Journal articles: 'CYP46'

1

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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4

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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5

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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8

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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9

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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10

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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11

Macé, Sandrine. "P4-044 Association analysis between Alzheimer's disease and the CYP46 gene polymorphisms." Neurobiology of Aging 25 (July 2004): S485. http://dx.doi.org/10.1016/s0197-4580(04)81602-6.

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12

Chalmers, Katy A., Doris Culpan, Patrick G. Kehoe, Gordon K. Wilcock, Anthony Hughes, and Seth Love. "APOE promoter, ACE1 and CYP46 polymorphisms and β-amyloid in Alzheimer’s disease." NeuroReport 15, no. 1 (January 2004): 95–98. http://dx.doi.org/10.1097/00001756-200401190-00019.

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13

Cartagena, Casandra M., Farid Ahmed, Mark P. Burns, Ahdeah Pajoohesh-Ganji, Daniel T. Pak, Alan I. Faden, and G. William Rebeck. "Cortical Injury Increases Cholesterol 24S Hydroxylase (Cyp46) Levels in the Rat Brain." Journal of Neurotrauma 25, no. 9 (September 2008): 1087–98. http://dx.doi.org/10.1089/neu.2007.0444.

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14

Hänggi, Jürgen, Christian R. A. Mondadori, Andreas Buchmann, Katharina Henke, and Christoph Hock. "A CYP46 T/C SNP modulates parahippocampal and hippocampal morphology in young subjects." Neurobiology of Aging 32, no. 6 (June 2011): 1023–32. http://dx.doi.org/10.1016/j.neurobiolaging.2009.07.001.

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15

Lai, Chiou-Lian, Li-Min Liou, Ching-Kuan Liu, Yuan-Han Yang, and Ruey-Tay Lin. "Effects of metabolic syndrome, apolipoprotein E, and CYP46 on cognition among Taiwanese Chinese." Kaohsiung Journal of Medical Sciences 30, no. 7 (July 2014): 343–49. http://dx.doi.org/10.1016/j.kjms.2014.03.005.

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16

Leon, Victoriano J., Susana Gomez-Castro, and Juan-Luis Garcia. "228-P: Association of CYP46 and DRB1*03 genes in rheumatoid arthritis disease." Human Immunology 70 (November 2009): S127. http://dx.doi.org/10.1016/j.humimm.2009.09.261.

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17

Leon, Victoriano J., Jesus L. Cacho, and Maria D. Sevillano. "227-P: CYP46 gene in multiple sclerosis patients in Castilla y Leon (Spain)." Human Immunology 70 (November 2009): S126. http://dx.doi.org/10.1016/j.humimm.2009.09.260.

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18

Golanska, Ewa, Krystyna Hulas-Bigoszewska, Monika Sieruta, Izabela Zawlik, Monika Witusik, Sylwia M. Gresner, Tomasz Sobow, et al. "Earlier Onset of Alzheimer's Disease: Risk Polymorphisms Within PRNP, PRND, CYP46, and APOE Genes." Journal of Alzheimer's Disease 17, no. 2 (June 5, 2009): 359–68. http://dx.doi.org/10.3233/jad-2009-1055.

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19

Lai, C. L., C. Y. Hsu, H. Y. Hsieh, and C. K. Liu. "P4-8 The effects of cholesterol and CYP46 polymorphism on cognitive event-related potentials." Clinical Neurophysiology 121 (October 2010): S122. http://dx.doi.org/10.1016/s1388-2457(10)60503-2.

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20

Li, Y., L. W. Chu, Y. Q. Chen, B. M. Y. Cheung, R. Y. H. Leung, P. Y. Yik, K. M. Ng, et al. "Intron 2 (T/C) CYP46 Polymorphism Is Associated with Alzheimer’s Disease in Chinese Patients." Dementia and Geriatric Cognitive Disorders 22, no. 5-6 (2006): 399–404. http://dx.doi.org/10.1159/000095723.

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21

Flirski, M., M. Sieruta, T. Sobow, P. P. Liberski, and I. Kloszewska. "APOE, CYP46, PRNP and PRND: Genetic polymorphisms in Alzheimer's disease and mild cognitive impairment." European Psychiatry 23 (April 2008): S197. http://dx.doi.org/10.1016/j.eurpsy.2008.01.308.

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22

Cellini, Elena, Andrea Tedde, Benedetta Nacmias, Silvia Bagnoli, and Sandro Sorbi. "P1-323: A cholesterol 24S-hydroxylase gene (Cyp46) polymorphism in Italian Alzheimer's disease patients." Alzheimer's & Dementia 2 (July 2006): S191—S192. http://dx.doi.org/10.1016/j.jalz.2006.05.701.

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23

Kuo, Ping-Hui, Ching-I. Lin, Yue-Hwa Chen, Wan-Chun Chiu, and Shyh-Hsiang Lin. "A high-cholesterol diet enriched with polyphenols from Oriental plums (Prunus salicina) improves cognitive function and lowers brain cholesterol levels and neurodegenerative-related protein expression in mice." British Journal of Nutrition 113, no. 10 (April 13, 2015): 1550–57. http://dx.doi.org/10.1017/s0007114515000732.

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Ageing accompanied by a decline in cognitive performance may be a result of the long-term effects of oxidative stress on neurologic processes. It has been shown that high-cholesterol contents in the blood and brain may lead to the deposition of the β-amyloid (Aβ) protein in the brain, which damages brain cells. The present study was designed to observe the effect of polyphenol-rich Oriental plums on cognitive function and cerebral neurodegeneration-related protein expression in mice that were fed a high-cholesterol diet for 5 months. The study consisted of four groups: the control (Ctrl) group, which was fed the American Institute of Nutrition (AIN)-93M diet; the high cholesterol (HC) group, which was fed the AIN-93M diet with 5 % cholesterol; the high cholesterol+low Oriental plum (LOP) group, which was fed the AIN-93M diet with 5 % cholesterol and 2 % Oriental plum powder; and the high cholesterol+high Oriental plum (HOP) group, which was fed the AIN-93M diet with 5 % cholesterol and 5 % Oriental plum powder. Measurements of cognitive function were assessed using the Morris water maze, and the mRNA expression of cholesterol hydroxylase (Cyp46), Aβ and β-secretase 1 (BACE1) were analysed. The results showed that cholesterol concentrations in both the blood and the brain were significantly higher in the HC group than in the Ctrl and HOP groups at the end of the trial. The high-cholesterol diet per se produced significant cognitive deficits, which were accompanied by a significantly increased mRNA expression of Cyp46, BACE1, Aβ and 24-hydroxycholesterol in the brain cortex and hippocampus. However, all of these variables were non-significantly increased in the HOP group as compared to the Ctrl group. In conclusion, incorporating polyphenol-enriched Oriental plum into a high-cholesterol diet can ameliorate some of the symptoms of neurodegenerative conditions.

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24

Desai, Purnima, Steven T. DeKosky, and M. Ilyas Kamboh. "Genetic variation in the cholesterol 24-hydroxylase (CYP46) gene and the risk of Alzheimer's disease." Neuroscience Letters 328, no. 1 (August 2002): 9–12. http://dx.doi.org/10.1016/s0304-3940(02)00443-3.

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25

Kabbara, Amro, Nathalie Payet, Dominique Cottel, Bernard Frigard, Philippe Amouyel, and Jean-Charles Lambert. "Exclusion of CYP46 and APOM as candidate genes for Alzheimer's disease in a French population." Neuroscience Letters 363, no. 2 (June 2004): 139–43. http://dx.doi.org/10.1016/j.neulet.2004.03.066.

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26

Ingelsson, Martin, Jennifer Jesneck, Michael C. Irizarry, Bradley T. Hyman, and G. William Rebeck. "Lack of association of the cholesterol 24-hydroxylase (CYP46) intron 2 polymorphism with Alzheimer’s disease." Neuroscience Letters 367, no. 2 (September 2004): 228–31. http://dx.doi.org/10.1016/j.neulet.2004.06.011.

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27

Tedde, Andrea, Mario Rotondi, Elena Cellini, Silvia Bagnoli, Laura Muratore, Benedetta Nacmias, and Sandro Sorbi. "Lack of association between the CYP46 gene polymorphism and Italian late-onset sporadic Alzheimer's disease." Neurobiology of Aging 27, no. 5 (May 2006): 773.e1–773.e3. http://dx.doi.org/10.1016/j.neurobiolaging.2005.03.029.

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Liberski, Pawel P., Ewa Golanska, Piotr Rieske, Maria Barcikowska, Beata Peplonska, Maria Styczynska, Tomasz Sobow, and Tomasz Gabryelewicz. "P4-085 A new polymorphism in the cholesterol 24S-hydroxylase (CYP46) gene in Alzheimer's disease." Neurobiology of Aging 25 (July 2004): S498. http://dx.doi.org/10.1016/s0197-4580(04)81643-9.

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Flirski, M., E. Golanska, T. Sobow, P. Liberski, and I. Kloszewska. "1.208 APOE, CYP46, PRNP and PRND: Genetic polymorphisms in Alzheimer's Disease and mild cognitive impairment." Parkinsonism & Related Disorders 13 (January 2007): S62. http://dx.doi.org/10.1016/s1353-8020(08)70481-4.

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Cacho, Jesus L., Victoriano J. Leon, and Maria D. Savillano. "CYP46 gene and DR3 in Alzheimer and other neurological diseases in Castilla y Leon (Spain)." Human Immunology 66, no. 8 (August 2005): 44. http://dx.doi.org/10.1016/j.humimm.2005.08.083.

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31

Juhász, Anna, Ágnes Rimanóczy, Krisztina Boda, Gábor Vincze, Győző Szlávik, Marianna Zana, Annamária Bjelik, et al. "CYP46 T/C Polymorphism is not Associated with Alzheimer’s Dementia in a Population from Hungary." Neurochemical Research 30, no. 8 (August 2005): 943–48. http://dx.doi.org/10.1007/s11064-005-5979-4.

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32

Helisalmi, S. "Association of CYP46 intron 2 polymorphism in Finnish Alzheimer's disease samples and a global scale summary." Journal of Neurology, Neurosurgery & Psychiatry 77, no. 3 (July 26, 2005): 421–22. http://dx.doi.org/10.1136/jnnp.2005.071928.

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33

Smiljanic, Kosara, Irena Lavrnja, Aleksandra Mladenovic Djordjevic, Sabera Ruzdijic, Mirjana Stojiljkovic, Sanja Pekovic, and Selma Kanazir. "Brain injury induces cholesterol 24-hydroxylase (Cyp46) expression in glial cells in a time-dependent manner." Histochemistry and Cell Biology 134, no. 2 (June 18, 2010): 159–69. http://dx.doi.org/10.1007/s00418-010-0718-6.

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34

Borroni, Barbara, Silvana Archetti, Chiara Agosti, Nabil Akkawi, Cristina Brambilla, Luigi Caimi, Carlo Caltagirone, Monica Di Luca, and Alessandro Padovani. "Intronic CYP46 polymorphism along with ApoE genotype in sporadic Alzheimer Disease: from risk factors to disease modulators." Neurobiology of Aging 25, no. 6 (July 2004): 747–51. http://dx.doi.org/10.1016/j.neurobiolaging.2003.08.004.

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35

Vega, Gloria Lena, and Myron F. Weiner. "Plasma 24S Hydroxycholesterol Response to Statins in Alzheimer’s Disease Patients: Effects of Gender, CYP46, and ApoE Polymorphisms." Journal of Molecular Neuroscience 33, no. 1 (June 22, 2007): 51–55. http://dx.doi.org/10.1007/s12031-007-0040-5.

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36

Wang, Fen, and Jianping Jia. "Polymorphisms of cholesterol metabolism genes CYP46 and ABCA1 and the risk of sporadic Alzheimer's disease in Chinese." Brain Research 1147 (May 2007): 34–38. http://dx.doi.org/10.1016/j.brainres.2007.02.005.

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37

Papassotiropoulos, Andreas, Johannes R. Streffer, Magdalini Tsolaki, Simon Schmid, Dietmar Thal, Francesca Nicosia, Vassiliki Iakovidou, et al. "Increased Brain β-Amyloid Load, Phosphorylated Tau, and Risk of Alzheimer Disease Associated With an Intronic CYP46 Polymorphism." Archives of Neurology 60, no. 1 (January 1, 2003): 29. http://dx.doi.org/10.1001/archneur.60.1.29.

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38

Milagre, Ines, Elsa Rodrigues, Maria J. Gama, and Maria C. Lechner. "P1-358: Identification of a CCAAT/Enhancer Binding Protein (C/EBP) responsive region in the human CYP46 promoter." Alzheimer's & Dementia 2 (July 2006): S202—S203. http://dx.doi.org/10.1016/j.jalz.2006.05.736.

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39

Bou-Fakhredin, Rayan, Batoul Dia, Hilda E. Ghadieh, Stefano Rivella, Maria Domenica Cappellini, Assaad A. Eid, and Ali T. Taher. "CYP450 Mediates Reactive Oxygen Species Production in a Mouse Model of β-Thalassemia through an Increase in 20-HETE Activity." International Journal of Molecular Sciences 22, no. 3 (January 23, 2021): 1106. http://dx.doi.org/10.3390/ijms22031106.

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Oxidative damage by reactive oxygen species (ROS) is one of the main contributors to cell injury and tissue damage in thalassemia patients. Recent studies suggest that ROS generation in non-transfusion-dependent (NTDT) patients occurs as a result of iron overload. Among the different sources of ROS, the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes and cytochrome P450 (CYP450) have been proposed to be major contributors for oxidative stress in several diseases. However, the sources of ROS in patients with NTDT remain poorly understood. In this study, Hbbth3/+ mice, a mouse model for β-thalassemia, were used. These mice exhibit an unchanged or decreased expression of the major NOX isoforms, NOX1, NOX2 and NOX4, when compared to their C57BL/6 control littermates. However, a significant increase in the protein synthesis of CYP4A and CYP4F was observed in the Hbbth3/+ mice when compared to the C57BL/6 control mice. These changes were paralleled by an increased production of 20-hydroxyeicosatetraenoic acid (20-HETE), a CYP4A and CYP4F metabolite. Furthermore, these changes corroborate with onset of ROS production concomitant with liver injury. To our knowledge, this is the first report indicating that CYP450 4A and 4F-induced 20-HETE production mediates reactive oxygen species overgeneration in Hbbth3/+ mice through an NADPH-dependent pathway.

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Vega, Gloria, Myron Weine, Heike Kolsch, Klaus Bergmann, Reinhard Heun, Dieter Lutjohan, Anh Nguyen, and Carol Moore. "The Effects of Gender and CYP46 and Apo E Polymorphism on 24S-Hydroxycholesterol Levels in Alzheimers Patients Treated with Statins." Current Alzheimer Research 1, no. 1 (February 1, 2004): 71–77. http://dx.doi.org/10.2174/1567205043480546.

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Plenty, Nicole L., Jessica L. Faulkner, Joshua Cotton, Shauna-Kay Spencer, Kedra Wallace, Babbette LaMarca, and Sydney R. Murphy. "Arachidonic acid metabolites of CYP4A and CYP4F are altered in women with preeclampsia." Prostaglandins & Other Lipid Mediators 136 (May 2018): 15–22. http://dx.doi.org/10.1016/j.prostaglandins.2018.03.001.

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Stec, David E., Averia Flasch, Richard J. Roman, and Jared A. White. "Distribution of cytochrome P-450 4A and 4F isoforms along the nephron in mice." American Journal of Physiology-Renal Physiology 284, no. 1 (January 1, 2003): F95—F102. http://dx.doi.org/10.1152/ajprenal.00132.2002.

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The production of 20-hydroxyeicosatetraenoic acid (20-HETE) in the kidney is thought to be involved in the control of renal vascular tone and tubular sodium and chloride reabsorption. 20-HETE production in the kidney has been extensively studied in rats and humans and occurs primarily via the actions of P-450 enzymes of the CYP4A and -4F families. Recent advancements in molecular genetics of the mouse have made it possible to disrupt genes in a cell-type-specific fashion. These advances could help in the creation of models that could distinguish between the vascular and tubular actions of 20-HETE. However, isoforms of the CYP4A and -4F families that may be responsible for the production of 20-HETE in the vascular and tubular segments in the kidney of the mouse are presently unknown. The goal of this study was to identify the isoforms of the CYP4A and -4F families along the nephron by RT-PCR of RNA isolated from microdissected renal blood vessels and nephron segments from 16- to 24-wk-old male and female C57BL/6J mice. CYP4A and -4F isoforms were detected in every segment analyzed, with sex differences only observed in the proximal tubule and glomeruli. In the proximal tubular segments from male mice, the 4A10 and -12 isoforms were present, whereas the 4A10 and -14 isoforms were detected in segments from female mice. In glomeruli, sex differences in the expression pattern of CYP4F isoforms were also observed, with male mice expressing the 4F13, -14, and -15 isoforms, whereas female mice expressed the 4F13, -16, and -18 isoforms. These results demonstrate that isolated nephron and renal vessel segments express multiple isoforms of the CYP4A and -4F families; therefore, elimination of a single CYP4A or -4F isoform may not decrease 20-HETE production in all nephron segments or the renal vasculature of male and female mice. However, the importance of CYP4A vs. -4F isoforms to the production of 20-HETE in each of these renal tubular and vascular segments of the mouse remains to be determined.

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Bogdanovic, Nenad, Lionel Bretillon, Erik G. Lund, Ulf Diczfalusy, Lars Lannfelt, Bengt Winblad, David W. Russell, and Ingemar Björkhem. "On the turnover of brain cholesterol in patients with Alzheimer's disease. Abnormal induction of the cholesterol-catabolic enzyme CYP46 in glial cells." Neuroscience Letters 314, no. 1-2 (November 2001): 45–48. http://dx.doi.org/10.1016/s0304-3940(01)02277-7.

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44

Hardwick, James P., and Liping Chen. "Something completely different?" Human & Experimental Toxicology 15, no. 6 (June 1996): 543–44. http://dx.doi.org/10.1177/096032719601500616.

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Three cDNAs clones, designated 4f-8, 4f-34 and 4f- 41, coding for three new forms of cytochrome P450 belonging to the CYP4F subfamily were isolated from an untreated rat brain cDNA library. CDNA 4f- 8, 4f-34 and 4f-41 coded for proteins of 522, 526 and 537 amino acids, respectively, and their amino acid sequence similarity to CYP4F ranged from 71 to 80%. These new P450s were thus named CYP4F4, 4F5 and 4F6, respectively. Northern blot analysis revealed that the expression levels of these forms of P450 in the brain were somewhat low and that similar forms of subfamily 4F P450 were expressed in liver and kidney at a relatively high level compared with brain. No CYP4A expression was detected by Northern blot analysis in untreated rat brain mRNA. All three clones were in vitro- translatable using a reticulocyte lysate system. These results show that multiple forms of subfamily 4F P450 exist in the brain and that the subfamily 4F P450 may be one of the major forms of P450 in the brain.

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45

Uehara, Shotaro, Norie Murayama, Yasuharu Nakanishi, Chika Nakamura, Takanori Hashizume, Darryl C. Zeldin, Hiroshi Yamazaki, and Yasuhiro Uno. "Immunochemical quantification of cynomolgus CYP2J2, CYP4A and CYP4F enzymes in liver and small intestine." Xenobiotica 45, no. 2 (August 20, 2014): 124–30. http://dx.doi.org/10.3109/00498254.2014.952800.

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46

Sodero, Alejandro O., Laura Trovò, Francesca Iannilli, Paul Van Veldhoven, Carlos G. Dotti, and Mauricio G. Martin. "Regulation of tyrosine kinase B activity by the Cyp46/cholesterol loss pathway in mature hippocampal neurons: relevance for neuronal survival under stress and in aging." Journal of Neurochemistry 116, no. 5 (January 7, 2011): 747–55. http://dx.doi.org/10.1111/j.1471-4159.2010.07079.x.

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Vaivoda, Rachel, Christine Vaine, Cassandra Boerstler, Kristy Galloway, and Peter Christmas. "CYP4F18-Deficient Neutrophils Exhibit Increased Chemotaxis to Complement Component C5a." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/250456.

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CYP4Fs were first identified as enzymes that catalyze hydroxylation of leukotriene B4(LTB4). CYP4F18 has an unusual expression in neutrophils and was predicted to play a role in regulating LTB4-dependent inflammation. We compared chemotaxis of wild-type andCyp4f18knockout neutrophils using anin vitroassay. There was no significant difference in the chemotactic response to LTB4, but the response to complement component C5a increased 1.9–2.25-fold in knockout cells compared to wild-type (P< 0.01). This increase was still observed when neutrophils were treated with inhibitors of eicosanoid synthesis. There were no changes in expression of other CYP4 enzymes in knockout neutrophils that might compensate for loss of CYP4F18 or lead to differences in activity. A mouse model of dextran sodium sulfate colitis was used to investigate the consequences of increased C5a-dependent chemotaxisin vivo, but there was no significant difference in weight loss, disease activity, or colonic tissue myeloperoxidase between wild-type andCyp4f18knockout mice. This study demonstrates the limitations of inferring CYP4F function based on an ability to use LTB4as a substrate, points to expanding roles for CYP4F enzymes in immune regulation, and underscores thein vivochallenges of CYP knockout studies.

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Li, Bing, Hua Zhang, Min Ni, Bin-bin Wang, Fan-chi Li, Kai-zhun Xu, Wei-de Shen, Qing-you Xia, and Ping Zhao. "Identification and characterization of six cytochrome P450 genes belonging to CYP4 and CYP6 gene families in the silkworm, Bombyx mori." Molecular Biology Reports 41, no. 8 (May 4, 2014): 5135–46. http://dx.doi.org/10.1007/s11033-014-3379-z.

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Kudoh, Tetsuhiro, Stephen W. Wilson, and Igor B. Dawid. "Distinct roles for Fgf, Wnt and retinoic acid in posteriorizing the neural ectoderm." Development 129, no. 18 (September 15, 2002): 4335–46. http://dx.doi.org/10.1242/dev.129.18.4335.

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Early neural patterning in vertebrates involves signals that inhibit anterior (A) and promote posterior (P) positional values within the nascent neural plate. In this study, we have investigated the contributions of, and interactions between, retinoic acid (RA), Fgf and Wnt signals in the promotion of posterior fates in the ectoderm. We analyze expression and function of cyp26/P450RAI, a gene that encodes retinoic acid 4-hydroxylase, as a tool for investigating these events. Cyp26 is first expressed in the presumptive anterior neural ectoderm and the blastoderm margin at the late blastula. When the posterior neural gene hoxb1b is expressed during gastrulation, it shows a strikingly complementary pattern to cyp26. Using these two genes, as well as otx2 and meis3 as anterior and posterior markers, we show that Fgf and Wnt signals suppress expression of anterior genes, including cyp26. Overexpression of cyp26 suppresses posterior genes, suggesting that the anterior expression of cyp26 is important for restricting the expression of posterior genes. Consistent with this, knock-down of cyp26 by morpholino oligonucleotides leads to the anterior expansion of posterior genes. We further show that Fgf- and Wnt-dependent activation of posterior genes is mediated by RA, whereas suppression of anterior genes does not depend on RA signaling. Fgf and Wnt signals suppress cyp26 expression, while Cyp26 suppresses the RA signal. Thus, cyp26 has an important role in linking the Fgf, Wnt and RA signals to regulate AP patterning of the neural ectoderm in the late blastula to gastrula embryo in zebrafish.

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Melo, N. R., G. P. Moran, A. G. S. Warrilow, E. Dudley, S. N. Smith, D. J. Sullivan, D. C. Lamb, D. E. Kelly, D. C. Coleman, and S. L. Kelly. "CYP56 (Dit2p) in Candida albicans: Characterization and Investigation of Its Role in Growth and Antifungal Drug Susceptibility." Antimicrobial Agents and Chemotherapy 52, no. 10 (July 28, 2008): 3718–24. http://dx.doi.org/10.1128/aac.00446-08.

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ABSTRACT The complete DNA sequence of Candida albicans DIT2, encoding cytochrome P450 family 56 (CYP56), was obtained, and heterologous expression was achieved in Escherichia coli, where CYP56 was targeted to the membrane fraction. In reconstituted assays with the purified enzyme, CYP56 was shown to catalyze the conversion of N-formyl tyrosine into N,N′-bisformyl dityrosine, a reaction that was dependent on cytochrome P450 reductase, NADPH, and oxygen, yielding a turnover of 21.6 min−1 and a ks of 26 μM. The Hill number was calculated as 1.6, indicating that two molecules of the substrate could bind to the protein. Azole antifungals could bind to the heme of CYP56 as a sixth ligand with high affinity. Both chromosomal alleles of CYP56 were disrupted using the SAT1 flipper technique, and CYP56 was found to be nonessential for cell viability under the culture conditions investigated. Susceptibility to azole drugs that bind to cytochromes P450 was tested, and the mutant showed unaltered susceptibility. However, the mutant showed increased susceptibility to the echinocandin drug caspofungin, suggesting an alteration in 1,3-glucan synthase and/or cell wall structure mediated by the presence of dityrosine. Phenotypically, the wild-type and mutant strains were morphologically similar when cultured in rich yeast extract-peptone-dextrose medium. However in minimal medium, the cyp56Δ mutant strain exhibited hyphal growth, in contrast to the wild-type strain, which grew solely in the yeast form. Furthermore, CYP56 was essential for chlamydospore formation.

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Journal articles on the topic 'CYP46'

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