CYP2C19, CPCJ, CYP2C, CYPIIC17, CYPIIC19, P450C2C, P450IIC19, cytochrome P450 family 2 subfamily C member 19
外部ID
HomoloGene: 133565 GeneCards: CYP2C19
EC番号
1.14.13.48
遺伝子の位置 (ヒト)
染色体
10番染色体 (ヒト)[1]
バンド
データ無し
開始点
94,762,681 bp[1]
終点
94,853,205 bp[1]
RNA発現パターン
さらなる参照発現データ
遺伝子オントロジー
分子機能
• iron ion binding • oxygen binding • arachidonic acid epoxygenase activity • metal ion binding • monooxygenase activity • steroid hydroxylase activity • heme binding • oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen • enzyme binding • oxidoreductase activity • oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen
• steroid metabolic process • exogenous drug catabolic process • epoxygenase P450 pathway • omega-hydroxylase P450 pathway • heterocycle metabolic process • drug metabolic process • monoterpenoid metabolic process • xenobiotic metabolic process • oxidation-reduction process • organic acid metabolic process
^“Cloning and expression of complementary DNAs for multiple members of the human cytochrome P450IIC subfamily”. Biochemistry30 (13): 3247–55. (April 1991). doi:10.1021/bi00227a012. PMID 2009263.
^“A 2.4-megabase physical map spanning the CYP2C gene cluster on chromosome 10q24”. Genomics28 (2): 328–32. (July 1995). doi:10.1006/geno.1995.1149. PMID 8530044.
^“CYP2C19 gene”. NIH Genetics Home Reference. 2017年9月6日閲覧。
^“Cytochrome P450 2C19 (CYP2C19) Genotype”. Mayo Medical Laboratories (2013年6月). 2016年4月15日時点のオリジナル[リンク切れ]よりアーカイブ。 Template:Cite webの呼び出しエラー：引数 accessdate は必須です。
^“Geographical/interracial differences in polymorphic drug oxidation. Current state of knowledge of cytochromes P450 (CYP) 2D6 and 2C19”. Clinical Pharmacokinetics29 (3): 192–209. (September 1995). doi:10.2165/00003088-199529030-00005. PMID 8521680.
^ abc“Clinical significance of the cytochrome P450 2C19 genetic polymorphism”. Clinical Pharmacokinetics41 (12): 913–58. (2002). doi:10.2165/00003088-200241120-00002. PMID 12222994.
^“American Association of Clinical Chemistry Annual Meeting 2014: Utility of Genetic Testing in Practical Pain Management”. AutoGenomics (2014年). 2018年2月3日閲覧。
^ abcCenter for Drug Evaluation and Research. “Drug Interactions & Labeling - Drug Development and Drug Interactions: Table of Substrates, Inhibitors and Inducers”. FDA. 2016年6月1日閲覧。
^ abcdefghijklmnopqrstuvwxyzaaabacadaeafagahaiajakalFlockhart, DA (2007年). “Drug Interactions: Cytochrome P450 Drug Interaction Table”. Indiana University School of Medicine. 2011年7月10日閲覧。
^ abcdefghijklmnopqrstSjöqvist, Folke. “Fakta för förskrivare: Interaktion mellan läkemedel” [Facts for prescribers: Interaction between drugs] (Swedish). FASS Vårdpersonal. 2011年7月10日閲覧。
^“Gene variants in CYP2C19 are associated with altered in vivo bupropion pharmacokinetics but not bupropion-assisted smoking cessation outcomes”. Drug Metabolism and Disposition42 (11): 1971–7. (November 2014). doi:10.1124/dmd.114.060285. PMC 4201132. PMID 25187485. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4201132/.
^“Metabolism of (+)- and (-)-limonenes to respective carveols and perillyl alcohols by CYP2C9 and CYP2C19 in human liver microsomes”. Drug Metabolism and Disposition30 (5): 602–7. (May 2002). doi:10.1124/dmd.30.5.602. PMID 11950794.
^“Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects”. British Journal of Clinical Pharmacology64 (1): 67–74. (July 2007). doi:10.1111/j.1365-2125.2007.02846.x. PMC 2000619. PMID 17298483. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2000619/.
^“Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide”. British Journal of Pharmacology153 (7): 1579–86. (April 2008). doi:10.1038/sj.bjp.0707685. PMC 2437900. PMID 18204476. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2437900/.
^“Chloramphenicol is a potent inhibitor of cytochrome P450 isoforms CYP2C19 and CYP3A4 in human liver microsomes”. Antimicrobial Agents and Chemotherapy47 (11): 3464–9. (November 2003). doi:10.1128/AAC.47.11.3464-3469.2003. PMC 253795. PMID 14576103. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC253795/.
^“Fluoxetine- and norfluoxetine-mediated complex drug-drug interactions: in vitro to in vivo correlation of effects on CYP2D6, CYP2C19, and CYP3A4”. Clinical Pharmacology and Therapeutics95 (6): 653–62. (June 2014). doi:10.1038/clpt.2014.50. PMC 4029899. PMID 24569517. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4029899/.
^ abPerucca, Emilio; Levy, René H. (2002). “Combination Therapy and Drug Interactions”. In Levy, René H.; Mattson, Richard H.; Meldrum,, Brian S. et al.. Antiepileptic drugs (5th ed.). Hagerstwon, MD: Lippincott Williams & Wilkins. p. 100. ISBN 0-7817-2321-3. OCLC 848759609. https://books.google.com/books?id=HAOY0qG-vAYC&pg=PA100.
^“Isoniazid is a mechanism-based inhibitor of cytochrome P450 1A2, 2A6, 2C19 and 3A4 isoforms in human liver microsomes”. European Journal of Clinical Pharmacology57 (11): 799–804. (January 2002). doi:10.1007/s00228-001-0396-3. PMID 11868802.
^“Isozyme-specific induction of low-dose aspirin on cytochrome P450 in healthy subjects”. Clinical Pharmacology and Therapeutics73 (3): 264–71. (March 2003). doi:10.1067/mcp.2003.14. PMID 12621391.
参考文献
“Biochemistry and molecular biology of the human CYP2C subfamily”. Pharmacogenetics4 (6): 285–99. (December 1994). doi:10.1097/00008571-199412000-00001. PMID 7704034.
“Molecular genetics of the human cytochrome P450 monooxygenase superfamily”. Xenobiotica28 (12): 1129–65. (December 1998). doi:10.1080/004982598238868. PMID 9890157.
“Human extrahepatic cytochromes P450: function in xenobiotic metabolism and tissue-selective chemical toxicity in the respiratory and gastrointestinal tracts”. Annual Review of Pharmacology and Toxicology43: 149–73. (2003). doi:10.1146/annurev.pharmtox.43.100901.140251. PMID 12171978.
“Genetic polymorphism of human cytochrome P-450 (S)-mephenytoin 4-hydroxylase. Studies with human autoantibodies suggest a functionally altered cytochrome P-450 isozyme as cause of the genetic deficiency”. Biochemistry26 (25): 8466–74. (December 1987). doi:10.1021/bi00399a065. PMID 3442670.
“Identification of a new genetic defect responsible for the polymorphism of (S)-mephenytoin metabolism in Japanese”. Molecular Pharmacology46 (4): 594–8. (October 1994). PMID 7969038.
“Cloning and expression of complementary DNAs for multiple members of the human cytochrome PH50IIC subfamily”. Biochemistry32 (5): 1390. (February 1993). doi:10.1021/bi00056a025. PMID 8095407.
“Evidence that CYP2C19 is the major (S)-mephenytoin 4'-hydroxylase in humans”. Biochemistry33 (7): 1743–52. (February 1994). doi:10.1021/bi00173a017. PMID 8110777.
“The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans”. The Journal of Biological Chemistry269 (22): 15419–22. (June 1994). PMID 8195181.
“Human CYP2C19 is a major omeprazole 5-hydroxylase, as demonstrated with recombinant cytochrome P450 enzymes”. Drug Metabolism and Disposition24 (10): 1081–7. (October 1996). PMID 8894508.
“Differences in the incidence of the CYP2C19 polymorphism affecting the S-mephenytoin phenotype in Chinese Han and Bai populations and identification of a new rare CYP2C19 mutant allele”. The Journal of Pharmacology and Experimental Therapeutics281 (1): 604–9. (April 1997). PMID 9103550.
“Kinetics of ferric cytochrome P450 reduction by NADPH-cytochrome P450 reductase: rapid reduction in the absence of substrate and variations among cytochrome P450 systems”. Biochemistry36 (48): 14741–50. (December 1997). doi:10.1021/bi9719399. PMID 9398194.
“A new genetic defect in human CYP2C19: mutation of the initiation codon is responsible for poor metabolism of S-mephenytoin”. The Journal of Pharmacology and Experimental Therapeutics284 (1): 356–61. (January 1998). PMID 9435198.
“Identification of new human CYP2C19 alleles (CYP2C19*6 and CYP2C19*2B) in a Caucasian poor metabolizer of mephenytoin”. The Journal of Pharmacology and Experimental Therapeutics286 (3): 1490–5. (September 1998). PMID 9732415.
“An additional defective allele, CYP2C19*5, contributes to the S-mephenytoin poor metabolizer phenotype in Caucasians”. Pharmacogenetics8 (2): 129–35. (April 1998). doi:10.1097/00008571-199804000-00006. PMID 10022751.
“Methadone N-demethylation in human liver microsomes: lack of stereoselectivity and involvement of CYP3A4”. British Journal of Clinical Pharmacology47 (4): 403–12. (April 1999). doi:10.1046/j.1365-2125.1999.00921.x. PMC 2014231. PMID 10233205. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014231/.
“A novel transversion in the intron 5 donor splice junction of CYP2C19 and a sequence polymorphism in exon 3 contribute to the poor metabolizer phenotype for the anticonvulsant drug S-mephenytoin”. The Journal of Pharmacology and Experimental Therapeutics290 (2): 635–40. (August 1999). PMID 10411572.
外部リンク
PharmGKB: Annotated PGx Gene Information for CYP2C19
Human CYP2C19 genome location and CYP2C19 gene details page in the UCSC Genome Browser.
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Per the Font of Magic feature, sorcerer can use Flexible Casting to create 5th-level spell slots at level 7, even though they are not typically available until level 9. You can transform unexpended sorcery points into one spell slot as a bonus action on your turn. The Creating Spell Slots table shows the cost of creating a spell slot of [5th level is 7] If such a sorcerer levels up while still having this 5th-level spell slot, can they choose a 5th-level spell as the spell they gain upon levelling up? The Spellcasting feature states: Additionally, when you gain a level in this class, you can choose one of the sorcerer spells you know and replace it with another spell from the sorcerer spell list, which also must be of a level for which you have spell slots.
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After the 2018 errata, the disintegrate spell description now reads: A creature targeted by this spell must make a Dexterity saving throw. On a failed save, the target takes 10d6 + 40 force damage. The target is disintegrated if this damage leaves it with 0 hit points. If you were to polymorph an enemy into a rat and then disintegrate it, would the enemy be disintegrated or would it just return to its original form? I know that for Druids, it’s not an instant kill anymore, but is this the case for polymorph as well?
dnd-5e spells polymorph errata
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Recently, I saw a construction of topological invariant for $pi_3(U(n))$ with $ngeq 2$ : $$ N=frac{1}{24pi^2}int_{S^3} d^3x epsilon^{ijk} Tr[(U^{-1}partial_{x_i}U)(U^{-1}partial_{x_j}U)(U^{-1}partial_{x_k}U)] , $$ where $Uin U(n)$ depends on $boldsymbol{x}=(x_1,x_2,x_3)in S^3$ , $epsilon^{ijk}$ is the Levi-Civita symbol, $i,j,k=1,2,3$ , and the duplicated indexes are summed over. It is claimed that $N$ is an integer, but why? Update 02/02/2019 I think I got an argument for $n=2$ . In this case, $U=e^{i varphi} q$ with $qin SU(2)$ . Due to the trace and the Levi-Civita symbol in $N$ , $varphi$ does not contribute to $N$ . As $Tr[q^{dagger}partial_i q]=0$ and $(q^{dagger}partial_i q)^{dagger}=-q^{dagger}partial_i q$ , $q^{dagger}partial_i q$ in geneeral has the form $q^{dagger}partia
Mixing
