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The Journal of cell biology, ISSN 0021-9525, 6/2002, Volume 157, Issue 6, pp. 929 - 939
Journal Article
Journal Article
European Journal of Cancer, ISSN 0959-8049, 2016, Volume 58, pp. 52 - 61
...). Interestingly, a strong reduction of ErbB-3 expression was observed in W12G. Loss of the E2 and E5 viral genes occurs in W12G and this may affect ErbB-3 receptor expression... 
Hematology, Oncology and Palliative Medicine | ErbB-3 | E2 protein | IHC | CIN | W12 cell line | Nrdp-1 | Cervical cancer | EGFR | HPV | TRANSFORMATION | GROWTH-FACTOR RECEPTOR | ELEMENT | ONCOLOGY | TRANSACTIVATION | HPV TYPE-16 | Cervical Intraepithelial Neoplasia - pathology | Receptor, ErbB-3 - metabolism | Cell Proliferation | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Uterine Cervical Neoplasms - pathology | DNA-Binding Proteins - metabolism | Papillomavirus Infections - pathology | Young Adult | Cervical Intraepithelial Neoplasia - enzymology | Ubiquitination | Transfection | Time Factors | Proteolysis | Adult | Female | Oncogene Proteins, Viral - genetics | Papillomavirus Infections - virology | Oncogene Proteins, Viral - metabolism | Genome, Viral | Uterine Cervical Neoplasms - enzymology | Papillomavirus Infections - enzymology | Ubiquitin-Protein Ligases - metabolism | Receptor, ErbB-3 - genetics | DNA-Binding Proteins - genetics | Uterine Cervical Neoplasms - genetics | Virus Integration | Human papillomavirus 16 - metabolism | Cervical Intraepithelial Neoplasia - virology | Papillomavirus Infections - genetics | Gene Expression Regulation, Enzymologic | Host-Pathogen Interactions | Gene Expression Regulation, Viral | Cell Line, Tumor | Protein Binding | Uterine Cervical Neoplasms - virology | Aged | Cervical Intraepithelial Neoplasia - genetics | Ubiquitin-Protein Ligases - genetics | Human papillomavirus 16 - genetics | Cell Transformation, Viral | Ubiquitin | Tyrosine | Genetic transcription | Ligases | Papillomavirus infections | Genomics
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, p. e0128360
.... In our work, we separately investigated the EGFR and ErbB-3 heterodimerization, regarded as the origin of intracellular signaling pathways... 
BREAST-CANCER | GROWTH-FACTOR RECEPTOR | ACTIVATION | EXON 19 | MECHANISM | MULTIDISCIPLINARY SCIENCES | C-MET | STRUCTURAL-ANALYSIS | TYROSINE KINASE INHIBITOR | FACTOR-I | CLINICAL-RESPONSE | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Receptor, ErbB-3 - metabolism | Humans | Thermodynamics | Protein Binding - drug effects | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Signal Transduction - genetics | Mutation - genetics | Molecular Dynamics Simulation | Receptor, Epidermal Growth Factor - chemistry | Disease-Free Survival | Regression Analysis | Drug Resistance, Neoplasm - genetics | Signal Transduction - drug effects | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Erlotinib Hydrochloride - pharmacology | Mutant Proteins - chemistry | Erlotinib Hydrochloride - therapeutic use | Protein Kinase Inhibitors - pharmacology | Structural Homology, Protein | Carcinoma, Non-Small-Cell Lung - drug therapy | Quinazolines - pharmacology | Protein Multimerization - drug effects | Care and treatment | Erlotinib | Analysis | Development and progression | Genetic aspects | Lung cancer, Non-small cell | Gefitinib | Health aspects | Energy consumption | Medical innovations | Lung cancer | Molecular dynamics | Intracellular signalling | Insulin-like growth factors | Drug resistance | Drug development | Kinases | Cancer therapies | c-Met protein | Proteins | Computational chemistry | Signal transduction | Cell growth | Epidermal growth factor | Pathways | Rodents | Dimerization | Protein-tyrosine kinase | Binding | Tyrosine | Dynamic structural analysis | Medical research | Computer simulation | Epidermal growth factor receptors | ErbB protein | Molecular interactions | Non-small cell lung carcinoma | Breast cancer | Lung carcinoma | ErbB-3 protein | Regression analysis | Survival | ErbB-2 protein | Free energy | Mutants | Studies | Inhibitors | Ligands | Mutation | Intracellular | Drug discovery | Binding sites | Structural analysis | Cancer
Journal Article
Journal Article
Cancer Research, ISSN 0008-5472, 10/2013, Volume 73, Issue 19, pp. 6024 - 6035
HER2/HER3 dimerization resulting from overexpression of HER2 or neuregulin (NRG1) in cancer leads to HER3-mediated oncogenic activation of phosphoinositide... 
BREAST-CANCER | EXTRACELLULAR REGION | COMPLEX | DOMAIN | ACTIVATION | ERBB3 | ONCOLOGY | AFFINITY | CRYSTAL-STRUCTURE | FACTOR RECEPTOR | TRASTUZUMAB RESISTANCE | Receptor, ErbB-3 - metabolism | Immunoprecipitation | Humans | Protein Conformation - drug effects | Receptor, ErbB-2 - metabolism | Immunoblotting | Receptor, ErbB-3 - chemistry | Breast Neoplasms - metabolism | Receptor, Epidermal Growth Factor - metabolism | Receptor, ErbB-3 - immunology | Antibodies, Monoclonal, Humanized - pharmacology | Female | Receptor, ErbB-2 - antagonists & inhibitors | Receptor, ErbB-2 - immunology | Phosphorylation - drug effects | Tumor Cells, Cultured | Proto-Oncogene Proteins c-akt - metabolism | Signal Transduction | Receptor, ErbB-3 - antagonists & inhibitors | Survival Rate | Mice, SCID | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - pathology | Mice, Nude | Neuregulin-1 - metabolism | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Breast Neoplasms - mortality | Mice, Inbred NOD | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | Protein Multimerization - drug effects | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | BASIC BIOLOGICAL SCIENCES | 60 APPLIED LIFE SCIENCES | PI-3 kinase | NRG | ligand-independent | Antibody | neuregulin | SCCHN | EGFR | resistance | feedback | HER | PIK3CA | cancer | HER2 | HER3 | ligand-dependent
Journal Article
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 09/2009, Volume 15, Issue 17, pp. 5445 - 5456
Purpose: The insulin-like growth factor (IGF) signaling axis is frequently dysregulated in hepatocellular carcinoma (HCC). Therefore, we investigated whether... 
targeted therapy | AVE1642 | gefitinib | HER3/erbB-3 | hepatocellular carcinoma | CANCER-CELLS | HUMAN HEPATOMA | ACTIVATION | ONCOLOGY | TYROSINE KINASE | MYELOMA CELLS | ACQUIRED-RESISTANCE | SENSITIVITY | CELL-LINES | MESENCHYMAL TRANSITION | EXPRESSION | Phosphorylation - physiology | Receptor, ErbB-3 - metabolism | Receptor, IGF Type 1 - antagonists & inhibitors | Antibiotics, Antineoplastic - pharmacology | Humans | Antibodies, Monoclonal - therapeutic use | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | Carcinoma, Hepatocellular - drug therapy | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Cell Survival - physiology | Cell Survival - drug effects | Antibodies, Monoclonal - pharmacology | Liver Neoplasms - drug therapy | Receptor, ErbB-3 - antagonists & inhibitors | Receptor, ErbB-3 - agonists | Sirolimus - pharmacology | Drug Synergism | Insulin - metabolism | Signal Transduction - drug effects | Liver Neoplasms - metabolism | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Signal Transduction - physiology | Quinazolines - pharmacology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Carcinoma, Hepatocellular - metabolism | RNA, Small Interfering - metabolism | Index Medicus
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2016, Volume 291, Issue 3, pp. 1029 - 1052
N-MYC downstream-regulated gene-1 (NDRG1) is a potent growth and metastasis suppressor that acts through its inhibitory effects on a wide variety of cellular... 
BREAST-CANCER | ISONICOTINOYL HYDRAZONE CLASS | ACTIVATED PROTEIN-KINASE | TGF-BETA | IRON CHELATORS | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | EPIDERMAL-GROWTH-FACTOR | EFFECTIVE ANTIPROLIFERATIVE AGENTS | PANCREATIC-CANCER | SELECTIVE ANTITUMOR-ACTIVITY | Receptor, ErbB-3 - metabolism | Pancreatic Neoplasms - metabolism | Receptor, ErbB-2 - genetics | Humans | Antineoplastic Agents - therapeutic use | Intracellular Signaling Peptides and Proteins - metabolism | Antineoplastic Agents - administration & dosage | Colonic Neoplasms - metabolism | RNA Interference | Receptor, ErbB-2 - antagonists & inhibitors | Intracellular Signaling Peptides and Proteins - genetics | ErbB Receptors - antagonists & inhibitors | Pancreatic Neoplasms - pathology | Cell Cycle Proteins - metabolism | Receptor, ErbB-3 - antagonists & inhibitors | Recombinant Proteins - chemistry | Random Allocation | Receptor, ErbB-3 - agonists | Receptor, ErbB-3 - genetics | Mice, Nude | Cell Line, Tumor | Receptor, ErbB-2 - agonists | Colonic Neoplasms - drug therapy | ErbB Receptors - genetics | Receptor, ErbB-2 - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Pancreatic Neoplasms - drug therapy | Cell Cycle Proteins - genetics | Female | Antineoplastic Agents - pharmacology | Thiosemicarbazones - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Pyridines - therapeutic use | Recombinant Proteins - metabolism | ErbB Receptors - metabolism | Epidermal Growth Factor - genetics | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Epidermal Growth Factor - metabolism | Cell Cycle Proteins - agonists | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Thiosemicarbazones - therapeutic use | Tumor Burden - drug effects | Colonic Neoplasms - pathology | Intracellular Signaling Peptides and Proteins - agonists | Epidermal Growth Factor - antagonists & inhibitors | Pyridines - pharmacology | ErbB Receptors - agonists | Molecular Bases of Disease | cancer therapy | anticancer drug | pharmaceutics | metastasis suppressor | molecular pharmacology | pharmacology | thiosemicarbazones | tumor cell biology | NDRG1 | Dp44mT
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2017, Volume 292, Issue 31, pp. 12772 - 12782
The iron-regulated metastasis suppressor N-myc downstream-regulated gene 1 (NDRG1) has been shown to inhibit numerous oncogenic signaling pathways in cancer... 
ANTIPROLIFERATIVE ACTIVITY | TGF-BETA | epidermal growth factor receptor (EGFR) | BIOCHEMISTRY & MOLECULAR BIOLOGY | PANCREATIC-CANCER | TYROSINE KINASES | NDRG1 | EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | cancer therapy | TUMOR-CELL MIGRATION | metastasis | cell signaling | PROSTATE-CANCER | GENE-1 NDRG1 | iron | SELECTIVE ANTITUMOR-ACTIVITY | Receptor, ErbB-3 - metabolism | Humans | Protein Multimerization | Receptor, ErbB-2 - chemistry | Receptor, ErbB-2 - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Receptor, ErbB-3 - chemistry | Receptors, Transferrin - agonists | Carcinogenesis | Antigens, CD - metabolism | Cell Cycle Proteins - chemistry | Endocytosis | Receptor, Epidermal Growth Factor - metabolism | Clathrin-Coated Vesicles | Proteolysis | Receptor, ErbB-2 - antagonists & inhibitors | Signal Transduction | Cell Cycle Proteins - metabolism | Receptor, ErbB-3 - antagonists & inhibitors | Receptor, ErbB-3 - agonists | Iron - metabolism | Receptors, Transferrin - metabolism | Receptor, Epidermal Growth Factor - chemistry | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Models, Biological | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Ligands | Endosomes - enzymology | Receptor, ErbB-2 - agonists | Transferrin - metabolism | Index Medicus | Minireviews
Journal Article
Nature Cell Biology, ISSN 1465-7392, 01/2018, Volume 20, Issue 1, pp. 46 - 57
Human pluripotent stem cells (hPSCs) can be directed to differentiate into skeletal muscle progenitor cells (SMPCs). However, the myogenicity of hPSC-SMPCs... 
PLURIPOTENT STEM-CELLS | DIRECTED DIFFERENTIATION | IN-VITRO | MYOGENIC DIFFERENTIATION | RNA-SEQ | FUNCTIONAL-ANALYSIS | DUCHENNE MUSCULAR-DYSTROPHY | SATELLITE CELLS | FETAL | LARGE GENE LISTS | CELL BIOLOGY | Receptor, ErbB-3 - metabolism | Humans | Middle Aged | PAX7 Transcription Factor - genetics | Male | PAX7 Transcription Factor - metabolism | Receptors, Nerve Growth Factor - metabolism | Muscle Fibers, Skeletal - metabolism | Myoblasts - metabolism | Gene Expression Regulation, Developmental | Myoblasts - cytology | Adult | Female | Myosins - metabolism | Cell Differentiation | Induced Pluripotent Stem Cells - cytology | Muscular Dystrophy, Duchenne - therapy | Dystrophin - metabolism | Induced Pluripotent Stem Cells - metabolism | Signal Transduction | Muscular Dystrophy, Duchenne - pathology | Receptor, ErbB-3 - genetics | Myosins - genetics | Nerve Tissue Proteins - genetics | Gene Editing | Receptors, Nerve Growth Factor - genetics | Nerve Tissue Proteins - metabolism | Transforming Growth Factor beta - genetics | Dystrophin - genetics | CRISPR-Cas Systems | Muscle Development - genetics | Muscle Fibers, Skeletal - cytology | Aged | Muscular Dystrophy, Duchenne - metabolism | Muscular Dystrophy, Duchenne - genetics | Transforming Growth Factor beta - metabolism | RNA sequencing | Usage | Growth | Stem cells | Muscle cells | Fetus | Research | Comparative analysis | Transforming growth factors | CRISPR | Satellite RNA | Fetuses | Muscles | Satellite cells | ErbB-3 protein | Ribonucleic acid--RNA | Cell surface | Myogenesis | Muscular dystrophy | Skeletal muscle | Gene sequencing | Musculoskeletal system | Signaling | Receptors | Nerve growth factor receptors | Duchenne's muscular dystrophy | Cells (biology) | Dystrophy | Differentiation | Dystrophin | Pluripotency
Journal Article