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Nature medicine, ISSN 1546-170X, 2011, Volume 17, Issue 5, pp. 589 - 595
Hepatitis C virus (HCV) is a major cause of liver disease, but therapeutic options are limited and there are no prevention strategies. Viral entry is the first... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | B TYPE-I | NEUTRALIZING ANTIBODIES | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | FACTOR RECEPTOR | CELL BIOLOGY | EPIDERMAL-GROWTH-FACTOR | CELL TRANSMISSION | HUMAN LIVER | INFECTION | ERLOTINIB | Erlotinib Hydrochloride | RNA, Small Interfering - genetics | Receptor, Epidermal Growth Factor - genetics | Hepatitis C - therapy | Humans | Virus Internalization - drug effects | RNA Interference | Membrane Proteins - physiology | Base Sequence | Hepacivirus - physiology | Hepatitis C - prevention & control | Receptor, Epidermal Growth Factor - physiology | Hepacivirus - drug effects | Cell Line | Antiviral Agents - pharmacology | Receptor, EphA2 - physiology | Tetraspanin 28 | Claudin-1 | Animals | Hepatitis C - virology | Receptor, EphA2 - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antigens, CD - physiology | Hepatitis C - physiopathology | Ligands | Mice | Protein Kinase Inhibitors - pharmacology | Receptor, EphA2 - antagonists & inhibitors | Quinazolines - pharmacology | Host-Pathogen Interactions - physiology | Ephrin A | Antiviral agents | Care and treatment | Patient outcomes | Physiological aspects | Research | Hepatitis C | Hepatitis | Viruses | Drug therapy | Antiviral drugs | Receptor, EphA2 | Hépatology and Gastroenterology | Antigens, CD81 | Antiviral Agents | Quinazolines | Virus Internalization | Membrane Proteins | Host-Pathogen Interactions | Life Sciences | Human health and pathology | Protein Kinase Inhibitors | RNA, Small Interfering | Hepacivirus | Antigens, CD | Receptor, Epidermal Growth Factor | Liver | HCV escape variants | Cell-cell transmission | genetics | pharmacology | Antiviral | therapy | physiology | drug effects | prevention & control | antagonists & inhibitors | physiopathology | Phosphotyrosine kinase | virology
Journal Article
Placenta, ISSN 0143-4004, 2014, Volume 36, Issue 3, pp. 270 - 278
Abstract Introduction The epidermal growth factor (EGF) signaling system regulates trophoblast differentiation, and its disruption could contribute to... 
Internal Medicine | Obstetrics and Gynecology | Epidermal growth factors | Preeclampsia | Placenta | TROPHOBLAST CELLS | APOPTOSIS | OXIDATIVE STRESS | CYTOTROPHOBLASTS | EGF | HUMAN-PLACENTA | DEVELOPMENTAL BIOLOGY | FACTOR RECEPTOR | OBSTETRICS & GYNECOLOGY | WOMEN | RETARDATION | REPRODUCTIVE BIOLOGY | ENDOMETRIAL | Receptor, Epidermal Growth Factor - genetics | Humans | Trophoblasts - pathology | Young Adult | Receptor, Epidermal Growth Factor - metabolism | Protein Isoforms - metabolism | Protein Isoforms - chemistry | Transforming Growth Factor alpha - blood | Epidermal Growth Factor - chemistry | Heparin-binding EGF-like Growth Factor - blood | Peptide Fragments - blood | Adult | Female | Pre-Eclampsia - metabolism | Transforming Growth Factor alpha - metabolism | Peptide Fragments - metabolism | Trophoblasts - metabolism | Placentation | Down-Regulation | Epidermal Growth Factor - metabolism | Chorionic Villi - metabolism | Pre-Eclampsia - pathology | Epidermal Growth Factor - blood | Receptor, Epidermal Growth Factor - chemistry | Heparin-binding EGF-like Growth Factor - metabolism | Placenta - metabolism | Pregnancy | Chorionic Villi - pathology | Pre-Eclampsia - blood | Placenta - pathology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Line, Transformed | Apoptosis | Cohort Studies | Protein Isoforms - genetics | Physiological aspects | Medical colleges | Epidermal growth factor | Cells | placenta | epidermal growth factors | preeclampsia
Journal Article
Journal Article
Journal of Clinical Neuroscience, ISSN 0967-5868, 2009, Volume 16, Issue 6, pp. 748 - 754
Abstract Glioblastoma multiforme (GBM) is the most common brain tumour and has the worst prognosis. Epidermal growth factor receptor (EGFR) gene amplification,... 
Neurology | EGFRvIII | Therapy | Glioma | Signalling | TARGETED THERAPY | MONOCLONAL-ANTIBODY 425 | TYROSINE KINASE INHIBITION | PHASE-II | MOLECULAR DETERMINANTS | NEUROSCIENCES | CLINICAL NEUROLOGY | TUMOR XENOGRAFTS | FACTOR RECEPTOR EGFR | EPIDERMAL-GROWTH-FACTOR | RECURRENT MALIGNANT GLIOMAS | SIGNALING NETWORKS | Antibodies - therapeutic use | Receptor, Epidermal Growth Factor - genetics | Protein Binding - genetics | Biomarkers, Tumor - analysis | Humans | Brain Neoplasms - genetics | Protein Structure, Tertiary - genetics | Signal Transduction - genetics | Brain Neoplasms - metabolism | Receptor, Epidermal Growth Factor - chemistry | Antibodies - pharmacology | Glioblastoma - therapy | Glioblastoma - genetics | Cell Transformation, Neoplastic - genetics | Brain Neoplasms - therapy | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Glioblastoma - metabolism | Antineoplastic Agents - pharmacology | Receptor, Epidermal Growth Factor, genetics | Tumor Markers, Biological, analysis | Glioblastoma, therapy | Glioblastoma, metabolism | Protein Structure, Tertiary, genetics | Brain Neoplasms, genetics | Cell Transformation, Neoplastic, genetics | Glioblastoma, genetics | Antineoplastic Agents, pharmacology | Receptor, Epidermal Growth Factor, chemistry | Protein Binding, genetics | Antibodies, therapeutic use | Brain Neoplasms, metabolism | Antibodies, pharmacology | Brain Neoplasms, therapy | Receptor, Epidermal Growth Factor, antagonists and inhibitors | Signal Transduction, genetics
Journal Article
Nature (London), ISSN 1476-4687, 2013, Volume 506, Issue 7487, pp. 230 - 234
There are no clinically relevant treatments available that improve function in the growing population of very preterm infants (less than 32 weeks' gestation)... 
MULTIPLE-SCLEROSIS | LOW-BIRTH-WEIGHT | OLIGODENDROCYTE PROGENITORS | MULTIDISCIPLINARY SCIENCES | HYPOXIC INJURY | CENTRAL-NERVOUS-SYSTEM | MOUSE CORPUS-CALLOSUM | PRETERM INFANTS | RAT-BRAIN | WHITE-MATTER ABNORMALITIES | FACTOR RECEPTOR | Epidermal Growth Factor - administration & dosage | Oligodendroglia - metabolism | Receptor, Epidermal Growth Factor - genetics | Demyelinating Diseases - congenital | Brain Injuries - drug therapy | Humans | Brain Injuries - congenital | Male | Stem Cells - cytology | Demyelinating Diseases - metabolism | Epidermal Growth Factor - therapeutic use | Molecular Targeted Therapy | Stem Cells - metabolism | Cell Lineage - drug effects | Hypoxia - metabolism | Receptor, Epidermal Growth Factor - metabolism | Oligodendroglia - drug effects | Time Factors | Oligodendroglia - cytology | Demyelinating Diseases - pathology | Disease Models, Animal | Animals, Newborn | Cell Survival - drug effects | Demyelinating Diseases - prevention & control | Administration, Intranasal | Infant, Premature, Diseases - drug therapy | Cell Division - drug effects | Brain Injuries - prevention & control | Oligodendroglia - pathology | Hypoxia - genetics | Regeneration - drug effects | Animals | Signal Transduction - drug effects | Cell Differentiation - drug effects | Hypoxia - pathology | Stem Cells - drug effects | Hypoxia - physiopathology | Infant, Premature, Diseases - metabolism | Mice | Epidermal Growth Factor - pharmacology | Brain Injuries - pathology | Infant, Premature, Diseases - pathology | Brain | Medical research | Care and treatment | Infants (Premature) | Risk factors | Complications and side effects | Epidermal growth factor | Physiological aspects | Medicine, Experimental | Hypoxia | Diagnosis | Health aspects | Injuries | Brain damage | Attention Deficit Hyperactivity Disorder | Rodents | Apoptosis
Journal Article