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Cancer Letters, ISSN 0304-3835, 05/2017, Volume 394, pp. 22 - 32
Hepatitis B virus X protein (HBx) plays an important role in the progression of hepatocellular carcinoma. Here we reported that overexpression of HBx in... 
High mobility group box 1 | Calmodulin dependent protein kinase | Hepatocellular carcinoma | Metastasis | Hepatitis B virus X protein | CELLS | DNA-BINDING | PHOSPHATIDYLINOSITOL 3-KINASE | HMGB1 | RELEASE | HBX PROTEIN | LIVER-CANCER | IN-VITRO | ONCOLOGY | NUCLEAR FACTOR | NF-KAPPA-B | Hepatitis B - metabolism | Hepatitis B - genetics | Humans | Lung Neoplasms - metabolism | Middle Aged | Hepatitis B - virology | Male | Antineoplastic Agents - therapeutic use | Viral Load | Hepatitis B - complications | Time Factors | HMGB1 Protein - metabolism | Liver Neoplasms - pathology | Calcium Chelating Agents - pharmacology | HMGB1 Protein - antagonists & inhibitors | Liver Neoplasms - virology | Carcinoma, Hepatocellular - virology | Host-Pathogen Interactions | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - antagonists & inhibitors | Cell Movement - drug effects | Lung Neoplasms - prevention & control | Gene Expression Regulation, Viral | Hepatitis B virus - genetics | Liver Neoplasms - metabolism | Cell Line, Tumor | Mice, Inbred NOD | Hepatitis B virus - metabolism | DNA, Viral - genetics | Carcinoma, Hepatocellular - metabolism | Prognosis | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - metabolism | Carcinoma, Hepatocellular - secondary | Liver Neoplasms - therapy | Transfection | Lung Neoplasms - secondary | Trans-Activators - genetics | Female | Calcium Signaling | Proportional Hazards Models | Lung Neoplasms - virology | Mice, SCID | Antibodies - pharmacology | Xenograft Model Antitumor Assays | Animals | Calcium-Calmodulin-Dependent Protein Kinase Kinase - antagonists & inhibitors | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Trans-Activators - metabolism | Carcinoma, Hepatocellular - therapy | Protein Kinase Inhibitors - pharmacology | Medical colleges | Chromosomal proteins | Liver | Antibodies | Development and progression | Hepatoma | Viral antibodies | International cooperation | Analysis | Cellular signal transduction | Hepatitis B virus | Health aspects | Hepatitis B | Protein kinases | Calmodulin | Cell culture | Transcription factors | Ca2+/calmodulin-dependent protein kinase IV | Error analysis | Bcl-2 protein | Mobility | AKT protein | Mesothelioma | Biochemistry | ADP | Risk factors | Metastases | Proteins | Liver cancer | Hepatitis | Signal transduction | Cell activation | Ischemia | Surgery | Membrane potential | Deoxyribonucleic acid--DNA | Binding | Liver diseases | Biochemical analysis | Mortality | Activator protein 1 | Hazards | Regression analysis | Gene expression | Survival | 1-Phosphatidylinositol 3-kinase | Hypoxia | Viability | Biotechnology | Calcium | Viruses | Stimulation | Infections | Activation | Kinases | DNA repair | Carcinogenesis | Rodents | Bacteria | Calcium (intracellular) | Statistical analysis | Invasiveness | Tumor cells | Markers | Inflammation | Permeability | Computer programs | Cell death | Medical prognosis | Bcl protein | In vivo methods and tests | Cytoplasm | Apoptosis | Cancer
Journal Article
Journal Article
FEBS Letters, ISSN 0014-5793, 2004, Volume 557, Issue 1, pp. 73 - 80
Ligand activation of peroxisome proliferator‐activated receptor γ (PPARγ) has been reported to induce growth inhibition and apoptosis in various cancers... 
Peroxisome proliferator-activated receptor γ | Transactivation | Protein–protein interaction | Hepatitis B virus X protein | IFA, immunofluorescence assay | HBV, hepatitis B virus | HBx-TG, hepatitis B virus X protein transgenic | HBx, hepatitis B virus X protein | RXR, retinoid X receptor | DBD, DNA binding domain | NLS, nuclear localization signal | rHBx, recombinant hepatitis B virus X protein | PPARγ, peroxisome proliferator-activated receptor γ | PPRE, peroxisome proliferator response element | HA, hemagglutinin | NE, nuclear extract | HCC, hepatocellular carcinoma | EMSA, electrophoretic mobility shift assay | LBD, ligand binding domain | Protein-protein interaction | DNA-BINDING | TRANSCRIPTIONAL ACTIVITY | NUCLEAR RECEPTORS | BIOCHEMISTRY & MOLECULAR BIOLOGY | transactivation | CELL BIOLOGY | LIVER-CANCER | hepatitis B virus X protein | HUMAN PROSTATE-CANCER | HEPATOCELLULAR-CARCINOMA | BIOPHYSICS | RESPONSE ELEMENTS | protein-protein interaction | HEPATOMA-CELL LINES | peroxisome proliferator-activated receptor gamma | MOLECULAR-BASIS | TRANSGENIC MICE | Green Fluorescent Proteins | Adenoviridae | Transcription Factors - chemistry | Apoptosis - drug effects | Humans | Hepatitis B Antigens - chemistry | Protein Transport - drug effects | Trans-Activators - chemistry | Recombinant Fusion Proteins - metabolism | Recombinant Fusion Proteins - drug effects | Transcription Factors - drug effects | Transfection | Base Sequence | Receptors, Cytoplasmic and Nuclear - chemistry | Liver Neoplasms - pathology | Trans-Activators - pharmacology | Hepatitis B Antigens - pharmacology | Tumor Cells, Cultured | Genes, Reporter | Liver Neoplasms - virology | Cell Line | Receptors, Cytoplasmic and Nuclear - drug effects | Carcinoma, Hepatocellular - virology | Receptors, Cytoplasmic and Nuclear - genetics | Recombinant Fusion Proteins - chemistry | Transcription Factors - genetics | DNA Primers | Reverse Transcriptase Polymerase Chain Reaction | Cell Division - drug effects | Transcription Factors - metabolism | Carcinoma, Hepatocellular - pathology | Ligands | Luminescent Proteins - genetics | Trans-Activators - metabolism | Genetic Vectors | Receptors, Cytoplasmic and Nuclear - metabolism
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2017, Volume 12, Issue 1, p. e0169648
The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this... 
CELLS | NUCLEAR-BODIES | HEPATITIS-B-VIRUS | REPLICATION | DNA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | EPIGENETIC REGULATION | COMPONENTS | BINDING | HUMANIZED MICE | Autoantigens - metabolism | Hepatitis B - metabolism | Antigens, Nuclear - metabolism | Humans | Hepatitis B - virology | Male | Hepatocytes - metabolism | Autoantigens - genetics | Hepatitis B - immunology | Hepatocytes - cytology | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Promyelocytic Leukemia Protein - metabolism | Nuclear Proteins - genetics | Cytokines - genetics | Hepatitis B virus - immunology | Promyelocytic Leukemia Protein - genetics | Cytokines - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Chromosomal Proteins, Non-Histone | Nuclear Proteins - metabolism | Mice, SCID | Immunity, Innate - immunology | Animals | Antigens, Nuclear - genetics | Virus Replication | Trans-Activators - metabolism | Mice | Immune response | Analysis | Genetic aspects | Hepatitis B virus | Research | Genetic transcription | Hepatitis B | Cell culture | HBX protein | Pathogenesis | Viruses | Infections | Genomes | Degradation | Proteins | Hepatitis | Hepatology | Localization | Bioinformatics | Chromosomes | Deoxyribonucleic acid--DNA | Immune system | Antigens | Cytokines | Chromosome 5 | Gene expression | Ribonucleic acid--RNA | Hepatocytes | Interferon | Kinetics | X protein | RNA | Deoxyribonucleic acid | Ribonucleic acid
Journal Article
Scientific Reports, ISSN 2045-2322, 01/2017, Volume 7, Issue 1, p. 40783
Journal Article
Journal Article
Molecular Medicine Reports, ISSN 1791-2997, 02/2016, Volume 13, Issue 2, pp. 1345 - 1352
Transforming growth factor (TGF)-β induces cell growth arrest in well-differentiated hepatocellular carcinoma (HCC) while hepatitis B virus X protein (HBx)... 
cell growth | hepatitis B virus X protein | c-Jun N-terminal kinase inhibitor | transforming growth factor-β | hepatocellular carcinoma | C-Jun N-terminal kinase inhibitor | Hepatocellular carcinoma | Cell growth | Transforming growth factor-β | Hepatitis B virus X protein | SIGNAL | MEDICINE, RESEARCH & EXPERIMENTAL | TRANSCRIPTIONAL ACTIVATION | TGF-BETA | ONCOGENESIS | TUMOR SUPPRESSION | SMAD3 PHOSPHORYLATION | HBX PROTEIN | CANCER | transforming growth factor-beta | DIRECT BINDING | REPRESSION | ONCOLOGY | Humans | JNK Mitogen-Activated Protein Kinases - biosynthesis | Transforming Growth Factor beta - biosynthesis | Smad3 Protein - genetics | Proto-Oncogene Proteins c-myc - biosynthesis | Hepatitis B, Chronic - genetics | Smad4 Protein - genetics | Carcinoma, Hepatocellular - genetics | Trans-Activators - genetics | Liver Neoplasms - pathology | Gene Expression Regulation, Neoplastic - drug effects | JNK Mitogen-Activated Protein Kinases - genetics | Smad4 Protein - biosynthesis | Hepatitis B, Chronic - pathology | Liver Neoplasms - virology | Liver Neoplasms - genetics | Carcinoma, Hepatocellular - virology | Hepatitis B, Chronic - virology | Hepatitis B virus - drug effects | Protein Kinase Inhibitors - administration & dosage | Transforming Growth Factor beta - genetics | Signal Transduction - drug effects | Carcinoma, Hepatocellular - pathology | Hepatitis B virus - genetics | Cell Line, Tumor | Trans-Activators - metabolism | Cell Proliferation - drug effects | Proto-Oncogene Proteins c-myc - genetics | Biotechnology | Transcription factors | Transforming growth factor-b | c-Myc protein | Infections | Myc protein | Kinases | Smad4 protein | Proteins | Liver cancer | Signal transduction | Hepatitis | Cell activation | Rodents | Penicillin | Growth factors | Antiviral agents | Cytomegalovirus | Immunoglobulins | c-Jun protein | Gene expression | Lymphocytes B | Plasmids | Medical prognosis | X protein | Viral infections | Hepatitis B
Journal Article