Clinical Microbiology Reviews, ISSN 0893-8512, 10/2010, Volume 23, Issue 4, pp. 689 - 712
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DNA-POLYMERASE GENE | ACQUIRED-IMMUNODEFICIENCY-SYNDROME | CONFERRING FOSCARNET RESISTANCE | AMINO-ACID CHANGES | REAL-TIME PCR | HERPES-SIMPLEX-VIRUS | OPEN READING FRAME | BACTERIAL ARTIFICIAL CHROMOSOME | MICROBIOLOGY | UL97 PROTEIN-KINASE | STEM-CELL TRANSPLANTATION | Cytomegalovirus - genetics | Cytosine - analogs & derivatives | Genome, Viral | Antiviral Agents - pharmacology | Foscarnet - pharmacology | Organophosphonates - therapeutic use | Antiviral Agents - therapeutic use | Humans | Phosphotransferases (Alcohol Group Acceptor) - genetics | Sequence Analysis, DNA | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Drug Resistance, Viral - genetics | Organophosphonates - pharmacology | Cytomegalovirus Infections - drug therapy | Ganciclovir - therapeutic use | Ganciclovir - pharmacology | Cytosine - pharmacology | Cytosine - therapeutic use | Foscarnet - therapeutic use | DNA-Directed DNA Polymerase | Cytomegalovirus - drug effects | Reviews
DNA-POLYMERASE GENE | ACQUIRED-IMMUNODEFICIENCY-SYNDROME | CONFERRING FOSCARNET RESISTANCE | AMINO-ACID CHANGES | REAL-TIME PCR | HERPES-SIMPLEX-VIRUS | OPEN READING FRAME | BACTERIAL ARTIFICIAL CHROMOSOME | MICROBIOLOGY | UL97 PROTEIN-KINASE | STEM-CELL TRANSPLANTATION | Cytomegalovirus - genetics | Cytosine - analogs & derivatives | Genome, Viral | Antiviral Agents - pharmacology | Foscarnet - pharmacology | Organophosphonates - therapeutic use | Antiviral Agents - therapeutic use | Humans | Phosphotransferases (Alcohol Group Acceptor) - genetics | Sequence Analysis, DNA | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Drug Resistance, Viral - genetics | Organophosphonates - pharmacology | Cytomegalovirus Infections - drug therapy | Ganciclovir - therapeutic use | Ganciclovir - pharmacology | Cytosine - pharmacology | Cytosine - therapeutic use | Foscarnet - therapeutic use | DNA-Directed DNA Polymerase | Cytomegalovirus - drug effects | Reviews
Journal Article
Antiviral Research, ISSN 0166-3542, 2010, Volume 85, Issue 1, pp. 210 - 231
Antiretroviral therapy has led to a significant decrease in human immunodeficiency virus (HIV)-related mortality. Approved antiretroviral drugs target...
Phosphorolysis | Thymidine analogues | Reverse transcriptase | HIV | DNA polymerase | Drug resistance | NUCLEOSIDE ANALOG INHIBITORS | DEPENDENT PRIMER UNBLOCKING | HIGH-LEVEL RESISTANCE | AMINO-ACID SUBSTITUTIONS | DOUBLE-STRANDED DNA | VIROLOGY | VIRAL REPLICATION CAPACITY | THYMIDINE NUCLEOTIDE ANALOGS | TREATMENT-EXPERIENCED PATIENTS | MUTATIONS CONFERRING RESISTANCE | PHARMACOLOGY & PHARMACY | HIV-1 REVERSE-TRANSCRIPTASE | Anti-HIV Agents - pharmacology | Humans | Drug Resistance, Viral | Viral Proteins - genetics | HIV - genetics | Mutation, Missense | HIV - drug effects
Phosphorolysis | Thymidine analogues | Reverse transcriptase | HIV | DNA polymerase | Drug resistance | NUCLEOSIDE ANALOG INHIBITORS | DEPENDENT PRIMER UNBLOCKING | HIGH-LEVEL RESISTANCE | AMINO-ACID SUBSTITUTIONS | DOUBLE-STRANDED DNA | VIROLOGY | VIRAL REPLICATION CAPACITY | THYMIDINE NUCLEOTIDE ANALOGS | TREATMENT-EXPERIENCED PATIENTS | MUTATIONS CONFERRING RESISTANCE | PHARMACOLOGY & PHARMACY | HIV-1 REVERSE-TRANSCRIPTASE | Anti-HIV Agents - pharmacology | Humans | Drug Resistance, Viral | Viral Proteins - genetics | HIV - genetics | Mutation, Missense | HIV - drug effects
Journal Article
Clinical Microbiology Reviews, ISSN 0893-8512, 04/2002, Volume 15, Issue 2, pp. 247 - 277
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PATIENTS RECEIVING COMBINATIONS | ORALLY BIOAVAILABLE INHIBITOR | PROTEASE INHIBITOR THERAPY | ACTIVE ANTIRETROVIRAL THERAPY | HIGH-LEVEL RESISTANCE | IN-VITRO SELECTION | LINE PROBE ASSAY | MUTATIONS CONFERRING RESISTANCE | MICROBIOLOGY | HIV-1 REVERSE-TRANSCRIPTASE | SAQUINAVIR-CONTAINING REGIMEN | Anti-HIV Agents - pharmacology | HIV-1 - drug effects | HIV Infections - virology | Humans | HIV Protease - genetics | Reverse Transcriptase Inhibitors - pharmacology | Genotype | HIV Reverse Transcriptase - genetics | HIV-1 - genetics | Drug Resistance, Viral - genetics | Anti-HIV Agents - therapeutic use | HIV Infections - drug therapy | HIV-1 - enzymology | Reverse Transcriptase Inhibitors - therapeutic use | Drug Therapy, Combination | Microbial Sensitivity Tests - methods | Review
PATIENTS RECEIVING COMBINATIONS | ORALLY BIOAVAILABLE INHIBITOR | PROTEASE INHIBITOR THERAPY | ACTIVE ANTIRETROVIRAL THERAPY | HIGH-LEVEL RESISTANCE | IN-VITRO SELECTION | LINE PROBE ASSAY | MUTATIONS CONFERRING RESISTANCE | MICROBIOLOGY | HIV-1 REVERSE-TRANSCRIPTASE | SAQUINAVIR-CONTAINING REGIMEN | Anti-HIV Agents - pharmacology | HIV-1 - drug effects | HIV Infections - virology | Humans | HIV Protease - genetics | Reverse Transcriptase Inhibitors - pharmacology | Genotype | HIV Reverse Transcriptase - genetics | HIV-1 - genetics | Drug Resistance, Viral - genetics | Anti-HIV Agents - therapeutic use | HIV Infections - drug therapy | HIV-1 - enzymology | Reverse Transcriptase Inhibitors - therapeutic use | Drug Therapy, Combination | Microbial Sensitivity Tests - methods | Review
Journal Article
Reviews in Medical Virology, ISSN 1052-9276, 05/2016, Volume 26, Issue 3, pp. 161 - 182
Summary Human cytomegalovirus (HCMV) infection is a major cause of morbidity and mortality in allogeneic hematopoietic stem cell transplant recipients. The...
ACQUIRED-IMMUNODEFICIENCY-SYNDROME | CONFERRING GANCICLOVIR RESISTANCE | IN-VITRO | VIROLOGY | IMMUNOCOMPROMISED PATIENTS | BONE-MARROW-TRANSPLANTATION | DNA-POLYMERASE MUTATIONS | COMPOUND AIC246 LETERMOVIR | CMV INFECTION | MULTIDRUG-RESISTANCE | UL97 PHOSPHOTRANSFERASE MUTATIONS | Cytomegalovirus - genetics | Antiviral Agents - pharmacology | Antiviral Agents - therapeutic use | Humans | Drug Resistance, Viral | Viral Proteins - genetics | Genotype | Phosphotransferases (Alcohol Group Acceptor) - genetics | Cytomegalovirus Infections - immunology | Host-Pathogen Interactions - drug effects | DNA-Directed DNA Polymerase - genetics | Host-Pathogen Interactions - immunology | Cytomegalovirus - immunology | Phenotype | Cytomegalovirus Infections - drug therapy | Hematopoietic Stem Cell Transplantation - adverse effects | Cytomegalovirus Infections - virology | Disease Management | Mutation | Cytomegalovirus - drug effects | Antiviral agents | Stem cells | Development and progression | Cytomegalovirus infections | Transplantation | Drug resistance | Hematopoietic stem cells
ACQUIRED-IMMUNODEFICIENCY-SYNDROME | CONFERRING GANCICLOVIR RESISTANCE | IN-VITRO | VIROLOGY | IMMUNOCOMPROMISED PATIENTS | BONE-MARROW-TRANSPLANTATION | DNA-POLYMERASE MUTATIONS | COMPOUND AIC246 LETERMOVIR | CMV INFECTION | MULTIDRUG-RESISTANCE | UL97 PHOSPHOTRANSFERASE MUTATIONS | Cytomegalovirus - genetics | Antiviral Agents - pharmacology | Antiviral Agents - therapeutic use | Humans | Drug Resistance, Viral | Viral Proteins - genetics | Genotype | Phosphotransferases (Alcohol Group Acceptor) - genetics | Cytomegalovirus Infections - immunology | Host-Pathogen Interactions - drug effects | DNA-Directed DNA Polymerase - genetics | Host-Pathogen Interactions - immunology | Cytomegalovirus - immunology | Phenotype | Cytomegalovirus Infections - drug therapy | Hematopoietic Stem Cell Transplantation - adverse effects | Cytomegalovirus Infections - virology | Disease Management | Mutation | Cytomegalovirus - drug effects | Antiviral agents | Stem cells | Development and progression | Cytomegalovirus infections | Transplantation | Drug resistance | Hematopoietic stem cells
Journal Article
Journal of Antimicrobial Chemotherapy, ISSN 0305-7453, 4/2012, Volume 67, Issue 4, pp. 928 - 932
Objectives It has been proposed that antimicrobial resistance could be associated with a fitness cost in bacteria, which is often determined by competition...
Biofitness | In vitro time growth | Modelling | Multidrug-resistant bacteria | INFECTIOUS DISEASES | multidrug-resistant bacteria | ANTIBIOTIC-RESISTANCE | CONFERRING MUTATIONS | VANCOMYCIN RESISTANCE | MICROBIOLOGY | BIOLOGICAL COST | modelling | biofitness | PSEUDOMONAS-AERUGINOSA | PHARMACOLOGY & PHARMACY | in vitro time growth | STAPHYLOCOCCUS-AUREUS | MULTIDRUG-RESISTANCE | Models, Theoretical | Acinetobacter baumannii - physiology | Energy Metabolism | Time Factors | Humans | Pseudomonas aeruginosa - growth & development | Drug Resistance, Bacterial | Pseudomonas aeruginosa - physiology | Bacterial Load | Acinetobacter baumannii - growth & development | Competition | Antibiotics | Growth rate | Abundance | Mathematical models | Colony-forming cells | Drug resistance | Fitness
Biofitness | In vitro time growth | Modelling | Multidrug-resistant bacteria | INFECTIOUS DISEASES | multidrug-resistant bacteria | ANTIBIOTIC-RESISTANCE | CONFERRING MUTATIONS | VANCOMYCIN RESISTANCE | MICROBIOLOGY | BIOLOGICAL COST | modelling | biofitness | PSEUDOMONAS-AERUGINOSA | PHARMACOLOGY & PHARMACY | in vitro time growth | STAPHYLOCOCCUS-AUREUS | MULTIDRUG-RESISTANCE | Models, Theoretical | Acinetobacter baumannii - physiology | Energy Metabolism | Time Factors | Humans | Pseudomonas aeruginosa - growth & development | Drug Resistance, Bacterial | Pseudomonas aeruginosa - physiology | Bacterial Load | Acinetobacter baumannii - growth & development | Competition | Antibiotics | Growth rate | Abundance | Mathematical models | Colony-forming cells | Drug resistance | Fitness
Journal Article
Expert Opinion on Investigational Drugs, ISSN 1354-3784, 03/2008, Volume 17, Issue 3, pp. 303 - 319
Background: With 170 million people infected worldwide and an inadequate current standard of care, hepatitis C virus (HCV) infection represents a major unmet...
small molecule antivirals | HCV protease inhibitors | drug discovery | HCV polymerase inhibitors | HCV replicon | NS5A | NS5B | HCV | HCV drug resistance | antiviral therapy | NS3 | Antiviral therapy | Drug discovery | Small molecule antivirals | NS5B POLYMERASE | DEPENDENT RNA-POLYMERASE | HEPATITIS-C-VIRUS | HCVNS5B POLYMERASE | NS3/4A PROTEASE | PEG-INTERFERON-ALPHA-2A PEG-IFN | IN-VITRO | PROTEASE INHIBITOR TELAPREVIR | MUTATIONS CONFERRING RESISTANCE | PHARMACOLOGY & PHARMACY | SERINE-PROTEASE | Hepacivirus - drug effects | Antiviral Agents - pharmacology | Hepatitis C - drug therapy | Humans | Enzyme Inhibitors - pharmacology | Models, Molecular | Clinical Trials as Topic | Drug Resistance, Viral - genetics | Hepacivirus - enzymology | Drug Resistance, Viral - drug effects | Molecular Structure | Viral Nonstructural Proteins - antagonists & inhibitors | Binding Sites
small molecule antivirals | HCV protease inhibitors | drug discovery | HCV polymerase inhibitors | HCV replicon | NS5A | NS5B | HCV | HCV drug resistance | antiviral therapy | NS3 | Antiviral therapy | Drug discovery | Small molecule antivirals | NS5B POLYMERASE | DEPENDENT RNA-POLYMERASE | HEPATITIS-C-VIRUS | HCVNS5B POLYMERASE | NS3/4A PROTEASE | PEG-INTERFERON-ALPHA-2A PEG-IFN | IN-VITRO | PROTEASE INHIBITOR TELAPREVIR | MUTATIONS CONFERRING RESISTANCE | PHARMACOLOGY & PHARMACY | SERINE-PROTEASE | Hepacivirus - drug effects | Antiviral Agents - pharmacology | Hepatitis C - drug therapy | Humans | Enzyme Inhibitors - pharmacology | Models, Molecular | Clinical Trials as Topic | Drug Resistance, Viral - genetics | Hepacivirus - enzymology | Drug Resistance, Viral - drug effects | Molecular Structure | Viral Nonstructural Proteins - antagonists & inhibitors | Binding Sites
Journal Article
Hepatology, ISSN 0270-9139, 04/2009, Volume 49, Issue 4, pp. 1069 - 1082
The efficacy of specifically targeted anti‐viral therapy for hepatitis C virus (HCV) (STAT‐C), including HCV protease and polymerase inhibitors, is limited by...
NONNUCLEOSIDE POLYMERASE INHIBITOR | RESPONSES | NUCLEOSIDE | VARIANTS | RNA REPLICATION | MUTATIONS CONFERRING RESISTANCE | SENSITIVITY | HCV PROTEASE INHIBITOR | IDENTIFICATION | COMBINATION | GASTROENTEROLOGY & HEPATOLOGY | Genome, Viral | Antiviral Agents - therapeutic use | Humans | Selection, Genetic | Adaptation, Biological | Hepacivirus - genetics | Hepatitis C, Chronic - virology | Molecular Sequence Data | Viral Nonstructural Proteins - genetics | Genotype | HLA Antigens - genetics | Hepatitis C, Chronic - complications | Amino Acids - genetics | Hepatitis C, Chronic - drug therapy | Genetic Variation | Drug Resistance, Viral - genetics | DNA Mutational Analysis | HIV Infections - complications | Hepatitis C, Chronic - immunology | Cohort Studies
NONNUCLEOSIDE POLYMERASE INHIBITOR | RESPONSES | NUCLEOSIDE | VARIANTS | RNA REPLICATION | MUTATIONS CONFERRING RESISTANCE | SENSITIVITY | HCV PROTEASE INHIBITOR | IDENTIFICATION | COMBINATION | GASTROENTEROLOGY & HEPATOLOGY | Genome, Viral | Antiviral Agents - therapeutic use | Humans | Selection, Genetic | Adaptation, Biological | Hepacivirus - genetics | Hepatitis C, Chronic - virology | Molecular Sequence Data | Viral Nonstructural Proteins - genetics | Genotype | HLA Antigens - genetics | Hepatitis C, Chronic - complications | Amino Acids - genetics | Hepatitis C, Chronic - drug therapy | Genetic Variation | Drug Resistance, Viral - genetics | DNA Mutational Analysis | HIV Infections - complications | Hepatitis C, Chronic - immunology | Cohort Studies
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 25, pp. 10290 - 10295
Clinical trials of direct-acting antiviral agents in patients chronically infected with hepatitis C virus (HCV) have demonstrated that viral resistance is...
RNA | Cell lines | Antivirals | Fluorescence | Drug resistance | Dosage | Genetic mutation | Hepacivirus | Genotypes | Replicon | Evolution | Virology | NONNUCLEOSIDE POLYMERASE INHIBITOR | REPLICATION | TELAPREVIR | HEPATITIS-C VIRUS | MECHANISM | virology | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | evolution | REPLICON VARIANTS | COMBINATION | CONFERRING RESISTANCE | Hepacivirus - drug effects | Cell Line | Antiviral Agents - pharmacology | Replicon - drug effects | Hepatitis C - drug therapy | Antiviral Agents - therapeutic use | Humans | Hepacivirus - genetics | Clinical Trials as Topic | Recombinant Fusion Proteins - metabolism | Drug Resistance, Viral - genetics | Recombinant Fusion Proteins - genetics | Mutation | Genes, Reporter | Replicon - genetics | Antiviral agents | Viral drug resistance | Microbial mutation | Genetic aspects | Research | Hepatitis C | Drug therapy | Health aspects | Biological Sciences
RNA | Cell lines | Antivirals | Fluorescence | Drug resistance | Dosage | Genetic mutation | Hepacivirus | Genotypes | Replicon | Evolution | Virology | NONNUCLEOSIDE POLYMERASE INHIBITOR | REPLICATION | TELAPREVIR | HEPATITIS-C VIRUS | MECHANISM | virology | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | evolution | REPLICON VARIANTS | COMBINATION | CONFERRING RESISTANCE | Hepacivirus - drug effects | Cell Line | Antiviral Agents - pharmacology | Replicon - drug effects | Hepatitis C - drug therapy | Antiviral Agents - therapeutic use | Humans | Hepacivirus - genetics | Clinical Trials as Topic | Recombinant Fusion Proteins - metabolism | Drug Resistance, Viral - genetics | Recombinant Fusion Proteins - genetics | Mutation | Genes, Reporter | Replicon - genetics | Antiviral agents | Viral drug resistance | Microbial mutation | Genetic aspects | Research | Hepatitis C | Drug therapy | Health aspects | Biological Sciences
Journal Article
Bulletin of Mathematical Biology, ISSN 0092-8240, 8/2012, Volume 74, Issue 8, pp. 1789 - 1817
Telaprevir, a novel hepatitis C virus (HCV) NS3-4A serine protease inhibitor, has demonstrated substantial antiviral activity in patients infected with HCV....
Direct-acting antiviral agents | Life Sciences, general | Mathematical and Computational Biology | Quasispecies | Mathematics | Telaprevir | Mutation | Mathematical model | Cell Biology | Fitness | VIRAL-RNA | VIRUS SERINE-PROTEASE | HCV PROTEASE | CONFERRING RESISTANCE | IN-VITRO | HIV-INFECTION | REPLICON CELLS | BIOLOGY | MATHEMATICAL & COMPUTATIONAL BIOLOGY | GENOTYPE 1 INFECTION | PEGYLATED INTERFERON-ALPHA-2B | ANTIRETROVIRAL TREATMENT | Hepatitis C - drug therapy | Proline - analogs & derivatives | Humans | Drug Resistance, Viral | Hepacivirus - genetics | Hepatitis C - genetics | Oligopeptides - therapeutic use | Proline - therapeutic use | Hepacivirus - enzymology | Numerical Analysis, Computer-Assisted | Hepatitis C - virology | Hepatocytes - virology | Cell Proliferation - drug effects | Models, Genetic | Protease Inhibitors - therapeutic use | Antiviral agents | Protease inhibitors | Analysis | Thrombin | Models | Drug resistance | Drug therapy | Hepatitis C virus | Hepatitis C | Anti-HIV agents | Prevalence studies (Epidemiology) | mathematical model | mutation | direct-acting antiviral agents | fitness | quasispecies
Direct-acting antiviral agents | Life Sciences, general | Mathematical and Computational Biology | Quasispecies | Mathematics | Telaprevir | Mutation | Mathematical model | Cell Biology | Fitness | VIRAL-RNA | VIRUS SERINE-PROTEASE | HCV PROTEASE | CONFERRING RESISTANCE | IN-VITRO | HIV-INFECTION | REPLICON CELLS | BIOLOGY | MATHEMATICAL & COMPUTATIONAL BIOLOGY | GENOTYPE 1 INFECTION | PEGYLATED INTERFERON-ALPHA-2B | ANTIRETROVIRAL TREATMENT | Hepatitis C - drug therapy | Proline - analogs & derivatives | Humans | Drug Resistance, Viral | Hepacivirus - genetics | Hepatitis C - genetics | Oligopeptides - therapeutic use | Proline - therapeutic use | Hepacivirus - enzymology | Numerical Analysis, Computer-Assisted | Hepatitis C - virology | Hepatocytes - virology | Cell Proliferation - drug effects | Models, Genetic | Protease Inhibitors - therapeutic use | Antiviral agents | Protease inhibitors | Analysis | Thrombin | Models | Drug resistance | Drug therapy | Hepatitis C virus | Hepatitis C | Anti-HIV agents | Prevalence studies (Epidemiology) | mathematical model | mutation | direct-acting antiviral agents | fitness | quasispecies
Journal Article
Tuberculosis, ISSN 1472-9792, 2016, Volume 98, pp. 50 - 55
Summary Tuberculosis (TB) is one of the leading causes of death due to an infectious disease in the world. Understanding the mechanisms of drug resistance has...
Infectious Disease | Pulmonary/Respiratory | Drug resistance progression | Single nucleotide polymorphism | Mycobacterium tuberculosis | Whole genome sequencing | Isoniazid | Rifampin | CATALASE-PEROXIDASE | STRAINS | TOXIN-ANTITOXIN SYSTEMS | CONFERRING MUTATIONS | MICROBIOLOGY | KATG | IMMUNOLOGY | DISCOVERY | ISONIAZID RESISTANCE | GENE | RESPIRATORY SYSTEM | DNA | SEQUENCING DATA | Antitubercular Agents - adverse effects | Humans | Bacterial Proteins - chemistry | Tuberculosis - microbiology | Structure-Activity Relationship | Mycobacterium tuberculosis - drug effects | Tuberculosis - diagnosis | Microbial Sensitivity Tests | Mycobacterium tuberculosis - pathogenicity | Time Factors | DNA Mutational Analysis | Tuberculosis - drug therapy | Bacterial Toxins - genetics | Isoniazid - therapeutic use | Rifampin - therapeutic use | Antitubercular Agents - therapeutic use | Genome, Bacterial | Catalase - genetics | Bacterial Proteins - genetics | Models, Molecular | Genotype | Treatment Outcome | Bacterial Toxins - chemistry | Phenotype | Protein Conformation | Polymorphism, Single Nucleotide | Mutation | Drug Resistance, Multiple, Bacterial - genetics | Catalase - chemistry | Mycobacterium tuberculosis - genetics | Medical colleges | Drug resistance in microorganisms | Biological products | Communicable diseases | Genomics | Genomes | Genetic polymorphisms | Tuberculosis | Codon | Analysis | Nucleotide sequencing | Drug therapy | DNA sequencing | Single nucleotide polymorphisms
Infectious Disease | Pulmonary/Respiratory | Drug resistance progression | Single nucleotide polymorphism | Mycobacterium tuberculosis | Whole genome sequencing | Isoniazid | Rifampin | CATALASE-PEROXIDASE | STRAINS | TOXIN-ANTITOXIN SYSTEMS | CONFERRING MUTATIONS | MICROBIOLOGY | KATG | IMMUNOLOGY | DISCOVERY | ISONIAZID RESISTANCE | GENE | RESPIRATORY SYSTEM | DNA | SEQUENCING DATA | Antitubercular Agents - adverse effects | Humans | Bacterial Proteins - chemistry | Tuberculosis - microbiology | Structure-Activity Relationship | Mycobacterium tuberculosis - drug effects | Tuberculosis - diagnosis | Microbial Sensitivity Tests | Mycobacterium tuberculosis - pathogenicity | Time Factors | DNA Mutational Analysis | Tuberculosis - drug therapy | Bacterial Toxins - genetics | Isoniazid - therapeutic use | Rifampin - therapeutic use | Antitubercular Agents - therapeutic use | Genome, Bacterial | Catalase - genetics | Bacterial Proteins - genetics | Models, Molecular | Genotype | Treatment Outcome | Bacterial Toxins - chemistry | Phenotype | Protein Conformation | Polymorphism, Single Nucleotide | Mutation | Drug Resistance, Multiple, Bacterial - genetics | Catalase - chemistry | Mycobacterium tuberculosis - genetics | Medical colleges | Drug resistance in microorganisms | Biological products | Communicable diseases | Genomics | Genomes | Genetic polymorphisms | Tuberculosis | Codon | Analysis | Nucleotide sequencing | Drug therapy | DNA sequencing | Single nucleotide polymorphisms
Journal Article
Molecular Microbiology, ISSN 0950-382X, 08/2008, Volume 69, Issue 4, pp. 827 - 840
Summary Overexpression of the MDR1 gene, encoding a multi‐drug efflux pump of the major facilitator superfamily, is a major cause of resistance to the widely...
ABC TRANSPORTERS CDR1 | CONTRIBUTE | VIRUS-INFECTED PATIENTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | GENE DISRUPTION | MICROBIOLOGY | DRUG-RESISTANCE | AZOLE ANTIFUNGAL AGENTS | UP-REGULATION | CONFERRING RESISTANCE | MOLECULAR-MECHANISMS | Antifungal Agents - pharmacology | Gene Expression Regulation, Fungal | Protein Structure, Tertiary | Promoter Regions, Genetic | Up-Regulation | Fluconazole - pharmacology | Drug Resistance, Multiple, Fungal - genetics | Transcriptional Activation | Molecular Sequence Data | Fungal Proteins - genetics | Transcription Factors - genetics | Loss of Heterozygosity | Candida albicans - genetics | Transcription Factors - metabolism | Candida albicans - drug effects | ATP-Binding Cassette, Sub-Family B, Member 1 - genetics | Recombination, Genetic | Base Sequence | Candida albicans - isolation & purification | Alleles | Genes, Regulator | Mutation | Fungal Proteins - metabolism | Gene mutations | Genetic aspects | Index Medicus
ABC TRANSPORTERS CDR1 | CONTRIBUTE | VIRUS-INFECTED PATIENTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | GENE DISRUPTION | MICROBIOLOGY | DRUG-RESISTANCE | AZOLE ANTIFUNGAL AGENTS | UP-REGULATION | CONFERRING RESISTANCE | MOLECULAR-MECHANISMS | Antifungal Agents - pharmacology | Gene Expression Regulation, Fungal | Protein Structure, Tertiary | Promoter Regions, Genetic | Up-Regulation | Fluconazole - pharmacology | Drug Resistance, Multiple, Fungal - genetics | Transcriptional Activation | Molecular Sequence Data | Fungal Proteins - genetics | Transcription Factors - genetics | Loss of Heterozygosity | Candida albicans - genetics | Transcription Factors - metabolism | Candida albicans - drug effects | ATP-Binding Cassette, Sub-Family B, Member 1 - genetics | Recombination, Genetic | Base Sequence | Candida albicans - isolation & purification | Alleles | Genes, Regulator | Mutation | Fungal Proteins - metabolism | Gene mutations | Genetic aspects | Index Medicus
Journal Article