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Oncogene, ISSN 0950-9232, 09/2008, Volume 27, Issue 38, pp. 5115 - 5123
Cancer development results from deregulated control of stem cell populations and alterations in their surrounding environment. Notch signaling is an important... 
Epigenetics | Keratinocytes | Cancer stem cells | p63 | Rho signaling | p53 | SIGNALING PATHWAYS | RBP-J-KAPPA | HAIR FOLLICLE | BIOCHEMISTRY & MOLECULAR BIOLOGY | keratinocytes | BETA-CATENIN | P53 HOMOLOG | epigenetics | CELL BIOLOGY | ONCOLOGY | GROWTH ARREST | CERVICAL-CANCER CELLS | GENETICS & HEREDITY | NEGATIVE TRANSCRIPTIONAL REGULATOR | KERATINOCYTE STEM-CELLS | cancer stem cells | NF-KAPPA-B | Species Specificity | Keratinocytes - radiation effects | Humans | Receptors, Notch - genetics | Tumor Suppressor Protein p53 - physiology | Neoplasms - virology | Neoplasms - genetics | Cell Transformation, Neoplastic - genetics | Tumor Virus Infections - physiopathology | Tumor Suppressor Proteins - genetics | Female | Neoplasms - physiopathology | Cell Differentiation - physiology | Genes, Tumor Suppressor | Oncogene Proteins, Viral - physiology | Receptors, Notch - physiology | Uterine Cervical Neoplasms - physiopathology | Uterine Cervical Neoplasms - genetics | Ultraviolet Rays - adverse effects | Tumor Suppressor Proteins - physiology | Keratinocytes - pathology | Animals | Uterine Cervical Neoplasms - virology | Signal Transduction - physiology | Mice | Apoptosis - physiology | DNA Damage | Receptor, Notch1 - genetics | Receptor, Notch1 - physiology | Care and treatment | Tumor suppressor genes | Cellular signal transduction | Genetic aspects | Research | Health aspects | Risk factors | Cancer | Signal transduction | Gene expression | Stem cells | Cell cycle | cancer therapy | carcinogenesis
Journal Article
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2012, Volume 7, Issue 12, p. e52580
Journal Article
The EMBO Journal, ISSN 0261-4189, 12/2005, Volume 24, Issue 23, pp. 4018 - 4028
Viral infection or TLR3 engagement causes activation of the transcription factors IRF‐3 and NF‐κB, which collaborate to induce transcription of type I IFN... 
NF‐κB | TBK1 | antiviral response | IKKε | IRF‐3 | IRF-3 | NF-κB | Antiviral response | TRANSCRIPTION FACTORS | DOUBLE-STRANDED-RNA | COMPLEX | IKK-EPSILON | BIOCHEMISTRY & MOLECULAR BIOLOGY | TANK-BINDING KINASE-1 | VIRAL-INFECTION | BETA | CELL BIOLOGY | NF-kappa B | IKK epsilon | SIGNALING PATHWAY | NF-KAPPA-B | ANTIVIRAL IMMUNITY | Humans | Molecular Sequence Data | NF-kappa B - metabolism | Toll-Like Receptor 3 - antagonists & inhibitors | Adaptor Proteins, Vesicular Transport - metabolism | I-kappa B Kinase - physiology | Protein Kinase Inhibitors - chemistry | I-kappa B Kinase - metabolism | Interferon-beta - genetics | Response Elements - physiology | Intracellular Signaling Peptides and Proteins - genetics | Herpesvirus 3, Human - physiology | Protein-Serine-Threonine Kinases - metabolism | Amino Acid Sequence | Promoter Regions, Genetic | Receptors, Retinoic Acid - metabolism | Protein Kinase Inhibitors - isolation & purification | Interferon-beta - antagonists & inhibitors | Interferon Regulatory Factor-3 - physiology | Toll-Like Receptor 3 - physiology | Animals | Poly I-C - metabolism | Interferon Regulatory Factor-3 - antagonists & inhibitors | Intracellular Signaling Peptides and Proteins - isolation & purification | Signal Transduction - physiology | Mice | Intracellular Signaling Peptides and Proteins - physiology
Journal Article
PLoS Pathogens, ISSN 1553-7366, 07/2017, Volume 13, Issue 7, p. e1006503
Myeloid-derived suppressor cells (MDSCs) are expanded in tumor microenvironments, including that of Epstein-Barr virus (EBV)-associated nasopharyngeal... 
AIM2 INFLAMMASOME | CANCER CELLS | INFLAMMASOME ACTIVATION | MICROBIOLOGY | NLRP3 INFLAMMASOME | VIROLOGY | EPITHELIAL-CELLS | GLUCOSE-METABOLISM | AEROBIC GLYCOLYSIS | NF-KAPPA-B | GLUT1 EXPRESSION | EPSTEIN-BARR-VIRUS | PARASITOLOGY | Nasopharyngeal Neoplasms - genetics | Nasopharyngeal Neoplasms - metabolism | Viral Matrix Proteins - genetics | Cell Proliferation | Herpesvirus 4, Human - genetics | Granulocyte-Macrophage Colony-Stimulating Factor - metabolism | Humans | Carcinoma - virology | Gene Expression Regulation, Neoplastic | Nasopharyngeal Neoplasms - virology | Nasopharyngeal Neoplasms - physiopathology | Myeloid-Derived Suppressor Cells - cytology | Epstein-Barr Virus Infections - genetics | Viral Matrix Proteins - metabolism | Interleukin-6 - metabolism | Myeloid-Derived Suppressor Cells - metabolism | Epstein-Barr Virus Infections - physiopathology | Nasopharyngeal Carcinoma | Epstein-Barr Virus Infections - virology | Interleukin-6 - genetics | Signal Transduction | Carcinoma - physiopathology | Granulocyte-Macrophage Colony-Stimulating Factor - genetics | Host-Pathogen Interactions | Cell Line, Tumor | Glycolysis | Carcinoma - genetics | Carcinoma - metabolism | Herpesvirus 4, Human - metabolism | Epstein-Barr Virus Infections - metabolism | Genetic aspects | Epstein-Barr virus | Research | Nasopharyngeal cancer | Membrane proteins | Laboratories | Viruses | Oncology | Infections | In vitro testing | Suppressor cells | Degradation | Interleukin 6 | Proteins | Nasopharyngeal carcinoma | Mitochondria | Ubiquitination | Interleukin 1 | Life sciences | Expansion | Glucose transporter | Biodegradation | GLUT1 protein | Granulocyte-macrophage colony-stimulating factor | Roles | Gene expression | Medicine | Immunosuppression | Collaboration | Microenvironments | Cyclooxygenase-2 | Transporter | Cancer | Latent membrane protein 1 | Tumors
Journal Article
European Journal of Immunology, ISSN 0014-2980, 06/2017, Volume 47, Issue 6, pp. 1022 - 1031
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2017, Volume 12, Issue 2, p. e0171812
Human cytomegalovirus (HCMV) is a species-specific beta-herpesvirus that infects for life up to 80% of the world's population and causes severe morbidity in... 
INTERFERON | ACTIVATION | VIRUS | REPLICATION | TYROSINE PHOSPHORYLATION | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | NEGATIVE REGULATORS | NECROSIS-FACTOR-ALPHA | PROTEINS | Suppressor of Cytokine Signaling 1 Protein - genetics | Macrophages - pathology | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Up-Regulation - genetics | Suppressor of Cytokine Signaling 1 Protein - metabolism | Suppressor of Cytokine Signaling 3 Protein - genetics | Herpesviridae Infections - pathology | Macrophages - metabolism | Animals | Macrophages - virology | Host-Pathogen Interactions - genetics | Muromegalovirus - physiology | Herpesviridae Infections - metabolism | Female | Transcription, Genetic | Mice | Mice, Inbred BALB C | Herpesviridae Infections - genetics | Suppressor of Cytokine Signaling 3 Protein - metabolism | Cytomegalovirus infections | Care and treatment | Macrophages | Gene expression | Analysis | Risk factors | Cell culture | Regulators | Phosphorylation | Tegument | Laboratories | Glands | Tissue culture | Viruses | Retina | Stimulation | Biology | Infections | Kinases | Proteins | Signal transduction | Ganciclovir | Negative feedback | Immunology | Acquired immune deficiency syndrome--AIDS | Rodents | Fibroblasts | Deoxyribonucleic acid--DNA | Cytomegalovirus | Cytokines | Salivary glands | Embryo fibroblasts | SOCS-1 protein | Embryos | Suppressors | Morbidity | Signaling | Retinitis | Viral infections | Acquired immune deficiency syndrome | Deoxyribonucleic acid | AIDS | DNA
Journal Article