	142-147
10479456-5	1999	P19 embryonal carcinoma (EC) cell lines stably expressing hCYP26 undergo extensive and rapid neuronal differentiation in monolayer at already low concentrations of RA, while normally P19 cells under these conditions differentiate only in endoderm-like cells.	Tretinoin	164-166	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	58-64
9740237-0	1998	Retinoic acid receptors regulate expression of retinoic acid 4-hydroxylase that specifically inactivates all-trans retinoic acid in human keratinocyte HaCaT cells.	2-octenal	109-114	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-74
9716180-6	1998	The RA-induced CYP26 was shown to be highly specific for the hydroxylation of all-trans-RA and did not recognize the 13-cis and 9-cis isomers.	Tretinoin	4-6	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
10953040-1	2000	In this study, the expression of CYP26 is examined in relation to retinoid-induced mucosecretory differentiation in human tracheobronchial epithelial (HTBE) cells and compared with that in human lung carcinoma cell lines.	Retinoids	66-74	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	33-38
10953040-4	2000	RA is required but not sufficient to induce RARbeta, CYP26, and MUC2 mRNA because induction is only observed in confluent but not in logarithmic cultures, suggesting that additional factors are critical in their regulation.	Tretinoin	0-2	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	53-58
10953040-5	2000	CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302.	retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid	47-125	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10953040-5	2000	CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302.	4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)benzoic acid	127-131	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10727725-1	2000	CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development.	Tretinoin	36-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10727725-1	2000	CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development.	Tretinoin	36-49	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	7-14
10727725-1	2000	CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development.	Tretinoin	11-13	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10727725-1	2000	CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development.	Retinoids	116-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
10727725-1	2000	CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development.	Retinoids	116-124	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	7-14
10421060-8	1999	[3H]Retinoic acid showed a more rapid metabolism to 4-hydroxy/4-keto-retinoic acid in HaCaT cells than in HEK, which could be explained by a higher expression of cytochrome p450RAI in the former cells.	Tritium	1-3	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	162-180
10421060-8	1999	[3H]Retinoic acid showed a more rapid metabolism to 4-hydroxy/4-keto-retinoic acid in HaCaT cells than in HEK, which could be explained by a higher expression of cytochrome p450RAI in the former cells.	Tretinoin	4-17	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	162-180
10421060-8	1999	[3H]Retinoic acid showed a more rapid metabolism to 4-hydroxy/4-keto-retinoic acid in HaCaT cells than in HEK, which could be explained by a higher expression of cytochrome p450RAI in the former cells.	4-hydroxy/4-keto-retinoic acid	52-82	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	162-180
9716180-1	1998	We report on the isolation of a cytochrome P450 (CYP)-like retinoic acid (RA) 4-hydroxylase cDNA from T-47D human breast cancer cells that is identical to the recently cloned hCYP26, which is involved in the metabolic breakdown of RA.	Tretinoin	74-76	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	175-181
9716180-2	1998	Northern analysis showed that this novel human CYP26 is induced within 1 h upon RA treatment in RA-sensitive T-47D breast carcinoma cells but not in RA-resistant MDA-MB-231 breast cancer cells and HCT 116 colon cancer cells.	Tretinoin	80-82	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-52
9716180-2	1998	Northern analysis showed that this novel human CYP26 is induced within 1 h upon RA treatment in RA-sensitive T-47D breast carcinoma cells but not in RA-resistant MDA-MB-231 breast cancer cells and HCT 116 colon cancer cells.	Tretinoin	96-98	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	47-52
9716180-3	1998	Stable introduction of different RA receptor (RAR) subtypes in HCT 116 cells showed that CYP26 expression is dependent on RARalpha and RARgamma and, to a lesser extent, on RARbeta and closely paralleled RA metabolism, suggesting that it represents the major RA 4-hydroxylase in these human cells.	Tretinoin	33-35	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	89-94
9716180-5	1998	Interestingly, CYP26 activity was efficiently inhibited by liarozole, an inhibitor of RA metabolism, leading to enhanced growth inhibition by RA.	liarozole	59-68	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
9716180-5	1998	Interestingly, CYP26 activity was efficiently inhibited by liarozole, an inhibitor of RA metabolism, leading to enhanced growth inhibition by RA.	Tretinoin	86-88	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
9716180-5	1998	Interestingly, CYP26 activity was efficiently inhibited by liarozole, an inhibitor of RA metabolism, leading to enhanced growth inhibition by RA.	Tretinoin	142-144	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	15-20
9564181-0	1998	The cloning and characterization of a novel cytochrome P450 family, CYP26, with specificity toward retinoic acid.	Tretinoin	99-112	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	68-73
9564181-2	1998	CYP26 displays specificity toward retinoic acid and it may function as an important regulator or differentiation and a possible modulator of disease states by controlling retinoid concentration and homeostasis.	Tretinoin	34-47	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
9564181-2	1998	CYP26 displays specificity toward retinoic acid and it may function as an important regulator or differentiation and a possible modulator of disease states by controlling retinoid concentration and homeostasis.	Retinoids	171-179	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-5
9857269-4	1998	Recently, a novel cytochrome P450 enzyme (CYP26) with specific RA 4-hydroxylase activity, which is rapidly induced by RA, has been cloned from man, mouse and zebra fish, fullfilling all requirements of an enzyme which could be of crucial importance in controlling steady-state levels of active retinoids in cells and target tissues, thus protecting against excessive exposure.	Tretinoin	63-65	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-47
9857269-4	1998	Recently, a novel cytochrome P450 enzyme (CYP26) with specific RA 4-hydroxylase activity, which is rapidly induced by RA, has been cloned from man, mouse and zebra fish, fullfilling all requirements of an enzyme which could be of crucial importance in controlling steady-state levels of active retinoids in cells and target tissues, thus protecting against excessive exposure.	Retinoids	294-303	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	42-47
9857269-5	1998	Besides the putative role of this newly identified CYP26 in contributing to susceptibility of cancer cells to retinoids, the possible function of this gene in early embryonic development is discussed.	Retinoids	110-119	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	51-56
9228017-0	1997	cDNA cloning of human retinoic acid-metabolizing enzyme (hP450RAI) identifies a novel family of cytochromes P450.	Tretinoin	22-35	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	57-65
9200700-14	1997	In contrast, the Triton X-100-solubilized LHCII is highly depleted in CP26 (CP 29 type I gene product) and is contaminated by a variety of unidentified polypeptides.	Octoxynol	17-29	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	70-74
9228017-11	1997	In this paper, we describe the cloning and characterization of the first mammalian retinoic acid-inducible retinoic acid-metabolizing cytochrome P450 (hP450RAI), which belongs to a novel class of cytochromes (CYP26).	Tretinoin	83-96	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	145-159
9228017-12	1997	We demonstrate that hP450RAI is responsible for generation of several hydroxylated forms of RA, including 4-OH-RA, 4-oxo-RA, and 18-OH-RA.	4-oh-ra	106-113	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-28
9228017-12	1997	We demonstrate that hP450RAI is responsible for generation of several hydroxylated forms of RA, including 4-OH-RA, 4-oxo-RA, and 18-OH-RA.	4-oxoretinoic acid	115-123	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-28
9228017-12	1997	We demonstrate that hP450RAI is responsible for generation of several hydroxylated forms of RA, including 4-OH-RA, 4-oxo-RA, and 18-OH-RA.	18-oh-ra	129-137	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	20-28
8757760-9	1996	These data demonstrate that, at doses used here, liarozole, although an effective inhibitor of retinoic acid 4-hydroxylase, cannot function alone like a retinoid in vivo, probably because of retinoic acid 4-hydroxylase induction.	liarozole	49-58	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	95-122
9228017-13	1997	We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-26
9228017-13	1997	We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	19-26
9228017-13	1997	We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	18-26
9228017-13	1997	We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression.	Tretinoin	64-66	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	19-26
8757760-0	1996	Liarozole inhibits human epidermal retinoic acid 4-hydroxylase activity and differentially augments human skin responses to retinoic acid and retinol in vivo.	liarozole	0-9	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	35-62
8757760-2	1996	We investigated the effects of liarozole on the retinoic acid 4-hydroxylase activity of human epidermis and its ability to modify in vivo human skin responses to retinoic acid and all-trans retinol.	liarozole	31-40	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	48-75
8757760-3	1996	Retinoic acid 4-hydroxylase activity induced in vivo by 4 d treatment with retinoic acid (0.1%) was inhibited in vitro by liarozole in a concentration-dependent manner.	Tretinoin	75-88	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-27
8757760-3	1996	Retinoic acid 4-hydroxylase activity induced in vivo by 4 d treatment with retinoic acid (0.1%) was inhibited in vitro by liarozole in a concentration-dependent manner.	liarozole	122-131	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	0-27
8757760-9	1996	These data demonstrate that, at doses used here, liarozole, although an effective inhibitor of retinoic acid 4-hydroxylase, cannot function alone like a retinoid in vivo, probably because of retinoic acid 4-hydroxylase induction.	liarozole	49-58	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	191-218
8601734-1	1996	Application of all-trans retinoic acid to human skin for 4 d under occlusion produces a marked increase in retinoic acid 4-hydroxylase activity.	2-octenal	19-24	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-134
8601734-1	1996	Application of all-trans retinoic acid to human skin for 4 d under occlusion produces a marked increase in retinoic acid 4-hydroxylase activity.	Tretinoin	25-38	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	107-134
8601734-3	1996	Application of 0.1% all-trans, 0.1% 9-cis, and 0.1% 13-cis retinoic acid to human skin for 2 d resulted in induction of only all-trans retinoic acid 4-hydroxylase activity.	Isotretinoin	52-72	cytochrome P450 family 26 subfamily A member 1	Homo sapiens	135-162