^“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. PMID2009263.
^“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. PMID8530044.
^“CYP2C19 gene”. NIH Genetics Home Reference. 6 September 2017閲覧。
^“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. PMID8521680.
^“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. PMID11950794.
^“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. PMID11868802.
^“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. PMID12621391.
“Molecular genetics of the human cytochrome P450 monooxygenase superfamily”. Xenobiotica28 (12): 1129–65. (December 1998). doi:10.1080/004982598238868. PMID9890157.
“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. PMID12171978.
“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. PMID3442670.
“Identification of a new genetic defect responsible for the polymorphism of (S)-mephenytoin metabolism in Japanese”. Molecular Pharmacology46 (4): 594–8. (October 1994). PMID7969038.
“Cloning and expression of complementary DNAs for multiple members of the human cytochrome PH50IIC subfamily”. Biochemistry32 (5): 1390. (February 1993). doi:10.1021/bi00056a025. PMID8095407.
“Evidence that CYP2C19 is the major (S)-mephenytoin 4'-hydroxylase in humans”. Biochemistry33 (7): 1743–52. (February 1994). doi:10.1021/bi00173a017. PMID8110777.
“The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans”. The Journal of Biological Chemistry269 (22): 15419–22. (June 1994). PMID8195181.
“Human CYP2C19 is a major omeprazole 5-hydroxylase, as demonstrated with recombinant cytochrome P450 enzymes”. Drug Metabolism and Disposition24 (10): 1081–7. (October 1996). PMID8894508.
“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). PMID9103550.
“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. PMID9398194.
“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). PMID9435198.
“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). PMID9732415.
“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. PMID10022751.
“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). PMID10411572.