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Nature Medicine, ISSN 1078-8956, 07/2018, Volume 24, Issue 7, pp. 954 - 960
The ubiquitously expressed non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, is involved in signal transduction downstream of multiple growth... 
MEDICINE, RESEARCH & EXPERIMENTAL | PANCREATIC DUCTAL ADENOCARCINOMA | TYROSINE PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL BIOLOGY | COLON-CANCER | SHP2 | INHIBITION | K-RAS | CELL LUNG-CARCINOMA | MOUSE MODEL | PROGRESSION | PHOSPHOTYROSINE PHOSPHATASE | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Pancreatic Neoplasms - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Lung Neoplasms - metabolism | Pancreatic Neoplasms - pathology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Lung Neoplasms - pathology | Mutation - genetics | Carcinogenesis - metabolism | Disease Progression | Carcinogenesis - pathology | Mitogen-Activated Protein Kinase Kinases - metabolism | Animals | Protein Kinase Inhibitors - therapeutic use | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - deficiency | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Tyrosine | Care and treatment | Cellular signal transduction | Genetic aspects | Research | Gene expression | Cancer | Adenocarcinoma | Animal models | Xenotransplantation | Lung cancer | Phosphatase | Carcinogenesis | K-Ras protein | Proteins | Signal transduction | Carcinogens | Allosteric properties | Clonal deletion | Organoids | Dependence | Xenografts | Deletion | Protein-tyrosine kinase receptors | Inhibition | Pancreas | Protein-tyrosine kinase | MAP kinase | Tumor cell lines | Signaling | Transduction | Tumors | Protein-tyrosine-phosphatase | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7610, pp. 148 - 152
The non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, has an important role in signal transduction downstream of growth factor receptor... 
TARGET | POTENT | PTPN11 | PROTOONCOGENE | MULTIDISCIPLINARY SCIENCES | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Humans | Extracellular Signal-Regulated MAP Kinases - metabolism | Oncogene Protein p21(ras) - metabolism | Pyrimidines - chemistry | Piperidines - pharmacology | Inhibitory Concentration 50 | Female | Allosteric Regulation - drug effects | Piperidines - chemistry | Reproducibility of Results | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - antagonists & inhibitors | Models, Molecular | Neoplasms - enzymology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - chemistry | Pyrimidines - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Mice, Nude | Piperidines - therapeutic use | Pyrimidines - therapeutic use | Protein Stability - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Neoplasms - pathology | Protein Structure, Tertiary - drug effects | Phosphatases | Observations | Health aspects | Phosphotransferases | Protein-protein interactions | Signal transduction | Cell growth | Peptides | Kinases | Phosphatase | Drug dosages | Cancer | Index Medicus | BASIC BIOLOGICAL SCIENCES
Journal Article
Nature Genetics, ISSN 1061-4036, 07/2016, Volume 48, Issue 7, pp. 747 - 757
Genome-wide association studies have identified several loci associated with pancreatic cancer risk; however, the mechanisms by which genetic factors influence... 
U-BOX | REGULATORY RNA | RETINOIC ACID | LONG NONCODING RNA | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | GENE-EXPRESSION | SUSCEPTIBILITY LOCI | UBIQUITIN LIGASES | IDENTIFY MULTIPLE | GENOME-WIDE ASSOCIATION | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Cell Proliferation | Pancreatic Neoplasms - metabolism | Humans | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Case-Control Studies | RNA Splicing Factors - metabolism | STAT1 Transcription Factor - metabolism | Ubiquitination | Proteolysis | DNA Repair Enzymes - metabolism | src-Family Kinases - metabolism | Nuclear Proteins - genetics | Binding Sites | Genome-Wide Association Study | Signal Transduction | Pancreatic Neoplasms - pathology | Nuclear Proteins - metabolism | Pancreatic Neoplasms - genetics | RNA, Long Noncoding - genetics | Pancreas - metabolism | RNA Splicing Factors - genetics | STAT1 Transcription Factor - genetics | Polymorphism, Single Nucleotide - genetics | MicroRNAs - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | src-Family Kinases - genetics | MicroRNA | Phosphatases | Genetic variation | Pancreatic cancer | Development and progression | Genetic aspects | Properties | Health aspects | Proteins | Studies | Confidence intervals | Research & development--R&D | Genomes | Mutation | Gene expression | Phosphatase | Cancer | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 04/2012, Volume 18, Issue 4, pp. 529 - 537
New cancer therapies are likely to arise from an in-depth understanding of the signaling networks influencing tumor initiation, progression and metastasis. We... 
MEDICINE, RESEARCH & EXPERIMENTAL | PROTEIN | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | NOONAN-SYNDROME | CELL BIOLOGY | GENE | STEM-CELL | MYELOID-LEUKEMIA | DIFFERENTIATION | MUTATIONS | IN-VITRO PROPAGATION | DUCTAL CARCINOMA | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Autoantigens - metabolism | Cell Proliferation | Oligonucleotide Array Sequence Analysis | Homeodomain Proteins - metabolism | Humans | Caspase 3 - metabolism | Receptor, ErbB-2 - metabolism | Ki-67 Antigen - metabolism | Gene Expression Profiling | Flow Cytometry | Time Factors | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Female | Membrane Proteins - metabolism | Gene Expression Regulation, Neoplastic - drug effects | Tumor Cells, Cultured | Gene Expression Regulation, Neoplastic - physiology | Computational Biology | Transcription Factors - genetics | Mice, SCID | src Homology Domains - physiology | Cell Adhesion Molecules - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Disease Progression | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Animals | Breast Neoplasms - pathology | Cell Polarity - physiology | Doxycycline - pharmacology | Luminescent Proteins - genetics | Signal Transduction - physiology | Mice | Proto-Oncogene Proteins c-myc - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Cell Transformation, Neoplastic - pathology | Luminescent Proteins - metabolism | Mitogen-Activated Protein Kinases - metabolism | RNA, Small Interfering - metabolism | Zinc Finger E-box-Binding Homeobox 1 | Transcription factors | Care and treatment | Phosphatases | Physiological aspects | Development and progression | Genetic aspects | Breast cancer | Research | Proteins | Signal transduction | Cellular biology | Gene expression | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 5, pp. 629 - 639
The human gene , which encodes the tyrosine phosphatase Shp2, may act as a proto-oncogene because dominantly activating mutations have been detected in several... 
BREAST-CANCER | CELLS | ACTIVATION | HUMAN-DISEASE | ONCOLOGY | SHP2 TYROSINE PHOSPHATASE | INFLAMMATION | STAT3 | LIVER | MUTATIONS | DIFFERENTIATION | CELL BIOLOGY | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Carcinoma, Hepatocellular - chemically induced | Liver - pathology | Hepatitis - enzymology | Liver - enzymology | Carcinoma, Hepatocellular - prevention & control | Humans | Hyperplasia | Lipopolysaccharides - administration & dosage | Adenoma, Liver Cell - pathology | Liver Neoplasms - chemically induced | Male | Necrosis | Liver - drug effects | Time Factors | Tumor Suppressor Proteins - deficiency | Carcinoma, Hepatocellular - genetics | Diethylnitrosamine | Hepatitis - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - deficiency | Tumor Suppressor Proteins - genetics | STAT3 Transcription Factor - deficiency | Liver Neoplasms - pathology | Adenoma, Liver Cell - enzymology | Liver Neoplasms - enzymology | Cytokines - genetics | Interleukin-6 - administration & dosage | Adenoma, Liver Cell - genetics | STAT3 Transcription Factor - genetics | Cytokines - blood | Liver Neoplasms - prevention & control | Liver Regeneration | Tumor Suppressor Proteins - metabolism | Liver Neoplasms - genetics | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Inflammation Mediators - blood | Hepatitis - pathology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - analysis | Carcinoma, Hepatocellular - enzymology | Mice, Knockout | Animals | Carcinoma, Hepatocellular - pathology | Mice | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Tyrosine | Liver cancer | Development and progression | Phosphatases | Leukemia | Index Medicus
Journal Article
Journal Article
Nature, ISSN 0028-0836, 06/2010, Volume 465, Issue 7299, pp. 808 - 812
The generation of reprogrammed induced pluripotent stem cells (iPSCs) from patients with defined genetic disorders holds the promise of increased understanding... 
SOMATIC PTPN11 MUTATIONS | SHP2 MUTATIONS | HUMAN ES | HEMATOPOIESIS | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | DISEASE | LEUKEMOGENESIS | DIFFERENTIATION | LEUKEMIA | FIBROBLASTS | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Embryonic Stem Cells - metabolism | Humans | Male | Gene Expression Profiling | LEOPARD Syndrome - drug therapy | Octamer Transcription Factor-3 - genetics | Phosphoproteins - analysis | SOXB1 Transcription Factors - genetics | Polymerase Chain Reaction | Adult | Female | Cell Differentiation | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Precision Medicine | Induced Pluripotent Stem Cells - pathology | Cell Line | Induced Pluripotent Stem Cells - enzymology | Nanog Homeobox Protein | LEOPARD Syndrome - metabolism | NFATC Transcription Factors - metabolism | Cells, Cultured | Fibroblasts - pathology | Homeodomain Proteins - genetics | Cell Lineage | Myocytes, Cardiac - pathology | Models, Biological | LEOPARD Syndrome - pathology | Myocytes, Cardiac - metabolism | Enzyme Activation | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Mitogen-Activated Protein Kinases - metabolism | NFATC Transcription Factors - genetics | Proteins | Signal transduction | Insects | Genes | Cardiomyocytes | Mutation | Kinases | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2013, Volume 499, Issue 7459, pp. 491 - 495
The tyrosine phosphatase SHP2, encoded by PTPN11, is required for the survival, proliferation and differentiation of various cell types(1,2). Germline... 
ENCHONDROMATOSIS | RANVIER | OSTEOCLASTS | MULTIDISCIPLINARY SCIENCES | OSSIFICATION GROOVE | PERICHONDRIAL RING | CELL PROLIFERATION | RECEPTOR | OSTEOGENESIS | CHONDROGENESIS | CARTILAGE | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Cartilage - pathology | Hedgehog Proteins - metabolism | Monocytes - metabolism | Bone Neoplasms - pathology | Bone Neoplasms - metabolism | MAP Kinase Signaling System | Fibroblast Growth Factors - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Mesenchymal Stromal Cells - cytology | Cell Division | Gene Deletion | Genes, Tumor Suppressor - physiology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - deficiency | Exostoses, Multiple Hereditary - genetics | Bone Neoplasms - genetics | Bone Neoplasms - drug therapy | Osteopetrosis - genetics | Osteopetrosis - pathology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Exostoses, Multiple Hereditary - metabolism | Mesenchymal Stromal Cells - metabolism | Mice, Transgenic | Osteopetrosis - metabolism | Chondromatosis - metabolism | Hedgehog Proteins - antagonists & inhibitors | Cartilage - metabolism | Osteoclasts - metabolism | Parathyroid Hormone-Related Protein - metabolism | Exostoses, Multiple Hereditary - pathology | Mice, Knockout | Exostoses, Multiple Hereditary - drug therapy | Gene Expression Regulation - drug effects | Cell Lineage | Cathepsin K - genetics | Macrophages - metabolism | Animals | Chondromatosis - drug therapy | Cathepsin K - metabolism | Chondromatosis - genetics | Signal Transduction - drug effects | Chondromatosis - pathology | Mice | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Cathepsin K - deficiency | Tyrosine | Phosphatases | Physiological aspects | Cellular signal transduction | Research | Bone diseases | Health aspects | Hedgehog proteins | Flow cytometry | Pathogenesis | Rodents | Bone density | Mutation | Kinases | Gene expression | Index Medicus
Journal Article
Journal Article