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Journal Article
PLoS genetics, ISSN 1553-7404, 2008, Volume 4, Issue 2, p. e24
In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR... 
MESSENGER-RNA | SIGNALING PATHWAY | INDUCED LONGEVITY | TOR | GENES | DAF-16 | GENETICS & HEREDITY | NEMATODE CAENORHABDITIS-ELEGANS | MEMBRANE-TRANSPORT | 3-KINASE COMPLEX | CELL-DEATH | Phosphotransferases (Alcohol Group Acceptor) - physiology | Genes, Helminth | rab GTP-Binding Proteins - genetics | Autophagy - physiology | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Trans-Activators - physiology | Caenorhabditis elegans - physiology | RNA Interference | Receptor, Insulin - genetics | Trans-Activators - genetics | Autophagy - genetics | Vesicular Transport Proteins | Caenorhabditis elegans - growth & development | Animals, Genetically Modified | Caenorhabditis elegans - genetics | Phosphotransferases (Alcohol Group Acceptor) - genetics | Longevity - genetics | Receptor, Insulin - physiology | Phosphatidylinositol 3-Kinases - genetics | rab GTP-Binding Proteins - physiology | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | Diet | Receptors, Nicotinic - physiology | Models, Biological | Phosphatidylinositol 3-Kinases - physiology | rab GTP-Binding Proteins - antagonists & inhibitors | Caenorhabditis elegans Proteins - physiology | Mutation | Trans-Activators - antagonists & inhibitors | Caenorhabditis elegans Proteins - genetics | Longevity - physiology | Receptors, Nicotinic - genetics | Proteins | Medical research | Kinases | Metabolism
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 12/2004, Volume 279, Issue 52, pp. 54708 - 54715
Suppressor of cytokine signaling (SOCS) proteins constitute a class of negative regulators for Janus kinase/signal transducer and activator of transcription... 
ACTIVATION | PATHWAY | IFN-GAMMA | MACROPHAGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | STAT INHIBITOR-1 (SSI-1)/SUPPRESSOR | GENE-EXPRESSION | LIPOPOLYSACCHARIDE | INTERFERON-BETA | INDUCTION | ADAPTER MOLECULE | CD40 Antigens - analysis | Toll-Like Receptor 2 | Toll-Like Receptor 3 | Receptors, Immunologic - physiology | Toll-Like Receptor 4 | Tumor Necrosis Factor-alpha - genetics | RNA, Messenger - analysis | Suppressor of Cytokine Signaling 1 Protein | Suppressor of Cytokine Signaling Proteins | Trans-Activators - physiology | Repressor Proteins - physiology | Toll-Like Receptors | Membrane Glycoproteins - physiology | Trans-Activators - genetics | Interferon Type I - physiology | Receptors, Cell Surface - physiology | Carrier Proteins - physiology | Cell Line | DNA-Binding Proteins - physiology | Gene Expression | Transcription Factors - physiology | Mice, Inbred C57BL | Receptors, Immunologic - deficiency | Repressor Proteins - genetics | Macrophages, Peritoneal - chemistry | Myeloid Differentiation Factor 88 | Transcription Factors - genetics | Chemokines, CXC - genetics | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Mice, Inbred C3H | Antigens, Differentiation - physiology | Chemokine CXCL10 | Carrier Proteins - genetics | Suppressor of Cytokine Signaling 3 Protein | Adaptor Proteins, Signal Transducing | Animals | Bone Marrow Cells | Lipopolysaccharides - pharmacology | NF-kappa B - physiology | Tumor Necrosis Factor-alpha - physiology | STAT1 Transcription Factor | Signal Transduction - physiology | Mice | Mice, Inbred BALB C | Macrophages, Peritoneal - metabolism
Journal Article
Neurobiology of disease, ISSN 0969-9961, 2007, Volume 26, Issue 1, pp. 112 - 124
Abstract Williams Syndrome (WS, [MIM 194050]) is a disorder caused by a hemizygous deletion of 25–30 genes on chromosome 7q11.23. Several of these genes... 
Neurology | Human | Genetic disorder | Mice | Cognition | Motor behavior | Muscle Proteins/genetics | In Situ Hybridization, Fluorescence | Trans-Activators/genetics | Conditioning, Operant/physiology | Motor Activity/physiology | Intelligence Tests | DNA/genetics | Mice, Knockout | Microtubule-Associated Proteins/genetics | Neuropsychological Tests | Eye Movements/physiology | Magnetic Resonance Imaging | Fear/psychology | Animals | Nerve Tissue Proteins/genetics | Postural Balance/physiology | Williams Syndrome/genetics | Cognition/physiology | Nuclear Proteins/genetics | Psychomotor Performance/physiology | MOUSE-BRAIN | CEREBELLAR | ATYPICAL 7Q11.23 DELETION | BEUREN-SYNDROME | cognition | motor behavior | mice | NEUROSCIENCES | RECORDING EYE-MOVEMENTS | CHILDREN | PROFILE | genetic disorder | CHROMOSOME 7Q11.23 | SYNDROME CRITICAL REGION | human | Motor Activity - physiology | Microtubule-Associated Proteins - genetics | Williams Syndrome - genetics | Conditioning, Operant - physiology | Psychomotor Performance - physiology | Williams Syndrome - psychology | Trans-Activators - physiology | Trans-Activators - genetics | Cognition - physiology | Fear - psychology | Nuclear Proteins - genetics | Muscle Proteins - physiology | Nerve Tissue Proteins - physiology | Eye Movements - physiology | Nerve Tissue Proteins - genetics | Microtubule-Associated Proteins - physiology | DNA - genetics | Muscle Proteins - genetics | Nuclear Proteins - physiology | Postural Balance - physiology | Williams Syndrome - pathology
Journal Article
Cell Cycle, ISSN 1551-4005, 2014, Volume 6, Issue 11, pp. 1329 - 1331
The circadian clock controls a large array of behavioral and physiological systems of fundamental importance to most organisms. Consequently, abnormal... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Circadian rhythms | Estrogen receptor α | Breast cancer | Cyclin D1 | CLOCK | MELATONIN | estrogen receptor alpha | TRANSCRIPTION | SENSITIVITY | breast cancer | circadian rhythms | ESTROGEN-RECEPTOR | CELL BIOLOGY | DISRUPTION | IN-VIVO | GENE-EXPRESSION | cyclin D1 | CELL-CYCLE | RECRUITS | PROMOTER | Chromatin - metabolism | Estrogens | Humans | Breast Neoplasms - etiology | Mammary Neoplasms, Experimental - physiopathology | Risk | Neoplasms, Hormone-Dependent - physiopathology | Breast Neoplasms - physiopathology | Melatonin - physiology | Mammary Neoplasms, Experimental - genetics | Neoplasms, Hormone-Dependent - genetics | Trans-Activators - physiology | Cyclin D1 - physiology | Cell Transformation, Neoplastic - genetics | Mammals - physiology | Female | Acetylation | Estrogen Receptor alpha - physiology | Genes, Tumor Suppressor | Breast Neoplasms - epidemiology | ARNTL Transcription Factors | Basic Helix-Loop-Helix Transcription Factors - physiology | Transcription Factors - physiology | Disease Susceptibility | Circadian Rhythm - genetics | Gene Expression Regulation | Circadian Rhythm - physiology | Histone Acetyltransferases - physiology | Protein Processing, Post-Translational - physiology | Animals | Breast Neoplasms - genetics | CLOCK Proteins | Developed Countries | Neoplasms, Hormone-Dependent - etiology | Models, Biological | Mice | Nuclear Proteins - physiology | Histones - metabolism | Mammary Neoplasms, Experimental - etiology
Journal Article
Nature reviews. Cancer, ISSN 1474-1768, 2002, Volume 2, Issue 1, pp. 38 - 47
Cells undergo a variety of biological responses when placed in hypoxic conditions, including activation of signalling pathways that regulate proliferation,... 
TARGET GENES | ACTIVATED PROTEIN-KINASE | P53-DEPENDENT APOPTOSIS | ONCOLOGY | INDUCIBLE FACTOR 1-ALPHA | GENE-EXPRESSION | BINDING-PROTEIN | FACTOR-I | FACTORS HIF-1-ALPHA | FACTOR (HIF)-1-ALPHA | UP-REGULATION | Oxidative Stress | Vascular Endothelial Growth Factors | Humans | Hypoxia-Inducible Factor 1, alpha Subunit | Trans-Activators - physiology | Aryl Hydrocarbon Receptor Nuclear Translocator | Antineoplastic Agents - pharmacokinetics | Dimerization | Basic Helix-Loop-Helix Transcription Factors | Endothelial Growth Factors - physiology | DNA-Binding Proteins - physiology | Hypoxia-Inducible Factor 1 | Oxidation-Reduction | Signal Transduction | Lymphokines - physiology | Neoplasms - blood supply | Forecasting | Trans-Activators - deficiency | Mice | Neovascularization, Pathologic - metabolism | DNA Damage | Hydrogen-Ion Concentration | Neoplasms - metabolism | Vascular Endothelial Growth Factor A | Erythropoietin - therapeutic use | Receptor Protein-Tyrosine Kinases - physiology | Transcription Factors - deficiency | Embryonic and Fetal Development | Oxygen - metabolism | Vascular Endothelial Growth Factor Receptor-1 | Cell Hypoxia | Neoplasms - genetics | Cell Division | Trans-Activators - genetics | Transcription Factors - physiology | Cell Survival | Gene Expression Regulation | Transcription Factors - genetics | Cyclic AMP Response Element-Binding Protein - physiology | Xenograft Model Antitumor Assays | Animals | Prodrugs - pharmacokinetics | NF-kappa B - physiology | Proto-Oncogene Proteins - physiology | Glycolysis | Neovascularization, Pathologic - genetics | Nuclear Proteins - physiology | Neoplasms - pathology | Receptors, Aryl Hydrocarbon | Apoptosis | Complications and side effects | Care and treatment | Prognosis | Growth | Physiological aspects | Hypoxia | Research | Tumors
Journal Article