PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27861128-0 2016 Retinoic acid catabolizing enzyme CYP26C1 is a genetic modifier in SHOX deficiency. Tretinoin 0-13 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 34-41 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 C member 1 Homo sapiens 53-60 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 C member 1 Homo sapiens 53-60 29731343-3 2018 We show that switching occurs during normal development and is mediated by feedback between segment identity and the retinoic acid degrading enzymes, cyp26b1 and cyp26c1. Tretinoin 117-130 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 162-169 29476041-0 2018 CYP26C1 Is a Hydroxylase of Multiple Active Retinoids and Interacts with Cellular Retinoic Acid Binding Proteins. Tretinoin 82-95 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 29476041-2 2018 The goal of this study was to establish the substrate specificity of CYP26C1, and determine whether CYP26C1 interacts with cellular retinoic acid binding proteins (CRABPs). Tretinoin 132-145 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 100-107 29476041-3 2018 CYP26C1 was found to effectively metabolize all-trans retinoic acid (atRA), 9-cis-retinoic acid (9-cis-RA), 13-cis-retinoic acid, and 4-oxo-atRA with the highest intrinsic clearance toward 9-cis-RA. Tretinoin 44-67 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 29476041-3 2018 CYP26C1 was found to effectively metabolize all-trans retinoic acid (atRA), 9-cis-retinoic acid (9-cis-RA), 13-cis-retinoic acid, and 4-oxo-atRA with the highest intrinsic clearance toward 9-cis-RA. Tretinoin 69-73 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 29706635-0 2018 Functional missense and splicing variants in the retinoic acid catabolizing enzyme CYP26C1 in idiopathic short stature. Tretinoin 49-62 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 83-90 29706635-3 2018 We have recently found that the retinoic acid degrading enzyme CYP26C1 modifies SHOX deficiency phenotypes toward more severe clinical manifestations. Tretinoin 32-45 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 63-70 29476041-7 2018 In support of this, CRABPs delivered 4-oxo-atRA and atRA for metabolism by CYP26C1. Tretinoin 43-47 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 75-82 29476041-8 2018 Despite the tight binding of 4-oxo-atRA and atRA with CRABPs, the apparent Michaelis-Menten constant in biological matrix (Km) value of these substrates with CYP26C1 was not increased when the substrates were bound with CRABPs, in contrast to what is predicted by free drug hypothesis. Tretinoin 35-39 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 158-165 27861128-4 2016 The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Tretinoin 31-44 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 65-72 27861128-5 2016 Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. Tretinoin 222-235 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 52-59 27861128-5 2016 Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. Tretinoin 222-235 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 139-146 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 C member 1 Homo sapiens 124-131 26009309-0 2016 Elevated expression of the retinoic acid-metabolizing enzyme CYP26C1 in primary breast carcinomas. Tretinoin 27-40 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 61-68 26009309-9 2016 Based on the RA-catabolizing activity of CYP26C1, our data suggest that CYP26C1 expression may contribute to neoplasia in the breast. Tretinoin 13-15 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 41-48 26009309-9 2016 Based on the RA-catabolizing activity of CYP26C1, our data suggest that CYP26C1 expression may contribute to neoplasia in the breast. Tretinoin 13-15 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 72-79 21906690-8 2011 CYP26C1 metabolism of all trans-RA could also be effectively competed with 9-cis RA, with IC(50) of 62nM, and was sensitive to ketoconazole inhibition. Tretinoin 32-34 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 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 C member 1 Homo sapiens 172-179 24360906-9 2014 In addition, they may modulate the transcriptional output of multiple signaling pathways involved in neural crest development (Wnt, Retinoic Acid) through the induction of key pathway regulators (Axin2 and Cyp26c1). Tretinoin 132-145 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 206-213 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 C member 1 Homo sapiens 124-131 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 C member 1 Homo sapiens 124-131 21906690-3 2011 CYP26C1 has also been shown to efficiently metabolize the 9-cis isomer of RA. Tretinoin 74-76 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 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 C member 1 Homo sapiens 103-110 18502188-8 2008 CYP26C1 transcription was significantly repressed by ATRA, and this downregulation also showed a neural differentiation-dependent pattern, in respect that CYP26C1 expression was kept in low-level even after the withdrawal of ATRA. Tretinoin 53-57 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 18502188-8 2008 CYP26C1 transcription was significantly repressed by ATRA, and this downregulation also showed a neural differentiation-dependent pattern, in respect that CYP26C1 expression was kept in low-level even after the withdrawal of ATRA. Tretinoin 225-229 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7 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 C member 1 Homo sapiens 47-54 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 C member 1 Homo sapiens 47-54 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 C member 1 Homo sapiens 47-54 14532297-0 2004 A novel human cytochrome P450, CYP26C1, involved in metabolism of 9-cis and all-trans isomers of retinoic acid. Tretinoin 97-110 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 31-38 14532297-6 2004 Transiently transfected cells expressing CYP26C1 convert atRA to polar water-soluble metabolites similar to those generated by CYP26A1 and -B1. Tretinoin 57-61 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 41-48 14532297-7 2004 Competition studies with all-trans, 13-cis, and 9-cis isomers of retinoic acid demonstrated that atRA was the preferred substrate for CYP26C1. Tretinoin 65-78 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 134-141 14532297-7 2004 Competition studies with all-trans, 13-cis, and 9-cis isomers of retinoic acid demonstrated that atRA was the preferred substrate for CYP26C1. Tretinoin 97-101 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 134-141 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 C member 1 Homo sapiens 14-21 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 C member 1 Homo sapiens 93-101