Relevant bibliographies by topics / CYP46

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'CYP46'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "CYP46"

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Wolozin, Benjamin. "Cyp46 (24S-Cholesterol Hydroxylase)." Archives of Neurology 60, no. 1 (January 1, 2003): 16. http://dx.doi.org/10.1001/archneur.60.1.16.

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Garcia, Anália Nusya Medeiros, Maria Tereza Cartaxo Muniz, Hugo Rafael Souza e Silva, Helker Albuquerque da Silva, and Luiz Athayde-Junior. "Cyp46 Polymorphisms in Alzheimer’s Disease: A Review." Journal of Molecular Neuroscience 39, no. 3 (August 25, 2009): 342–45. http://dx.doi.org/10.1007/s12031-009-9227-2.

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HENG, Yee M., C. W. Sharon KUO, Paul S. JONES, Richard SAVORY, Ruth M. SCHULZ, Simon R. TOMLINSON, Tim J. B. GRAY, and David R. BELL. "A novel murine P-450 gene, Cyp4a14, is part of a cluster of Cyp4a and Cyp4b, but not of CYP4F, genes in mouse and humans." Biochemical Journal 325, no. 3 (August 1, 1997): 741–49. http://dx.doi.org/10.1042/bj3250741.

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Genomic clones for Cyp4a12 and a novel member of the murine Cyp4a gene family were isolated. The novel gene, designated Cyp4a14, has a GC rich sequence immediately 5′ of the transcription start site, and is similar to the rat CYP4A2 and CYP4A3 genes. The Cyp4a14 gene spans approximately 13 kb, and contains 12 exons; sequence similarity to the rat CYP4A2 gene sequence falls off 300 bp upstream from the start site. In view of the known sex-specific expression of the rat CYP4A2 gene, the expression and inducibility of Cyp4a14 was examined. The gene was highly inducible in the liver when mice were treated with the peroxisome proliferator, methylclofenapate; induction levels were low in control animals and no sex differences in expression were observed. By contrast, the Cyp4a12 RNA was highly expressed in liver and kidney of control male mice but was expressed at very low levels in liver and kidney of female mice. Testosterone treatment increased the level of this RNA in female liver slightly, and to a greater extent in the kidney of female mice. In agreement with studies on the cognate RNA, expression of Cyp4a12 protein was male-specific in the liver of control mice and extremely high inducibility of Cyp4a10 protein, with no sex differences, was also demonstrated. In view of the overlapping patterns of inducibility of the three Cyp4a genes, we investigated whether the three genes were co-localized in the genome. Two overlapping yeast artificial chromosome (YAC) clones were isolated, and the three Cyp4a genes were shown to be present on a single YAC of 220 kb. The Cyp4a genes are adjacent to the Cyp4b1 gene, with Cyp4a12 most distant from Cyp4b1. The clustering of these two gene subfamilies in the mouse was replicated in the human, where the CYPA411 and CYP4B1 genes were present in a single YAC clone of 440 kb. However, the human CYP4F2 gene was mapped to chromosome 19. Phylogenetic analysis of the CYP4 gene families demonstrated that CYP4A and CYP4B are more closely related than CYP4F.
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Combarros, Onofre, Jon Infante, Javier Llorca, and José Berciano. "Genetic Association of CYP46 and Risk for Alzheimer’s Disease." Dementia and Geriatric Cognitive Disorders 18, no. 3-4 (2004): 257–60. http://dx.doi.org/10.1159/000080025.

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Kölsch, Heike, Dieter Lütjohann, Frank Jessen, Julius Popp, Frank Hentschel, Peter Kelemen, Sandra Schmitz, Wolfgang Maier, and Reinhard Heun. "CYP46A1 variants influence Alzheimer’s disease risk and brain cholesterol metabolism." European Psychiatry 24, no. 3 (April 2009): 183–90. http://dx.doi.org/10.1016/j.eurpsy.2008.12.005.

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AbstractBackgroundCholesterol 24S-hydroxylase (CYP46) catalyzes the conversion of cholesterol to 24S-hydroxycholesterol, the primary cerebral cholesterol elimination product. Only few gene variations in CYP46 gene (CYP46A1) have been investigated for their relevance as genetic risk factors of Alzheimer’s disease (AD) and results are contradictory.MethodsWe performed a gene variability screening in CYP46A1 and investigated the effect of gene variants on the risk of AD and on CSF levels of cholesterol and 24S-hydroxycholesterol.ResultsTwo of the identified 16 SNPs in CYP46A1 influenced AD risk in our study (rs7157609: p = 0.016; rs4900442: p = 0.019). The interaction term of both SNPs was also associated with an increased risk of AD (p = 0.006). Haplotypes including both SNPs were calculated and haplotype G–C was identified to influence the risk of AD (p = 0.005). AD patients and non-demented controls, who were carriers of the G–C haplotype, presented with reduced CSF levels of 24S-hydroxycholesterol (p = 0.001) and cholesterol (p < 0.001).ConclusionOur results suggest that CYP46A1 gene variations might act as risk factor for AD via an influence on brain cholesterol metabolism.
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Golanska, Ewa, Krystyna Hulas-Bigoszewska, Izabela Wojcik, Piotr Rieske, Maria Styczynska, Beata Peplonska, Anna Pfeffer, et al. "CYP46: A risk factor for Alzheimer's disease or a coincidence?" Neuroscience Letters 383, no. 1-2 (July 2005): 105–8. http://dx.doi.org/10.1016/j.neulet.2005.03.049.

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Martin, Mauricio G., Laura Trovò, Simona Perga, Agniezska Sadowska, Andrea Rasola, Federica Chiara, and Carlos G. Dotti. "Cyp46-mediated cholesterol loss promotes survival in stressed hippocampal neurons." Neurobiology of Aging 32, no. 5 (May 2011): 933–43. http://dx.doi.org/10.1016/j.neurobiolaging.2009.04.022.

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Lai, Chiou-lian, Chung-yao Hsu, Li-min Liou, Hsin-yi Hsieh, Yi-hsing Hsieh, and Ching-kuan Liu. "Effect of cholesterol and CYP46 polymorphism on cognitive event-related potentials." Psychophysiology 48, no. 11 (July 5, 2011): 1572–77. http://dx.doi.org/10.1111/j.1469-8986.2011.01221.x.

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Smiljanic, Kosara, Petar Marinkovic, Aleksandra Mladenovic, Sabera Ruzdijic, and Selma Kanazir. "P3-232: Dietary restriction modulates CYP46 expression in aging rat brain." Alzheimer's & Dementia 2 (July 2006): S443—S444. http://dx.doi.org/10.1016/j.jalz.2006.05.1501.

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Voronova, N. V., M. M. Varabyova, and Yu V. Bondarenko. "CYP4 and CYP6 gene variability in genome of Aphis fabae mordvilkoi Börner & Janisch, 1922." Faktori eksperimental'noi evolucii organizmiv 22 (September 9, 2018): 108–12. http://dx.doi.org/10.7124/feeo.v22.933.

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Aim. To estimate the variability of genes of 4th and 6th families of CYP450, which were extracted from the whole genome data of Aphis fabae mordvilkoi collected from Philadelphus coronaries L. in Belarus. Methods. The whole genome sequencing was carried out in the University of Utah DNA Sequencing and Genomic Core Facilities (USA). CYP4 and CYP6 gene sequences were extracted from the whole genome data by sequential mapping the whole genome reads to CYP4 and CYP6 CDSs of three reference genomes (Acyrthosiphon pisum Harris, 1776, Myzus persicae (Sulžer, 1776) и Diuraphis noxia (MordvilkoexKurdjumov, 1913)). All found uniqueversion of assembling were taken as a single gene. Results. In A. fabae mordvilkoi genome we found out 31 CYP4 genes and 24 from them were copies of CYP4C1s. We also found out 19 CYP6 gene sand 8 from them were identified as CYP6A13s. Variability of nucleotide an damino acid sequences of CYP4 and CYP6 CDSs were high. Conclusions. In A. fabae mordvilkoi genome most CYP4genes were identified as CYP4C1 and most CYP6 genes were CYP6A13s. Other CYP4 and CYP6 were mostly presented as single copies of different genes.Keywords: aphids, cytochrome p450, Aphis fabae, trophic specialization, gene copies.
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Dissertations / Theses on the topic "CYP46"

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GARCIA, Analia Nusya de Medeiros. "Polimorfismos dos genes CYP 46 e APOE e declínio cognitivo em idosos residentes no distrito de Fernando de Noronha-PE." Universidade Federal de Pernambuco, 2011. https://repositorio.ufpe.br/handle/123456789/8317.

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Made available in DSpace on 2014-06-12T22:59:08Z (GMT). No. of bitstreams: 2 arquivo5593_1.pdf: 9647965 bytes, checksum: 23ac0509ddb6353a3c91975edec8f243 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2011
O Declínio Cognitivo Leve (DCL) é um estado mental considerado a zona de transição entre o envelhecimento normal e a fase mais inicial de demência, sendo uma fase importante para a precocidade diagnóstica. Nos últimos anos, pesquisas estão sendo desenvolvidas na busca de marcadores genéticos para esta zona de pré-demência, como os polimorfismos dos genes da apolipoproteína E (APOE) representada por 3 alelos (E2, E3, E4) e do colesterol 24S-hidroxilase (CYP46) com alelos T e C. Indivíduos portadores do APOE E4 tem fator de risco quatro vezes maior de desenvolver a Demência de Alzheimer e dez vezes mais probabilidade se tiver associado os polimorfismos dos genes APOE e CYP46. O objetivo deste estudo foi investigar a possível associação entre o polimorfismo dos genes CYP46(T/C), APOE E4 e a presença de DCL na população idosa do Distrito de Fernando de Noronha, totalizando uma seleção de 52 indivíduos. A avaliação clínica foi realizada através de exame físico, funcional e mental. Foram aplicados testes neuropsiquiátricos (Mini Exame do Estado Mental, Teste de Fluência Verbal, Teste do Relógio) e a identificação do genótipo dos polimorfismos do APOE e CYP46 pelo método de PCR-RFLP. Como resultados observou-se que 87% da amostra apresentou declínio cognitivo leve. No Mini Exame do Estado Mental, Teste de Fluência Verbal e Teste do Relógio foi observado declínio cognitivo em 42,8%, 31,9% e 53,2% respectivamente. Foi observada uma frequência alélica de 10% para o alelo E4. Não foi observada associação entre APOE E4 e declínio cognitivo. Os alelos T (p = 0,628) e C (p = 0,2076) do gene Cyp46 não estão associadas ao DCL na população estudada. Não foi observada associação (p = 0,4286), quando analisado o sinergismo entre o polimorfismo dos genes Cyp46(T/C) e APOE E4 no desenvolvimento do DCL. Nesta população, os resultados sugerem que os polimorfismos dos genes Cyp46(T/C) e APOE E4 não estão associados ao DCL
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Sundin, Johanna. "Expression and Purification of Full-length CYP26 B1 and Spliced CYP26 B1." Thesis, Örebro University, School of Science and Technology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-7394.

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The goal of this project is to express both the normal CYP26 B1 and the spliced CYP26 B1 from human in Escherichia coli (E.coli) cells for further crystallization. This will be achieved by cloning in the DNA fragments into the Champion pET SUMO vector that is later transformed into E.coli cells. The CYP26 B1 contains a hydrophobic helix at the N-terminal of the protein, making both protein expression and crystallization difficult. Two variants of both full-length CYP26 B1 and the spliced variant will therefore be made, one with the trans-membrane helix present and one without the helix. The SUMO-vector will produce a fusion protein that will make CYP26 B1 more hydrophilic and improve the purification of the two proteins.

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Rydeen, Ariel B. "Requirements for Cyp26 enzymes in cardiovascular development." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1468335415.

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Graham, Richard Alan LeCluyse Edward L. "Biochemical and molecular characterization of beagle dog CYP4A." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,290.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the School of Pharmacy." Discipline: Pharmacy; Department/School: Pharmacy.
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Hood, Steven Richard. "Isolation and characterisation of a human CYP4A gene." Thesis, University of Surrey, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359859.

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Pautus, Stephane. "Design, synthesis and binding studies of novel CYP26 inhibitors." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55730/.

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All-frans-retinoic acid ATRA has shown spectacular success in the treatment of cancer and leukaemia, however ATRA is rapidly metabolised by the P450 enzyme CYP26. In order to enhance endogenous levels of ATRA and/or to extend the half life of externally administered ATRA, a CYP26 inhibitor is required. Two series of CYP26 inhibitors were synthesised a series of 4-alkyl/aryl-substituted 1-joeiizofuran-2-yl-phenylmethyl-1-triazoles and a series of benzoxazol-2-yl-phenylinn lazol The triazole derivatives were prepared using methodology previously described by our group. The aminobenzoxazole derivatives were envisaged from a docking experiment using a CYP26A1 homology model based on CYP3A4 template docking experiments were performed with MOE. The molecular docking of the amino-benzooxazole imidazole derivatives indicated multiple hydrogen bonding in addition to coordination between the imidazole nitrogen and the P450 haem transition metal. The triazole derivatives were evaluated for CYP26A1 inhibitory activity using a MCF-7 cell-based assay. The 4-ethyl-l,2,4-triazole and the 4-phenyl-l,2,4-triazole derivatives displayed inhibitory activity ICso 4.5 and ICso 7 uM respectively comparable with liarozole ICso 7 uM. On the other hand the aminobenzooxazole imidazole derivatives were only moderate inhibitors of the CYP26A1 enzyme in MCF-7 cells and did not achieve the promise shown in docking studies. The most potent inhibitor was the unsubstituted derivative IC5o 0.9 uM. Studies of the interaction of some of these inhibitors with hemin and TPP were also performed using different spectroscopic techniques mass spectrometry, X-ray crystallography, H NMR and UV/VIS spectroscopy and the binding constant was determined from the UV/VIS data for the unsubstituted compound of the aminobenzoxazole derivative with both hemin Km 1-69 0.31.105 M 1 and TPP Kt2 1.08 0.18.107 M2.
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Kuo, Chien-Wen Sharon. "The genomic structure of the CYP4 gene family." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310930.

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Gillett, Lorna. "Function of cytochrome P450s in the CYP4 family." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408051.

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Heng, Yee M. "Genomic cloning and identification of a novel murine Cyp4a gene." Thesis, University of Nottingham, 1997. http://eprints.nottingham.ac.uk/10399/.

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The mouse cytochrome P450 4a family of genes is poorly characterised. This thesis describes a detailed study of these genes. Using primers derived from exon 1 of the mouse cyp3a10 cDNA sequence, a 1.4kb genomic fragment was cloned which contained the promoter region of the gene. Additionally, a lambda genomic library was screened with probes derived from the partial cDNA clones of the mouse cyp4a10 and cyp4a12. Originally, two classes of phage lambda clones were isolated. One clone, lambda 16, was partially sequenced and was found to contain the 3' end of the cyp4a12 gene. The second clone, lambda 4, was subcloned and found to be distinct from previously known murine cyp4a genes. This novel gene has been designated cyp4a14. To obtain the full cyp4a14 gene, the genomic library was rescreened. Lambda clone 12 was subsequently isolated from the library, which was found to contain exons 1 to 5 of Cyp4a14. In order to study the promoter region of cyp4a14, a pcr-based approach was undertaken to clone 4.4 kb upstream of exon 1 of the gene and a 1.2kb fragment has been sequenced. Cyp4a14 RNA was also found to be highly induced by a peroxisome proliferator, methylclofenapate. Primer extension analyses were performed to determine the start of transcription of Cyp4a14, which was mapped to a single T nucleotide 26bp upstream of the putative start site of protein translation. The promoter region of Cyp4a14 is highly similar to the corresponding regions of the rat CYP4A2 genes. however, similarity is dramatically reduced about 350bp upstream of the start of transcription, which coincides with the presence of two 358bp repeats in teh CYP4A2 gene. The promoter also contains a highly conserved 19bp element which is also found in the promoter regions of the CYP4A1 and CYP4A2 genes. Cyp4a14 is a novel member of the murine Cyp4a subfamily. It contains 12 exons and is highly similar to the rat CYP4A2/3 genes. However, there is high conservation in exon 3 between Cyp4a14 and cyp4a3, which makes it marginally more related to this gene. In addition, cyp4a14 shows very high similarity in exons 4,8, 11 and 12 with other known CYP4A genes. Correspondingly, the peptide sequences encoded by these exons are highly conserved. Exon 8 encodes a 16 amino acid motif, LRAEVDTFMGEGHDTT, which is highly conserved in the CYP4 family. Exons 22 and 12 encode the well known RNCIG motif, containing the haem-binding domain, which is the proposed signature for a P450 protein. Exon 4 in the CYP4A genes encodes for a highly conserved, but previously unreported motif, HRRMLLTPGFHYDIL. Primary sequence alignments indicate that these motifs map very close to or within predicted substrate recognition sites and thus could have an important role in the enzyme activities of the CYP4A enzyme. The identification of Cyp4a14 also enables the analysis of the evolution of the murine Cyp4a subfamily. The mouse has 4 genes in the Cyp4a subfamily; however, the closely related rat has four CYP4A members. As the rat CYP4A2, which is very similar to CYP4AA3, was not to have a homologue in the mouse, it must have arisen after the mouse lineage had diverged from the rat in evolutionary history. As all three mouse Cyp4a genes are significantly more similar to their equivalents in the rat than to other murine Cyp4a genes, the gene duplication events giving rise to these three genes must have occurred before the mouse had diverged from the rat. Phylogenetic analyses of the CYP4A, CYP4B and CYp4F subfamilies demonstrate that CYP4A genes are more similar to the CYP4B family than to the CYP4F subfamily. This suggests that the gene duplication event giving rise to the CYP4A and CYP4B genes must be a more recent event than that giving rise to the CYP4F subfamily. In addition, the CYP4A subfamily of genes is more divergent than the CYP4B subfamily across species.
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Ning, Jia. "Allosteric effects of TPR domain-mediated protein-protein interactions." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31145.

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The tetratricopeptide repeat (TPR) motif contains 34 amino acids forming a helix-turn-helix structure. Different numbers of tandem TPR motifs assemble to form a TPR domain, thereby generating a polypeptide-binding interaction surface. The TPR domain provides a scaffold for mediating protein-protein interactions. Proteins that contain TPR domains exist in a broad range of organisms. These proteins have various functions. Cyclophilin 40 (Cyp40) and C-terminal Hsc70 interaction protein (CHIP) are two typical members of the family of TPR-containing proteins. Both proteins have the ability to bind the molecular chaperones Hsp70 and Hsp90. In most cases, TPR domains act as a scaffold to link chaperone and substrate or multi-protein complexes. Recent evidence suggests that Hsp90 binding to TPR domains can change the overall protein conformation but the allosteric mechanism triggered by ligand binding to the TPR domain remained unknown. This study focuses on using biophysical methods on the two TPR domain containing proteins Cyp40 and CHIP. In particular, this study reveals how the binding of the molecular chaperones Hsp70/90 to the TPR domains of Cyp40 and CHIP influences protein conformation and function. Here we show how conformational changes of the TPR domains affect structure and activity of Cyp40 and CHIP. By using biophysical methods, including thermal denaturation assay (TDA), differential scanning calorimetry (DSC), hydrogen deuterium exchange with mass spectrometry (HDX-MS) and small angle X-ray scattering (SAXS), together with enzymatic assays, we showed that (1) heat shock proteins allosterically affect the enzyme activity of both Cyp40 and CHIP, (2) heat shock proteins bind to the TPR domains of both Cyp40 and CHIP; (3) the binding increases the thermostability of both proteins. Further, by mutating an essential lysine in the TPR1 domain of both proteins (K30 for CHIP, and K227 for Cyp40) to alanine, the thermostability was significantly affected. The SAXS data showed in addition of the SRMEEVD peptide reduced the flexibility of CHIP. HDX-MS experiments suggest that the dynamic alteration due to binding with the Hsp90 peptide or the mutations further reduce the flexibility of the catalytic domains of both proteins. The results imply that the allosteric effects on the enzymatic activity are consequences of dynamic changes of the TPR domains. Hsp70 was also found to bind less tightly to CHIP-K30A than to wild-type CHIP, and thus showed less inhibition of enzymatic activity. These results further confirmed the discovery, that the dynamics of TPR domains allosterically affect enzymatic activity.
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Books on the topic "CYP46"

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Pianezza, Michael Lawrence. The influence of genetically variable CYP246 on tobacco dependence and smoking behaviour. Ottawa: National Library of Canada, 1998.

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Book chapters on the topic "CYP46"

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Rettie, Allan E., and Edward J. Kelly. "Chapter 12. The CYP4 Family." In Issues in Toxicology, 384–414. Cambridge: Royal Society of Chemistry, 2008. http://dx.doi.org/10.1039/9781847558428-00384.

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Sakai, Yasuo, and Ursula C. Dräger. "Detection of Retinoic Acid Catabolism with Reporter Systems and by In Situ Hybridization for CYP26 Enzymes." In Methods in Molecular Biology, 277–94. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-325-1_16.

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Hardwick, James P. "[26] CYP4A subfamily: Functional analysis by immunohistochemistry and in Situ hybridization." In Methods in Enzymology, 273–83. Elsevier, 1991. http://dx.doi.org/10.1016/0076-6879(91)06097-m.

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Stevison, Faith, Jing Jing, Sasmita Tripathy, and Nina Isoherranen. "Role of Retinoic Acid-Metabolizing Cytochrome P450s, CYP26, in Inflammation and Cancer." In Cytochrome P450 Function and Pharmacological Roles in Inflammation and Cancer, 373–412. Elsevier, 2015. http://dx.doi.org/10.1016/bs.apha.2015.04.006.

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Hoffman, Susan M. G., and Diane S. Keeney. "Fine-scale mapping of CYP gene clusters: An example from human CYP4 family." In Methods in Enzymology, 36–44. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)57663-1.

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Le, Thai-Hoang, Jiho Min, Sung-Kyu Lee, and Yang-Hoon Kim. "Gene Expressions of the Dhb, Vtg, Arnt, CYP4, CYP314 in Daphnia magna Induced by Toxicity of Glyphosate and Methidathion Pesticides." In Pesticides in the Modern World - Pests Control and Pesticides Exposure and Toxicity Assessment. InTech, 2011. http://dx.doi.org/10.5772/31797.

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Conference papers on the topic "CYP46"

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Oehlen, Bert, Gaifeng Ma, Siobhan McCormack, Dong Sung Lim, Jim Tarrant, Xiaokang Zhu, Bijoy Panicker, and Itzhak D. Goldberg. "Abstract B257: Identification of new CYP26 inhibitors with efficacy in breast cancer xenograft models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b257.

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Bridgens, Caroline E., Gareth J. Veal, Christopher P. F. Redfern, Mohamed S. Gomaa, Andrea Brancale, Jane L. Armstrong, and Claire Simons. "Abstract A158: Development of CYP26 inhibitors to optimize the treatment of neuroblastoma with retinoic acid." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a158.

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Wu, Cheng-Chia, Yunmeng Liu, Jonathan Chen, Katherine H. Gotlinger, Errabelli Ramu, John R. Falck, and Michal L. Schwartzman. "Abstract LB-160: CYP4F isoform expression and 20-HETE synthesis in prostate cancer cells are regulated by androgen and contribute to growth." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-160.

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