J. Fisher

发表

Induction of hepatic cytochrome P450 gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

J. Whitlock, M. Denison, E. Shen, 1989, Molecular biology & medicine.

OF ENHANCED ORAL AVAILABILITY OF CYP 3 A 4 SUBSTRATES BY GRAPEFRUIT CONSTITUENTS Decreased enterocyte CYP 3 A 4 concentration and mechanism-based inactivation by furanocoumarins

P. Watkins, P. Woster, K. Thummel, 1997 .

Control of cytochrome P1-450 gene expression by dioxin.

J. Whitlock, P. B. Jones, J. Fisher, 1985, Science.

Regulation of cytochrome P1-450 gene expression in mouse hepatoma cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

J. Whitlock, M. Denison, P. B. Jones, 1989, Drug metabolism reviews.

Activation of transcription as a general mechanism of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin action

J. Whitlock, K. Jones, J. Fisher, 1989, Molecular carcinogenesis.

Control of gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Multiple dioxin-responsive domains 5'-ward of the cytochrome P1-450 gene.

J. Whitlock, J. M. Fisher, P. B. Jones, 1986, The Journal of biological chemistry.

Mechanisms of enhanced oral availability of CYP3A4 substrates by grapefruit constituents. Decreased enterocyte CYP3A4 concentration and mechanism-based inactivation by furanocoumarins.

P. Watkins, P. Woster, K. He, 1997, Drug metabolism and disposition: the biological fate of chemicals.

Expression of enzymatically active CYP3A4 by Caco-2 cells grown on extracellular matrix-coated permeable supports in the presence of 1alpha,25-dihydroxyvitamin D3.

P. Watkins, K. Thummel, P. Schmiedlin-Ren, 1997, Molecular pharmacology.

Organization and function of a dioxin-responsive enhancer.

L. Wu, J. Whitlock, M. Denison, 1990, The Journal of biological chemistry.

Protein-DNA interactions at recognition sites for the dioxin-Ah receptor complex.

J. Whitlock, M. Denison, J. M. Fisher, 1989, The Journal of biological chemistry.

Characterization of interintestinal and intraintestinal variations in human CYP3A-dependent metabolism.

D. Shen, C. Marsh, J. Perkins, 1997, The Journal of pharmacology and experimental therapeutics.

Cytochrome P450 2E1 is the principal catalyst of human oxidative halothane metabolism in vitro.

E. Kharasch, K. Thummel, D. Hankins, 1997, The Journal of pharmacology and experimental therapeutics.

Inducible, receptor-dependent protein-DNA interactions at a dioxin-responsive transcriptional enhancer.

J. Whitlock, M. Denison, J. Fisher, 1988, Proceedings of the National Academy of Sciences of the United States of America.

Induction of CYP3A4 by 1 alpha,25-dihydroxyvitamin D3 is human cell line-specific and is unlikely to involve pregnane X receptor.

P. Watkins, K. Thummel, P. Schmiedlin-Ren, 2001, Drug metabolism and disposition: the biological fate of chemicals.

CYP2E1 activity before and after weight loss in morbidly obese subjects with nonalcoholic fatty liver disease

E. P. Dellinger, K. Kowdley, E. Kharasch, 2003, Hepatology.

The DNA recognition site for the dioxin-Ah receptor complex. Nucleotide sequence and functional analysis.

J. Whitlock, M. Denison, J. Fisher, 1988, The Journal of biological chemistry.

Midazolam metabolism by modified Caco-2 monolayers: effects of extracellular protein binding.

S. Wrighton, D. Shen, K. Thummel, 1999, The Journal of pharmacology and experimental therapeutics.

Cytochrome P 450 2 E 1 is the Principal Catalyst of Human Oxidative Halothane Metabolism in Vitro 1

E. Kharasch, K. Thummel, D. Hankins, 1997 .

First-pass midazolam metabolism catalyzed by 1alpha,25-dihydroxy vitamin D3-modified Caco-2 cell monolayers.

P. Watkins, S. Wrighton, D. Shen, 1999, The Journal of pharmacology and experimental therapeutics.

Effects of Steady-State Lasofoxifene on Cyp2D6- and Cyp2E1-Mediated Metabolism

R. Obach, R. Walsky, M. Gardner, 2006, The Annals of pharmacotherapy.