PUBLICACIÓN

Aryl-hydrocarbon receptor is an inhibitory regulator of lipid synthesis and of commitment to adipogenesis

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ACCEDER A LA PUBLICACIÓN: Scopus

Alexander D.L.

1998 Journal of Cell Science

CITAS

175

DOI

10.1242/jcs.111.22.3311

EID

2-s2.0-0031745543

ISSN

0021-9533

AUTORES DE LA UEX

Pedro María Fernández Salguero

OTRAS PUBLICACIONES DE INTERÉS

Modulation Of (Ca2+ + Mg2+)-Atpases And Ca2+ Fluxes Through The Plasma Membrane Of Synaptosomes And Sarcoplasmic Reticulum By Local Anaesthetics
Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment
Introducción: Carta Del Rector De La Uex
Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment
Introducción: Carta Del Rector De La Uex
The Ah Receptor From Toxicity To Therapeutics: Report From The 5th Ahr Meeting At Penn State University, Usa, June 2022
Introducción: Carta Del Rector De La Uex
The Ah Receptor From Toxicity To Therapeutics: Report From The 5th Ahr Meeting At Penn State University, Usa, June 2022
From Nucleus To Organs: Insights Of Aryl Hydrocarbon Receptor Molecular Mechanisms
The Ah Receptor From Toxicity To Therapeutics: Report From The 5th Ahr Meeting At Penn State University, Usa, June 2022
From Nucleus To Organs: Insights Of Aryl Hydrocarbon Receptor Molecular Mechanisms
Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
From Nucleus To Organs: Insights Of Aryl Hydrocarbon Receptor Molecular Mechanisms
Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Lack Of The Aryl Hydrocarbon Receptor Accelerates Aging In Mice
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Lack Of The Aryl Hydrocarbon Receptor Accelerates Aging In Mice
Vav Proteins Maintain Epithelial Traits In Breast Cancer Cells Using Mir-200c-Dependent And Independent Mechanisms
Lack Of The Aryl Hydrocarbon Receptor Accelerates Aging In Mice
Vav Proteins Maintain Epithelial Traits In Breast Cancer Cells Using Mir-200c-Dependent And Independent Mechanisms
Aryl Hydrocarbon Receptor Promotes Liver Polyploidization And Inhibits Pi3k, Erk, And Wnt/β-Catenin Signaling
Vav Proteins Maintain Epithelial Traits In Breast Cancer Cells Using Mir-200c-Dependent And Independent Mechanisms
Aryl Hydrocarbon Receptor Promotes Liver Polyploidization And Inhibits Pi3k, Erk, And Wnt/β-Catenin Signaling
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
Aryl Hydrocarbon Receptor Promotes Liver Polyploidization And Inhibits Pi3k, Erk, And Wnt/β-Catenin Signaling
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
Identification Of New Activators Of Mitochondrial Fusion Reveals A Link Between Mitochondrial Morphology And Pyrimidine Metabolism
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
Identification Of New Activators Of Mitochondrial Fusion Reveals A Link Between Mitochondrial Morphology And Pyrimidine Metabolism
Histone H4 Acetylation Regulates Behavioral Inter-Individual Variability In Zebrafish
Identification Of New Activators Of Mitochondrial Fusion Reveals A Link Between Mitochondrial Morphology And Pyrimidine Metabolism
Histone H4 Acetylation Regulates Behavioral Inter-Individual Variability In Zebrafish
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
Histone H4 Acetylation Regulates Behavioral Inter-Individual Variability In Zebrafish
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
A Dioxin-Like Compound Induces Hyperplasia And Branching Morphogenesis In Mouse Mammary Gland, Through Alterations In Tgf-Β1 And Aryl Hydrocarbon Receptor Signaling
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
A Dioxin-Like Compound Induces Hyperplasia And Branching Morphogenesis In Mouse Mammary Gland, Through Alterations In Tgf-Β1 And Aryl Hydrocarbon Receptor Signaling
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
A Dioxin-Like Compound Induces Hyperplasia And Branching Morphogenesis In Mouse Mammary Gland, Through Alterations In Tgf-Β1 And Aryl Hydrocarbon Receptor Signaling
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis
New Trends In Aryl Hydrocarbon Receptor Biology
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis
New Trends In Aryl Hydrocarbon Receptor Biology
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements
New Trends In Aryl Hydrocarbon Receptor Biology
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis.
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis.
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor.
Cd69 Controls The Uptake Of L-Tryptophan Through Lat1-Cd98 And Ahr-Dependent Secretion Of Il-22 In Psoriasis.
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor.
New Trends In Aryl Hydrocarbon Receptor Biology.
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor.
New Trends In Aryl Hydrocarbon Receptor Biology.
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements.
New Trends In Aryl Hydrocarbon Receptor Biology.
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements.
Skin Response To A Carcinogen Involves The Xenobiotic Receptor Pregnane X Receptor
Rna-Seq Analysis To Measure The Expression Of Sine Retroelements.
Skin Response To A Carcinogen Involves The Xenobiotic Receptor Pregnane X Receptor
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
Skin Response To A Carcinogen Involves The Xenobiotic Receptor Pregnane X Receptor
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
A Mesenchymal-Like Phenotype And Expression Of Cd44 Predict Lack Of Apoptotic Response To Sorafenib In Liver Tumor Cells
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
A Mesenchymal-Like Phenotype And Expression Of Cd44 Predict Lack Of Apoptotic Response To Sorafenib In Liver Tumor Cells
Bmi1 Regulates Murine Intestinal Stem Cell Proliferation And Self-Renewal Downstream Of Notch
A Mesenchymal-Like Phenotype And Expression Of Cd44 Predict Lack Of Apoptotic Response To Sorafenib In Liver Tumor Cells
Bmi1 Regulates Murine Intestinal Stem Cell Proliferation And Self-Renewal Downstream Of Notch
L-Kynurenine/aryl Hydrocarbon Receptor Pathway Mediates Brain Damage After Experimental Stroke
Bmi1 Regulates Murine Intestinal Stem Cell Proliferation And Self-Renewal Downstream Of Notch
L-Kynurenine/aryl Hydrocarbon Receptor Pathway Mediates Brain Damage After Experimental Stroke
The Dioxin Receptor Modulates Caveolin-1 Mobilization During Directional Migration: Role Of Cholesterol
L-Kynurenine/aryl Hydrocarbon Receptor Pathway Mediates Brain Damage After Experimental Stroke
The Dioxin Receptor Modulates Caveolin-1 Mobilization During Directional Migration: Role Of Cholesterol
Aryl Hydrocarbon Receptor-Dependent Induction Of Liver Fibrosis By Dioxin
The Dioxin Receptor Modulates Caveolin-1 Mobilization During Directional Migration: Role Of Cholesterol
Aryl Hydrocarbon Receptor-Dependent Induction Of Liver Fibrosis By Dioxin
The Dioxin Receptor Has Tumor Suppressor Activity In Melanoma Growth And Metastasis
Aryl Hydrocarbon Receptor-Dependent Induction Of Liver Fibrosis By Dioxin
The Dioxin Receptor Has Tumor Suppressor Activity In Melanoma Growth And Metastasis
Aryl Hydrocarbon Receptor Contributes To The Mek/erk-Dependent Maintenance Of The Immature State Of Human Dendritic Cells
The Dioxin Receptor Has Tumor Suppressor Activity In Melanoma Growth And Metastasis
Aryl Hydrocarbon Receptor Contributes To The Mek/erk-Dependent Maintenance Of The Immature State Of Human Dendritic Cells
The Dioxin Receptor Controls Β1 Integrin Activation In Fibroblasts Through A Cbp-Csk-Src Pathway
Aryl Hydrocarbon Receptor Contributes To The Mek/erk-Dependent Maintenance Of The Immature State Of Human Dendritic Cells
The Dioxin Receptor Controls Β1 Integrin Activation In Fibroblasts Through A Cbp-Csk-Src Pathway
Dioxin Receptor Expression Inhibits Basal And Transforming Growth Factor Β-Induced Epithelial-To-Mesenchymal Transition
The Dioxin Receptor Controls Β1 Integrin Activation In Fibroblasts Through A Cbp-Csk-Src Pathway
Dioxin Receptor Expression Inhibits Basal And Transforming Growth Factor Β-Induced Epithelial-To-Mesenchymal Transition
Oculomotor Deficits In Aryl Hydrocarbon Receptor Null Mouse
Dioxin Receptor Expression Inhibits Basal And Transforming Growth Factor Β-Induced Epithelial-To-Mesenchymal Transition
Oculomotor Deficits In Aryl Hydrocarbon Receptor Null Mouse
Aryl Hydrocarbon Receptor-Induced Adrenomedullin Mediates Cigarette Smoke Carcinogenicity In Humans And Mice
Oculomotor Deficits In Aryl Hydrocarbon Receptor Null Mouse
Aryl Hydrocarbon Receptor-Induced Adrenomedullin Mediates Cigarette Smoke Carcinogenicity In Humans And Mice
Dioxin Receptor And Slug Transcription Factors Regulate The Insulator Activity Of B1 Sine Retrotransposons Via An Rna Polymerase Switch
Aryl Hydrocarbon Receptor-Induced Adrenomedullin Mediates Cigarette Smoke Carcinogenicity In Humans And Mice
Dioxin Receptor And Slug Transcription Factors Regulate The Insulator Activity Of B1 Sine Retrotransposons Via An Rna Polymerase Switch
The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
Dioxin Receptor And Slug Transcription Factors Regulate The Insulator Activity Of B1 Sine Retrotransposons Via An Rna Polymerase Switch
The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
Aryl Hydrocarbon Receptor-Dependent Induction Of Apoptosis By 2,3,7,8-Tetrachlorodibenzo-P-Dioxin In Cerebellar Granule Cells From Mouse
The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
Aryl Hydrocarbon Receptor-Dependent Induction Of Apoptosis By 2,3,7,8-Tetrachlorodibenzo-P-Dioxin In Cerebellar Granule Cells From Mouse
Transcriptional Factor Aryl Hydrocarbon Receptor (Ahr) Controls Cardiovascular And Respiratory Functions By Regulating The Expression Of The Vav3 Proto-Oncogene
Aryl Hydrocarbon Receptor-Dependent Induction Of Apoptosis By 2,3,7,8-Tetrachlorodibenzo-P-Dioxin In Cerebellar Granule Cells From Mouse
Transcriptional Factor Aryl Hydrocarbon Receptor (Ahr) Controls Cardiovascular And Respiratory Functions By Regulating The Expression Of The Vav3 Proto-Oncogene
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis In Neural Growth Factor (Ngf)-Differentiated Pheochromocytoma Pc12 Cells
Transcriptional Factor Aryl Hydrocarbon Receptor (Ahr) Controls Cardiovascular And Respiratory Functions By Regulating The Expression Of The Vav3 Proto-Oncogene
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis In Neural Growth Factor (Ngf)-Differentiated Pheochromocytoma Pc12 Cells
A Remarkable New Target Gene For The Dioxin Receptor: The Vav3 Proto-Oncogene Links Ahr To Adhesion And Migration
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis In Neural Growth Factor (Ngf)-Differentiated Pheochromocytoma Pc12 Cells
A Remarkable New Target Gene For The Dioxin Receptor: The Vav3 Proto-Oncogene Links Ahr To Adhesion And Migration
Role Of Transforming Growth Factor Β In Cancer Microenvironment
A Remarkable New Target Gene For The Dioxin Receptor: The Vav3 Proto-Oncogene Links Ahr To Adhesion And Migration
Role Of Transforming Growth Factor Β In Cancer Microenvironment
Dioxin Receptor Deficiency Impairs Angiogenesis By A Mechanism Involving Vegf-A Depletion In The Endothelium And Transforming Growth Factor-Β Overexpression In The Stroma
Role Of Transforming Growth Factor Β In Cancer Microenvironment
Dioxin Receptor Deficiency Impairs Angiogenesis By A Mechanism Involving Vegf-A Depletion In The Endothelium And Transforming Growth Factor-Β Overexpression In The Stroma
Regulation Of Cell Survival By Resveratrol Involves Inhibition Of Nfκb-Regulated Gene Expression In Prostate Cancer Cells
Dioxin Receptor Deficiency Impairs Angiogenesis By A Mechanism Involving Vegf-A Depletion In The Endothelium And Transforming Growth Factor-Β Overexpression In The Stroma
Regulation Of Cell Survival By Resveratrol Involves Inhibition Of Nfκb-Regulated Gene Expression In Prostate Cancer Cells
The Dioxin Receptor Regulates The Constitutive Expression Of The Vav3 Proto-Oncogene And Modulates Cell Shape And Adhesion
Regulation Of Cell Survival By Resveratrol Involves Inhibition Of Nfκb-Regulated Gene Expression In Prostate Cancer Cells
The Dioxin Receptor Regulates The Constitutive Expression Of The Vav3 Proto-Oncogene And Modulates Cell Shape And Adhesion
Fitting A Xenobiotic Receptor Into Cell Homeostasis: How The Dioxin Receptor Interacts With Tgfβ Signaling
The Dioxin Receptor Regulates The Constitutive Expression Of The Vav3 Proto-Oncogene And Modulates Cell Shape And Adhesion
Fitting A Xenobiotic Receptor Into Cell Homeostasis: How The Dioxin Receptor Interacts With Tgfβ Signaling
Loss Of Dioxin-Receptor Expression Accelerates Wound Healing In Vivo By A Mechanism Involving Tgfβ
Fitting A Xenobiotic Receptor Into Cell Homeostasis: How The Dioxin Receptor Interacts With Tgfβ Signaling
Loss Of Dioxin-Receptor Expression Accelerates Wound Healing In Vivo By A Mechanism Involving Tgfβ
Recruitment Of Creb1 And Histone Deacetylase 2 (Hdac2) To The Mouse Ltbp-1 Promoter Regulates Its Constitutive Expression In A Dioxin Receptor-Dependent Manner
Loss Of Dioxin-Receptor Expression Accelerates Wound Healing In Vivo By A Mechanism Involving Tgfβ
Recruitment Of Creb1 And Histone Deacetylase 2 (Hdac2) To The Mouse Ltbp-1 Promoter Regulates Its Constitutive Expression In A Dioxin Receptor-Dependent Manner
Genome-Wide B1 Retrotransposon Binds The Transcription Factors Dioxin Receptor And Slug And Regulates Gene Expression In Vivo
Recruitment Of Creb1 And Histone Deacetylase 2 (Hdac2) To The Mouse Ltbp-1 Promoter Regulates Its Constitutive Expression In A Dioxin Receptor-Dependent Manner
Genome-Wide B1 Retrotransposon Binds The Transcription Factors Dioxin Receptor And Slug And Regulates Gene Expression In Vivo
Non-Genomic Action Of Resveratrol On Androgen And Oestrogen Receptors In Prostate Cancer: Modulation Of The Phosphoinositide 3-Kinase Pathway
Genome-Wide B1 Retrotransposon Binds The Transcription Factors Dioxin Receptor And Slug And Regulates Gene Expression In Vivo
Non-Genomic Action Of Resveratrol On Androgen And Oestrogen Receptors In Prostate Cancer: Modulation Of The Phosphoinositide 3-Kinase Pathway
Mechanisms Involved In Resveratrol-Induced Apoptosis And Cell Cycle Arrest In Prostate Cancer-Derived Cell Lines
Non-Genomic Action Of Resveratrol On Androgen And Oestrogen Receptors In Prostate Cancer: Modulation Of The Phosphoinositide 3-Kinase Pathway
Mechanisms Involved In Resveratrol-Induced Apoptosis And Cell Cycle Arrest In Prostate Cancer-Derived Cell Lines
The Aryl Hydrocarbon Receptor, More Than A Xenobiotic-Interacting Protein
Mechanisms Involved In Resveratrol-Induced Apoptosis And Cell Cycle Arrest In Prostate Cancer-Derived Cell Lines
The Aryl Hydrocarbon Receptor, More Than A Xenobiotic-Interacting Protein
The Dioxin Receptor Is Silenced By Promoter Hypermethylation In Human Acute Lymphoblastic Leukemia Through Inhibition Of Sp1 Binding
The Aryl Hydrocarbon Receptor, More Than A Xenobiotic-Interacting Protein
The Dioxin Receptor Is Silenced By Promoter Hypermethylation In Human Acute Lymphoblastic Leukemia Through Inhibition Of Sp1 Binding
Ltbp-1 Blockade In Dioxin Receptor-Null Mouse Embryo Fibroblasts Decreases Tgf-Β Activity: Role Of Extracellular Proteases Plasmin And Elastase
The Dioxin Receptor Is Silenced By Promoter Hypermethylation In Human Acute Lymphoblastic Leukemia Through Inhibition Of Sp1 Binding
Ltbp-1 Blockade In Dioxin Receptor-Null Mouse Embryo Fibroblasts Decreases Tgf-Β Activity: Role Of Extracellular Proteases Plasmin And Elastase
Improving Cancer Therapeutics By Molecular Profiling
Ltbp-1 Blockade In Dioxin Receptor-Null Mouse Embryo Fibroblasts Decreases Tgf-Β Activity: Role Of Extracellular Proteases Plasmin And Elastase
Improving Cancer Therapeutics By Molecular Profiling
Erratum: Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb (International Journal Of Cancer (2005) 115 (74-84))
Improving Cancer Therapeutics By Molecular Profiling
Erratum: Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb (International Journal Of Cancer (2005) 115 (74-84))
Immortalized Mouse Mammary Fibroblasts Lacking Dioxin Receptor Have Impaired Tumorigenicity In A Subcutaneous Mouse Xenograft Model
Erratum: Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb (International Journal Of Cancer (2005) 115 (74-84))
Immortalized Mouse Mammary Fibroblasts Lacking Dioxin Receptor Have Impaired Tumorigenicity In A Subcutaneous Mouse Xenograft Model
Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb
Immortalized Mouse Mammary Fibroblasts Lacking Dioxin Receptor Have Impaired Tumorigenicity In A Subcutaneous Mouse Xenograft Model
Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb
Resveratrol Modulates The Phosphoinositide 3-Kinase Pathway Through An Estrogen Receptor Α-Dependent Mechanism: Relevance In Cell Proliferation
Resveratrol-Induced Apoptosis In Mcf-7 Human Breast Cancer Cells Involves A Caspase-Independent Mechanism With Downregulation Of Bcl-2 And Nf-Κb
Resveratrol Modulates The Phosphoinositide 3-Kinase Pathway Through An Estrogen Receptor Α-Dependent Mechanism: Relevance In Cell Proliferation
Overexpression Of Latent Transforming Growth Factor-Β Binding Protein 1 (Ltbp-1) In Dioxin Receptor-Null Mouse Embryo Fibroblasts
Resveratrol Modulates The Phosphoinositide 3-Kinase Pathway Through An Estrogen Receptor Α-Dependent Mechanism: Relevance In Cell Proliferation
Overexpression Of Latent Transforming Growth Factor-Β Binding Protein 1 (Ltbp-1) In Dioxin Receptor-Null Mouse Embryo Fibroblasts
Liver Portal Fibrosis In Dioxin Receptor-Null Mice That Overexpress The Latent Transforming Growth Factor-Β-Binding Protein-1
Overexpression Of Latent Transforming Growth Factor-Β Binding Protein 1 (Ltbp-1) In Dioxin Receptor-Null Mouse Embryo Fibroblasts
Liver Portal Fibrosis In Dioxin Receptor-Null Mice That Overexpress The Latent Transforming Growth Factor-Β-Binding Protein-1
Proteasome Inhibition Induces Nuclear Translocation Of The Dioxin Receptor Through An Sp1 And Protein Kinase C-Dependent Pathway
Liver Portal Fibrosis In Dioxin Receptor-Null Mice That Overexpress The Latent Transforming Growth Factor-Β-Binding Protein-1
Proteasome Inhibition Induces Nuclear Translocation Of The Dioxin Receptor Through An Sp1 And Protein Kinase C-Dependent Pathway
Down-Regulation Of Cyp1a2 Induction During The Maturation Of Mouse Cerebellar Granule Cells In Culture: Role Of Nitric Oxide Accumulation
Proteasome Inhibition Induces Nuclear Translocation Of The Dioxin Receptor Through An Sp1 And Protein Kinase C-Dependent Pathway
Down-Regulation Of Cyp1a2 Induction During The Maturation Of Mouse Cerebellar Granule Cells In Culture: Role Of Nitric Oxide Accumulation
Thioridazine Steady-State Plasma Concentrations Are Influenced By Tobacco Smoking And Cyp2d6, But Not By The Cyp2c9 Genotype
Down-Regulation Of Cyp1a2 Induction During The Maturation Of Mouse Cerebellar Granule Cells In Culture: Role Of Nitric Oxide Accumulation
Thioridazine Steady-State Plasma Concentrations Are Influenced By Tobacco Smoking And Cyp2d6, But Not By The Cyp2c9 Genotype
Carcinogenesis Of The Food Mutagen Phip In Mice Is Dependent Of Cyp1a2
Thioridazine Steady-State Plasma Concentrations Are Influenced By Tobacco Smoking And Cyp2d6, But Not By The Cyp2c9 Genotype
Carcinogenesis Of The Food Mutagen Phip In Mice Is Dependent Of Cyp1a2
Polycyclic Aromatic Hydrocarbon-Inducible Dna Adducts: Evidence By 32p-Postlabeling And Use Of Knockout Mice For Ah Receptor-Independent Mechanisms Of Metabolic Activation In Vivo
Carcinogenesis Of The Food Mutagen Phip In Mice Is Dependent Of Cyp1a2
Polycyclic Aromatic Hydrocarbon-Inducible Dna Adducts: Evidence By 32p-Postlabeling And Use Of Knockout Mice For Ah Receptor-Independent Mechanisms Of Metabolic Activation In Vivo
El Resveratrol Presente En El Vino Como Potencial Inhibidor Del Desarrollo De Tumores En Humanos
Polycyclic Aromatic Hydrocarbon-Inducible Dna Adducts: Evidence By 32p-Postlabeling And Use Of Knockout Mice For Ah Receptor-Independent Mechanisms Of Metabolic Activation In Vivo
El Resveratrol Presente En El Vino Como Potencial Inhibidor Del Desarrollo De Tumores En Humanos
Neuroprotection Against Excitotoxicity By N-Alkylglycines In Rat Hippocampal Neurons
El Resveratrol Presente En El Vino Como Potencial Inhibidor Del Desarrollo De Tumores En Humanos
Neuroprotection Against Excitotoxicity By N-Alkylglycines In Rat Hippocampal Neurons
The Antiproliferative Activity Of Resveratrol Results In Apoptosis In Mcf-7 But Not In Mda-Mb-231 Human Breast Cancer Cells: Cell-Specific Alteration Of The Cell Cycle
Neuroprotection Against Excitotoxicity By N-Alkylglycines In Rat Hippocampal Neurons
The Antiproliferative Activity Of Resveratrol Results In Apoptosis In Mcf-7 But Not In Mda-Mb-231 Human Breast Cancer Cells: Cell-Specific Alteration Of The Cell Cycle
Resveratrol, Una Fitalexina Presente En El Vino, Inhibe Proliferación Celular En Líneas Tumorales Derivadas De Epitelio Mamario Humano
The Antiproliferative Activity Of Resveratrol Results In Apoptosis In Mcf-7 But Not In Mda-Mb-231 Human Breast Cancer Cells: Cell-Specific Alteration Of The Cell Cycle
Resveratrol, Una Fitalexina Presente En El Vino, Inhibe Proliferación Celular En Líneas Tumorales Derivadas De Epitelio Mamario Humano
Effect Of Thioridazine Dosage On The Debrisoquine Hydroxylation Phenotype In Psychiatric Patients With Different Cyp2d6 Genotypes
Resveratrol, Una Fitalexina Presente En El Vino, Inhibe Proliferación Celular En Líneas Tumorales Derivadas De Epitelio Mamario Humano
Effect Of Thioridazine Dosage On The Debrisoquine Hydroxylation Phenotype In Psychiatric Patients With Different Cyp2d6 Genotypes
Targeted Genomic Disruption Of H-Ras And N-Ras, Individually Or In Combination, Reveals The Dispensability Of Both Loci For Mouse Growth And Development
Effect Of Thioridazine Dosage On The Debrisoquine Hydroxylation Phenotype In Psychiatric Patients With Different Cyp2d6 Genotypes
Targeted Genomic Disruption Of H-Ras And N-Ras, Individually Or In Combination, Reveals The Dispensability Of Both Loci For Mouse Growth And Development
Proteasome Inhibition Induces Nuclear Translocation And Transcriptional Activation Of The Dioxin Receptor In Mouse Embryo Primary Fibroblasts In The Absence Of Xenobiotics
Targeted Genomic Disruption Of H-Ras And N-Ras, Individually Or In Combination, Reveals The Dispensability Of Both Loci For Mouse Growth And Development
Proteasome Inhibition Induces Nuclear Translocation And Transcriptional Activation Of The Dioxin Receptor In Mouse Embryo Primary Fibroblasts In The Absence Of Xenobiotics
Altered Cell Cycle Control At The G2/m Phases In Aryl Hydrocarbon Receptor-Null Embryo Fibroblast
Proteasome Inhibition Induces Nuclear Translocation And Transcriptional Activation Of The Dioxin Receptor In Mouse Embryo Primary Fibroblasts In The Absence Of Xenobiotics
Altered Cell Cycle Control At The G2/m Phases In Aryl Hydrocarbon Receptor-Null Embryo Fibroblast
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
Altered Cell Cycle Control At The G2/m Phases In Aryl Hydrocarbon Receptor-Null Embryo Fibroblast
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
Hepatic Fibrosis And Cytochrome P450: Experimental Models Of Fibrosis Compared To Ahr Knockout Mice
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
Hepatic Fibrosis And Cytochrome P450: Experimental Models Of Fibrosis Compared To Ahr Knockout Mice
Genomic Instability In Gadd45a-Deficient Mice
Hepatic Fibrosis And Cytochrome P450: Experimental Models Of Fibrosis Compared To Ahr Knockout Mice
Genomic Instability In Gadd45a-Deficient Mice
Cyp1a2 Is Not The Primary Enzyme Responsible For 4-Aminobiphenyl-Induced Hepatocarcinogenesis In Mice
Genomic Instability In Gadd45a-Deficient Mice
Cyp1a2 Is Not The Primary Enzyme Responsible For 4-Aminobiphenyl-Induced Hepatocarcinogenesis In Mice
Targeted Disruption Of The Microsomal Epoxide Hydrolase Gene. Microsomal Epoxide Hydrolase Is Required For The Carcinogenic Activity Of 7,12- Dimethylbenz[A]anthracene
Cyp1a2 Is Not The Primary Enzyme Responsible For 4-Aminobiphenyl-Induced Hepatocarcinogenesis In Mice
Targeted Disruption Of The Microsomal Epoxide Hydrolase Gene. Microsomal Epoxide Hydrolase Is Required For The Carcinogenic Activity Of 7,12- Dimethylbenz[A]anthracene
Expression Of Cyp2a Genes In Human Liver And Extrahepatic Tissues
Targeted Disruption Of The Microsomal Epoxide Hydrolase Gene. Microsomal Epoxide Hydrolase Is Required For The Carcinogenic Activity Of 7,12- Dimethylbenz[A]anthracene
Expression Of Cyp2a Genes In Human Liver And Extrahepatic Tissues
Amelioration Of Tcdd-Induced Teratogenesis In Aryl Hydrocarbon Receptor (Ahr)-Null Mice
Expression Of Cyp2a Genes In Human Liver And Extrahepatic Tissues
Amelioration Of Tcdd-Induced Teratogenesis In Aryl Hydrocarbon Receptor (Ahr)-Null Mice
The Aryl Hydrocarbon Receptor. Studies Using The Ahr-Null Mice
Amelioration Of Tcdd-Induced Teratogenesis In Aryl Hydrocarbon Receptor (Ahr)-Null Mice
The Aryl Hydrocarbon Receptor. Studies Using The Ahr-Null Mice
Aryl-Hydrocarbon Receptor Is An Inhibitory Regulator Of Lipid Synthesis And Of Commitment To Adipogenesis
The Aryl Hydrocarbon Receptor. Studies Using The Ahr-Null Mice
Aryl-Hydrocarbon Receptor Is An Inhibitory Regulator Of Lipid Synthesis And Of Commitment To Adipogenesis
Characterization Of The Human Dihydropyrimidine Dehydrogenase Gene
Aryl-Hydrocarbon Receptor Is An Inhibitory Regulator Of Lipid Synthesis And Of Commitment To Adipogenesis
Characterization Of The Human Dihydropyrimidine Dehydrogenase Gene
Effect Of Phenobarbital On Hepatic Cyp1a1 And Cyp1a2 In The Ahr-Null Mouse
Characterization Of The Human Dihydropyrimidine Dehydrogenase Gene
Effect Of Phenobarbital On Hepatic Cyp1a1 And Cyp1a2 In The Ahr-Null Mouse
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Caucasian Subjects
Effect Of Phenobarbital On Hepatic Cyp1a1 And Cyp1a2 In The Ahr-Null Mouse
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Caucasian Subjects
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Patients With Colorectal Cancer
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Caucasian Subjects
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Patients With Colorectal Cancer
Nomenclature For Human Dpyd Alleles
Dihydropyrimidine Dehydrogenase Pharmacogenetics In Patients With Colorectal Cancer
Nomenclature For Human Dpyd Alleles
The Involvement Of Aryl Hydrocarbon Receptor In The Activation Of Transforming Growth Factor-Β And Apoptosis
Nomenclature For Human Dpyd Alleles
The Involvement Of Aryl Hydrocarbon Receptor In The Activation Of Transforming Growth Factor-Β And Apoptosis
Aryl Hydrocarbon Receptor Deficient Mice (Ahr-/-) Exhibit An Accumulation Of Liver Retinylpalmitate
The Involvement Of Aryl Hydrocarbon Receptor In The Activation Of Transforming Growth Factor-Β And Apoptosis
Aryl Hydrocarbon Receptor Deficient Mice (Ahr-/-) Exhibit An Accumulation Of Liver Retinylpalmitate
Analysis Of The Selenocysteine (Sec) Trna Population In Mouse Embryonic Stem (Es) Cells Heterozygous For The Sec Trna Gene
Aryl Hydrocarbon Receptor Deficient Mice (Ahr-/-) Exhibit An Accumulation Of Liver Retinylpalmitate
Analysis Of The Selenocysteine (Sec) Trna Population In Mouse Embryonic Stem (Es) Cells Heterozygous For The Sec Trna Gene
Aryl Hydrocarbon Receptor Knockout Mice (Ahr(-/-)) Exhibit Liver Retinoid Accumulation And Reduced Retinoic Acid Metabolism
Analysis Of The Selenocysteine (Sec) Trna Population In Mouse Embryonic Stem (Es) Cells Heterozygous For The Sec Trna Gene
Aryl Hydrocarbon Receptor Knockout Mice (Ahr(-/-)) Exhibit Liver Retinoid Accumulation And Reduced Retinoic Acid Metabolism
Cyp2a6 Gene Polymorphism And Risk Of Liver Cancer And Cirrhosis
Aryl Hydrocarbon Receptor Knockout Mice (Ahr(-/-)) Exhibit Liver Retinoid Accumulation And Reduced Retinoic Acid Metabolism
Cyp2a6 Gene Polymorphism And Risk Of Liver Cancer And Cirrhosis
Selenocysteine Trna([Ser]sec) Levels And Selenium-Dependent Glutathione Peroxidase Activity In Mouse Embryonic Stem Cells Heterozygous For A Targeted Mutation In The Trna([Ser]sec) Gene
Cyp2a6 Gene Polymorphism And Risk Of Liver Cancer And Cirrhosis
Selenocysteine Trna([Ser]sec) Levels And Selenium-Dependent Glutathione Peroxidase Activity In Mouse Embryonic Stem Cells Heterozygous For A Targeted Mutation In The Trna([Ser]sec) Gene
Lack Of Correlation Between Phenotype And Genotype For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In A Family Of Pakistani Origin
Selenocysteine Trna([Ser]sec) Levels And Selenium-Dependent Glutathione Peroxidase Activity In Mouse Embryonic Stem Cells Heterozygous For A Targeted Mutation In The Trna([Ser]sec) Gene
Lack Of Correlation Between Phenotype And Genotype For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In A Family Of Pakistani Origin
Lesions Of Aryl-Hydrocarbon Receptor-Deficient Mice
Lack Of Correlation Between Phenotype And Genotype For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In A Family Of Pakistani Origin
Lesions Of Aryl-Hydrocarbon Receptor-Deficient Mice
Mutations At Codon 974 Of The Dpyd Gene Are A Rare Event
Lesions Of Aryl-Hydrocarbon Receptor-Deficient Mice
Mutations At Codon 974 Of The Dpyd Gene Are A Rare Event
Piperonyl Butoxide And Acenaphthylene Induce Cytochrome P450 1a2 And 1b1 Mrna In Aromatic Hydrocarbon-Responsive Receptor Knock-Out Mouse Liver
Mutations At Codon 974 Of The Dpyd Gene Are A Rare Event
Piperonyl Butoxide And Acenaphthylene Induce Cytochrome P450 1a2 And 1b1 Mrna In Aromatic Hydrocarbon-Responsive Receptor Knock-Out Mouse Liver
Transcriptional Induction Of The Cytochrome P4501a1 Gene By A Thiazolium Compound, Yh439
Piperonyl Butoxide And Acenaphthylene Induce Cytochrome P450 1a2 And 1b1 Mrna In Aromatic Hydrocarbon-Responsive Receptor Knock-Out Mouse Liver
Transcriptional Induction Of The Cytochrome P4501a1 Gene By A Thiazolium Compound, Yh439
The Role Of The Aryl Hydrocarbon Receptor In Animal Development, Physiological Homeostasis And Toxicity Of Tcdd
Transcriptional Induction Of The Cytochrome P4501a1 Gene By A Thiazolium Compound, Yh439
The Role Of The Aryl Hydrocarbon Receptor In Animal Development, Physiological Homeostasis And Toxicity Of Tcdd
Differential Regulation Of Mouse Ah Receptor Gene Expression In Cell Lines Of Different Tissue Origins
The Role Of The Aryl Hydrocarbon Receptor In Animal Development, Physiological Homeostasis And Toxicity Of Tcdd
Differential Regulation Of Mouse Ah Receptor Gene Expression In Cell Lines Of Different Tissue Origins
Molecular Basis Of The Human Dihydropyrimidine Dehydrogenase Deficiency And 5-Fluorouracil Toxicity
Differential Regulation Of Mouse Ah Receptor Gene Expression In Cell Lines Of Different Tissue Origins
Molecular Basis Of The Human Dihydropyrimidine Dehydrogenase Deficiency And 5-Fluorouracil Toxicity
Role Of Cyp2e1 In The Hepatotoxicity Of Acetaminophen
Molecular Basis Of The Human Dihydropyrimidine Dehydrogenase Deficiency And 5-Fluorouracil Toxicity
Role Of Cyp2e1 In The Hepatotoxicity Of Acetaminophen
Aryl-Hydrocarbon Receptor-Deficient Mice Are Resistant To 2,3,7,8-Tetrachlorodibenzo-P-Dioxin-Induced Toxicity
Role Of Cyp2e1 In The Hepatotoxicity Of Acetaminophen
Aryl-Hydrocarbon Receptor-Deficient Mice Are Resistant To 2,3,7,8-Tetrachlorodibenzo-P-Dioxin-Induced Toxicity
Hepatic Fibrosis In Ahr(-/-) Mice
Aryl-Hydrocarbon Receptor-Deficient Mice Are Resistant To 2,3,7,8-Tetrachlorodibenzo-P-Dioxin-Induced Toxicity
Hepatic Fibrosis In Ahr(-/-) Mice
The T/ebp Null Mouse: Thyroid-Specific Enhancer-Binding Protein Is Essential For The Organogenesis Of The Thyroid, Lung, Ventral Forebrain, And Pituitary
Hepatic Fibrosis In Ahr(-/-) Mice
The T/ebp Null Mouse: Thyroid-Specific Enhancer-Binding Protein Is Essential For The Organogenesis Of The Thyroid, Lung, Ventral Forebrain, And Pituitary
Pyrimidines And Cns Regulation
The T/ebp Null Mouse: Thyroid-Specific Enhancer-Binding Protein Is Essential For The Organogenesis Of The Thyroid, Lung, Ventral Forebrain, And Pituitary
Pyrimidines And Cns Regulation
Targeted Disruption Of Specific Cytochromes P450 And Xenobiotic Receptor Genes
Pyrimidines And Cns Regulation
Targeted Disruption Of Specific Cytochromes P450 And Xenobiotic Receptor Genes
Diagnostic-Analysis, Clinical Importance And Molecular-Basis Of Dihydropyrimidine Dehydrogenase-Deficiency
Targeted Disruption Of Specific Cytochromes P450 And Xenobiotic Receptor Genes
Diagnostic-Analysis, Clinical Importance And Molecular-Basis Of Dihydropyrimidine Dehydrogenase-Deficiency
Organization And Evolution Of The Cytochrome P450 Cyp2a-2b-2f Subfamily Gene Cluster On Human Chromosome 19
Diagnostic-Analysis, Clinical Importance And Molecular-Basis Of Dihydropyrimidine Dehydrogenase-Deficiency
Organization And Evolution Of The Cytochrome P450 Cyp2a-2b-2f Subfamily Gene Cluster On Human Chromosome 19
A Genetic Polymorphism In Coumarin 7-Hydroxylation: Sequence Of The Human Cyp2a Genes And Identification Of Variant Cyp2a6 Alleles
Organization And Evolution Of The Cytochrome P450 Cyp2a-2b-2f Subfamily Gene Cluster On Human Chromosome 19
A Genetic Polymorphism In Coumarin 7-Hydroxylation: Sequence Of The Human Cyp2a Genes And Identification Of Variant Cyp2a6 Alleles
Comparison Of Substrate Metabolism By Wild Type Cyp2d6 Protein And A Variant Containing Methionine, Not Valine, At Position 374
A Genetic Polymorphism In Coumarin 7-Hydroxylation: Sequence Of The Human Cyp2a Genes And Identification Of Variant Cyp2a6 Alleles
Comparison Of Substrate Metabolism By Wild Type Cyp2d6 Protein And A Variant Containing Methionine, Not Valine, At Position 374
Human Polymorphism In Drug Metabolism: Mutation In The Dihydropyrimidine Dehydrogenase Gene Results In Exon Skipping And Thymine Uracilurea
Comparison Of Substrate Metabolism By Wild Type Cyp2d6 Protein And A Variant Containing Methionine, Not Valine, At Position 374
Human Polymorphism In Drug Metabolism: Mutation In The Dihydropyrimidine Dehydrogenase Gene Results In Exon Skipping And Thymine Uracilurea
Genetic Polymorphism Of Cyp2c9 And Its Effect On Warfarin Maintenance Dose Requirement In Patients Undergoing Anticoagulation Therapy
Human Polymorphism In Drug Metabolism: Mutation In The Dihydropyrimidine Dehydrogenase Gene Results In Exon Skipping And Thymine Uracilurea
Genetic Polymorphism Of Cyp2c9 And Its Effect On Warfarin Maintenance Dose Requirement In Patients Undergoing Anticoagulation Therapy
Correlation Between Catalytic Activity And Protein Content For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In Human Lymphocytes
Genetic Polymorphism Of Cyp2c9 And Its Effect On Warfarin Maintenance Dose Requirement In Patients Undergoing Anticoagulation Therapy
Correlation Between Catalytic Activity And Protein Content For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In Human Lymphocytes
Neonatal Lethality Associated With Respiratory Distress In Mice Lacking Cytochrome P450 1a2
Correlation Between Catalytic Activity And Protein Content For The Polymorphically Expressed Dihydropyrimidine Dehydrogenase In Human Lymphocytes
Neonatal Lethality Associated With Respiratory Distress In Mice Lacking Cytochrome P450 1a2
Xenobiotic Receptor Knockout Mice
Neonatal Lethality Associated With Respiratory Distress In Mice Lacking Cytochrome P450 1a2
Xenobiotic Receptor Knockout Mice
Immune System Impairment And Hepatic Fibrosis In Mice Lacking The Dioxin-Binding Ah Receptor
Xenobiotic Receptor Knockout Mice
Immune System Impairment And Hepatic Fibrosis In Mice Lacking The Dioxin-Binding Ah Receptor
Targeted Disruption Of The Α Isoform Of The Peroxisome Proliferator- Activated Receptor Gene In Mice Results In Abolishment Of The Pleiotropic Effects Of Peroxisome Proliferators
Immune System Impairment And Hepatic Fibrosis In Mice Lacking The Dioxin-Binding Ah Receptor
Targeted Disruption Of The Α Isoform Of The Peroxisome Proliferator- Activated Receptor Gene In Mice Results In Abolishment Of The Pleiotropic Effects Of Peroxisome Proliferators
Cdna Cloning And Chromosome Mapping Of Human Dihydropyrimidine Dehydrogenase, An Enzyme Associated With 5-Fluorouracil Toxicity And Congenital Thymine Uraciluria
Targeted Disruption Of The Α Isoform Of The Peroxisome Proliferator- Activated Receptor Gene In Mice Results In Abolishment Of The Pleiotropic Effects Of Peroxisome Proliferators
Cdna Cloning And Chromosome Mapping Of Human Dihydropyrimidine Dehydrogenase, An Enzyme Associated With 5-Fluorouracil Toxicity And Congenital Thymine Uraciluria
Assignment Of The Human Dihydropyrimidine Dehydrogenase Gene (Dpyd) To Chromosome Region 1p22 By Fluorescence In Situ Hybridization
Cdna Cloning And Chromosome Mapping Of Human Dihydropyrimidine Dehydrogenase, An Enzyme Associated With 5-Fluorouracil Toxicity And Congenital Thymine Uraciluria
Assignment Of The Human Dihydropyrimidine Dehydrogenase Gene (Dpyd) To Chromosome Region 1p22 By Fluorescence In Situ Hybridization
Effect Of Immobilization On The Activity Of Rat Hepatic Microsomal Cytochrome P450 Enzymes
Assignment Of The Human Dihydropyrimidine Dehydrogenase Gene (Dpyd) To Chromosome Region 1p22 By Fluorescence In Situ Hybridization
Effect Of Immobilization On The Activity Of Rat Hepatic Microsomal Cytochrome P450 Enzymes
Differential Scanning Calorimetry Study Of Glycogen Phosphorylase B-Detergent Interactions
Effect Of Immobilization On The Activity Of Rat Hepatic Microsomal Cytochrome P450 Enzymes
Differential Scanning Calorimetry Study Of Glycogen Phosphorylase B-Detergent Interactions
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Differential Scanning Calorimetry Study Of Glycogen Phosphorylase B-Detergent Interactions
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Modulation Of (Ca2+ + Mg2+)-Atpases And Ca2+ Fluxes Through The Plasma Membrane Of Synaptosomes And Sarcoplasmic Reticulum By Local Anaesthetics
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Modulation Of (Ca2+ + Mg2+)-Atpases And Ca2+ Fluxes Through The Plasma Membrane Of Synaptosomes And Sarcoplasmic Reticulum By Local Anaesthetics
Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment
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