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Cancer cell, ISSN 1535-6108, 2012, Volume 22, Issue 2, pp. 153 - 166
... ALL). The genetic alterations that activate kinase signaling in Ph-like ALL are poorly understood... 
GROWTH-FACTOR RECEPTOR | BCR-JAK2 FUSION GENE | ONCOLOGY | NUCLEAR-PORE | MYELOPROLIFERATIVE NEOPLASMS | ACUTE MYELOID-LEUKEMIA | OF-FUNCTION MUTATIONS | FLT3 MUTATIONS | CHILDHOOD | B-PROGENITOR | CHRONIC MYELOMONOCYTIC LEUKEMIA | CELL BIOLOGY | Recurrence | Humans | Molecular Sequence Data | RNA, Messenger - metabolism | Receptor, Platelet-Derived Growth Factor beta - genetics | Protein-Tyrosine Kinases - genetics | DNA Mutational Analysis | Base Sequence | Trans-Activators - genetics | Phosphorylation - drug effects | Philadelphia Chromosome | Receptors, Cytokine - genetics | Genetic Predisposition to Disease | RNA, Messenger - genetics | Risk Factors | Gene Expression Regulation, Leukemic - drug effects | Signal Transduction - genetics | Enzyme Activation - drug effects | Mutation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Animals | Signal Transduction - drug effects | Cell Transformation, Neoplastic | Oncogene Proteins, Fusion - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Gene Rearrangement - genetics | Sequence Deletion - genetics | Tyrosine | Platelet-derived growth factor | Cytokines | Genes | Oncology, Experimental | Genomes | Research | Gene expression | Population genetics | Hunger | Medical genetics | Genetic research | Nucleotide sequencing | Acute lymphocytic leukemia | Cancer | DNA sequencing
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 06/2013, Volume 288, Issue 23, pp. 16761 - 16774
The objective of the study was to investigate how inflammatory cytokines, IL-1 beta, and TNF-alpha control NOTCH signaling activity in nucleus pulposus (NP) cells... 
MATRIX METALLOPROTEINASES | BACK-PAIN | TUMOR-NECROSIS-FACTOR | KAPPA-B ACTIVATION | BASIC SCIENCE | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEGRADATION | TNF-ALPHA | EXPRESSION | FACTOR-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Transcription Factor HES-1 | Homeodomain Proteins - metabolism | Humans | Middle Aged | Tumor Necrosis Factor-alpha - genetics | Male | Receptor, Notch2 - genetics | Interleukin-1beta - genetics | Promoter Regions, Genetic - genetics | Transcription Factor RelA - genetics | Intervertebral Disc Degeneration - metabolism | MAP Kinase Signaling System | Intervertebral Disc Degeneration - pathology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Interleukin-1beta - metabolism | Cell Cycle Proteins - genetics | Adult | Female | Intervertebral Disc - pathology | Repressor Proteins - metabolism | Intervertebral Disc Degeneration - genetics | Cell Line | Basic Helix-Loop-Helix Transcription Factors - genetics | Cell Cycle Proteins - metabolism | Receptor, Notch2 - metabolism | Rats | Repressor Proteins - genetics | Intervertebral Disc - metabolism | Receptor, Notch1 - metabolism | Homeodomain Proteins - genetics | Animals | Transcription Factor RelA - metabolism | Aged | Receptor, Notch1 - genetics | Intervertebral Disc | Nucleus Pulposus | Chondrocytes | Cytokine | Glycobiology and Extracellular Matrices | NF-kappa B (NF-KB) | Notch Pathway | Osteoarthritis
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, p. e9258
Background: The Notch pathway is essential for proper epidermal differentiation during embryonic skin development. Moreover, skin specific loss of Notch... 
HUMAN EPITHELIAL-CELLS | IN-VITRO | MOUSE KERATINOCYTES | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | GROWTH | IGM(+) B-CELLS | MICE | T-CELL | EXPRESSION | THYMIC STROMAL LYMPHOPOIETIN | Dermatitis, Atopic - genetics | Skin - metabolism | Humans | Receptor, Notch2 - genetics | Receptors, Notch - genetics | Myeloproliferative Disorders - genetics | Granulocyte Colony-Stimulating Factor - genetics | Dermatitis, Atopic - mortality | Flow Cytometry | Receptors, Cytokine - metabolism | Receptors, Cytokine - genetics | Granulocyte Colony-Stimulating Factor - metabolism | Skin - pathology | Immunoglobulins | Cytokines - metabolism | Mice, Inbred C57BL | Receptors, Notch - physiology | Mice, Transgenic | Survival Rate | Signal Transduction - genetics | Dermatitis, Atopic - physiopathology | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Receptor, Notch2 - physiology | Animals | Mice, Nude | Models, Biological | Survival Analysis | Myeloproliferative Disorders - physiopathology | Signal Transduction - physiology | Mice | Skin - physiopathology | Receptor, Notch1 - genetics | Myeloproliferative Disorders - mortality | Receptor, Notch1 - physiology | Embryonic development | Psoriasis | Atopic dermatitis | Bone marrow | Transplantation | Skin | B cells | Syngeneic grafts | Pathogenesis | Bone marrow transplantation | Homeostasis | Lichen planus | Inactivation | Dermatitis | Thymus | Signal transduction | Embryogenesis | Biomedical materials | Immunology | Granulocytes | Granulocyte colony-stimulating factor | Lymphocytes | Rodents | Biocompatibility | Drug dosages | Osteopenia | Neutropenia | Spleen | Repressing | Deactivation | Cytokines | Developmental biology | Dermatology | Leukocytes (eosinophilic) | Neutrophils | Keratinocytes | Breast cancer | Gene expression | Myeloproliferative diseases | Hemopoiesis | Signaling | Thymic stromal lymphopoietin | Stem cells | Mast cells | Infiltration | Notch protein | Hematopoietic system | Mutation | Eosinophils
Journal Article