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Journal of Biological Chemistry, ISSN 0021-9258, 12/2012, Volume 287, Issue 50, pp. 42352 - 42360
Interferons (IFNs) have important antiviral and antineoplastic properties, but the precise mechanisms required for generation of these responses remain to be... 
KINASE PATHWAY | ACTIVATION | ANTAGONIST | I INTERFERONS | PHOSPHORYLATION | MAP KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | GENES | GENERATION | CELLS RESPOND | Humans | Hematopoietic Stem Cells - pathology | Polycythemia Vera - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | Embryo, Mammalian - metabolism | MAP Kinase Signaling System | Polycythemia Vera - metabolism | U937 Cells | Interferon Type I - metabolism | Membrane Proteins - metabolism | Receptor, Interferon alpha-beta - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Polycythemia Vera - pathology | Intracellular Signaling Peptides and Proteins - genetics | Fibroblasts - metabolism | Receptor, Interferon alpha-beta - metabolism | Embryo, Mammalian - pathology | Membrane Proteins - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Hematopoietic Stem Cells - metabolism | Phosphoproteins - genetics | Fibroblasts - pathology | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Adaptor Proteins, Signal Transducing | Animals | Interferon Type I - genetics | Mice | MAP Kinases (MAPKs) | Signal Transduction | Cytokines | Cytokine | Cytokine Action | Innate Immunity | Antiviral Agents | Interferon | Polycythemia Vera | Protein Degradation
Journal Article
FASEB Journal, ISSN 0892-6638, 02/2012, Volume 26, Issue 2, pp. 894 - 906
The JAK2 mutation V617F is detectable in a majority of patients with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs). Enforced expression... 
Microenvironment | Cytokines | Fibrosis | Cancer | COLLAGEN PRODUCTION | POLYCYTHEMIA-VERA | BIOCHEMISTRY & MOLECULAR BIOLOGY | PRIMARY MYELOFIBROSIS | HEMATOPOIETIC PROGENITORS | CELL BIOLOGY | microenvironment | SIGNAL-TRANSDUCTION | CD34(+) CELLS | M RECEPTOR | MOUSE MODEL | BIOLOGY | TYROSINE KINASE JAK2 | cancer | cytokines | fibrosis | CELL-LINE | Humans | Neovascularization, Pathologic | Polycythemia Vera - genetics | Thrombocythemia, Essential - pathology | Myeloproliferative Disorders - pathology | Phosphatidylinositol 3-Kinases - metabolism | Mutation, Missense | Primary Myelofibrosis - pathology | RNA, Messenger - metabolism | Thrombocythemia, Essential - genetics | Myeloproliferative Disorders - genetics | Case-Control Studies | Gene Knockdown Techniques | Polycythemia Vera - metabolism | STAT5 Transcription Factor - metabolism | Base Sequence | Bone Marrow - metabolism | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Oncostatin M - metabolism | Polycythemia Vera - pathology | Janus Kinase 2 - antagonists & inhibitors | Primary Myelofibrosis - metabolism | Cell Line | RNA, Messenger - genetics | Janus Kinase 2 - genetics | Mutant Proteins - genetics | Mutant Proteins - metabolism | Oncostatin M - blood | Primary Myelofibrosis - genetics | Animals | Bone Marrow - pathology | Mice | Cytokines - biosynthesis | Oncostatin M - genetics | Thrombocythemia, Essential - metabolism | Amino Acid Substitution
Journal Article
Leukemia, ISSN 0887-6924, 2007, Volume 21, Issue 8, pp. 1658 - 1668
JAK2V617F and MPLW515L/K represent recently identified mutations in myeloproliferative disorders (MPD) that cause dysregulated JAK-STAT signaling, which is... 
MYELOFIBROSIS | JAK2(V617F) | POLYCYTHEMIA-VERA | ESSENTIAL THROMBOCYTHEMIA | JAK2V617F | myeloproliferative disorder | mutation | kinase inhibitor | MEGAKARYOBLASTIC LEUKEMIA | ACTIVATING MUTATION | ONCOLOGY | V617F | ACUTE LYMPHOBLASTIC-LEUKEMIA | JAK2 | HEMATOLOGY | MYELOID METAPLASIA | fms-Like Tyrosine Kinase 3 - antagonists & inhibitors | Apoptosis - drug effects | Humans | STAT Transcription Factors - metabolism | Polycythemia Vera - genetics | Myeloproliferative Disorders - genetics | Janus Kinase 3 - antagonists & inhibitors | Polycythemia Vera - metabolism | fms-Like Tyrosine Kinase 3 - genetics | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Colony-Forming Units Assay | Phosphorylation - drug effects | Janus Kinase 3 - metabolism | Janus Kinase 2 - antagonists & inhibitors | Primary Myelofibrosis - metabolism | Primary Myelofibrosis - drug therapy | Thrombopoietin - metabolism | Enzyme Inhibitors - pharmacology | Janus Kinase 2 - genetics | Myeloproliferative Disorders - drug therapy | Pyrimidines - pharmacology | Mice, SCID | Mutation - genetics | Sulfonamides - pharmacology | Receptors, Thrombopoietin - metabolism | Receptors, Thrombopoietin - antagonists & inhibitors | fms-Like Tyrosine Kinase 3 - metabolism | Receptors, Thrombopoietin - genetics | Primary Myelofibrosis - genetics | Animals | Janus Kinase 3 - genetics | Stem Cells - drug effects | Polycythemia Vera - drug therapy | Cell Proliferation - drug effects | Mice | Cell Cycle - drug effects | Antibody diversity | Chemical inhibitors | Genetic aspects | Research | Health aspects | Myeloproliferative disorders
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 2016, Volume 213, Issue 2, pp. 273 - 290
Journal Article
Journal of Molecular Medicine, ISSN 0946-2716, 1/2013, Volume 91, Issue 1, pp. 59 - 67
In Chuvash polycythemia, a homozygous 598C>T mutation in the von Hippel–Lindau gene (VHL) leads to an R200W substitution in VHL protein, impaired degradation... 
Human Genetics | Hypoxia-inducible factors | Biomedicine | Glycolysis | Internal Medicine | Molecular Medicine | VHL | Glucose | Insulin | Gluconeogenesis | MEDICINE, RESEARCH & EXPERIMENTAL | HYPOXIA-INDUCIBLE FACTOR | CELLS | PROMOTES GLYCOGEN ACCUMULATION | THROMBOSIS | ERYTHROPOIESIS | DEFICIENCY | GENETICS & HEREDITY | MICE | OXYGEN HOMEOSTASIS | EXPRESSION | Glucose Transport Proteins, Facilitative - metabolism | Polycythemia - genetics | Glucose-6-Phosphatase - genetics | Glycated Hemoglobin A - metabolism | Humans | Middle Aged | Polycythemia - blood | Male | Muscle, Skeletal - metabolism | Pyruvate Dehydrogenase Complex - genetics | Insulin - blood | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Adult | Female | Von Hippel-Lindau Tumor Suppressor Protein - genetics | Glucose Transport Proteins, Facilitative - genetics | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Pyruvate Dehydrogenase Complex - metabolism | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Liver - metabolism | Gene Expression Regulation | Genotype | Glucose-6-Phosphatase - metabolism | Homozygote | Hypoxia - blood | Hypoxia - genetics | Animals | Alleles | Hypoxia - physiopathology | Mice | Polycythemia - physiopathology | Mutation | Blood Glucose - metabolism | Glucose metabolism | Transcription factors | Polycythemia | Physiological aspects | Development and progression | Genetic aspects | Research | High altitude | Hypoxia-inducible factor 1 | Transcription | Liver | Genes | Inactivation | Degradation | Rodents | Hemoglobin | Skeleton | Glucose transporter | Enzymes | Fasting | Deactivation | Diabetes mellitus | Glycerol | Pharmacology | Hypoglycemia | Gene expression | Metabolism | Patients | Citric acid | Skeletal muscle | Homozygotes | Hippel-Lindau gene | Hypoxia | Neoplasia | glucose | hypoxia inducible factors | insulin | gluconeogenesis | glycolysis
Journal Article
Journal Article
Journal Article
American Journal of Hematology, ISSN 0361-8609, 05/2013, Volume 88, Issue 5, pp. 355 - 358
Myeloproliferative neoplasms (MPNs) are malignant disorders originating from clonal expansion of a single neoplastic stem cell and characteristically show an... 
MYELOFIBROSIS | PATHOGENESIS | GROWTH-FACTOR-BETA | COLLAGEN | CONSENSUS | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | MYELOID METAPLASIA | BONE-MARROW FIBROSIS | TGF-BETA-1 | Thrombocythemia, Essential - enzymology | Humans | Gene Expression Regulation, Neoplastic | Thrombocythemia, Essential - pathology | Bone Marrow - enzymology | Myeloproliferative Disorders - pathology | Primary Myelofibrosis - pathology | Neoplasm Proteins - metabolism | RNA, Messenger - metabolism | Amino Acid Oxidoreductases - metabolism | Amino Acid Oxidoreductases - genetics | Polycythemia Vera - metabolism | Myeloproliferative Disorders - blood | In Situ Hybridization | Isoenzymes - metabolism | Bone Marrow - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Myeloproliferative Disorders - metabolism | Polycythemia Vera - pathology | Neoplasm Proteins - genetics | Primary Myelofibrosis - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Isoenzymes - genetics | Polycythemia Vera - enzymology | Primary Myelofibrosis - enzymology | Image Processing, Computer-Assisted | Bone Marrow - pathology | Fibrosis | Protein-Lysine 6-Oxidase - metabolism | Amino Acid Oxidoreductases - blood | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Neoplasm Proteins - blood | Protein-Lysine 6-Oxidase - blood | Protein-Lysine 6-Oxidase - genetics | Thrombocythemia, Essential - metabolism | Cohort Studies
Journal Article