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Cell reports (Cambridge), ISSN 2211-1247, 2016, Volume 16, Issue 10, pp. 2576 - 2592
The mechanisms underlying Zika virus (ZIKV)-related microcephaly and other neurodevelopment defects remain poorly understood. Here, we describe the derivation... 
NEURAL PROGENITORS | LONG-TERM | HUMAN BRAIN | ADAPTER | CENTRAL-NERVOUS-SYSTEM | INFECTION | MICE | BINDING KINASE 1 | ORGANOIDS | INNATE IMMUNITY | CELL BIOLOGY | Neocortex - pathology | Neurons - pathology | Transcription, Genetic - drug effects | Brain - embryology | Neuroglia - ultrastructure | Neuroglia - pathology | Humans | Brain - virology | Centrosome - drug effects | Gene Expression Profiling | Microcephaly - virology | Neural Stem Cells - ultrastructure | Zika Virus Infection - virology | Neural Stem Cells - immunology | Neuroepithelial Cells - immunology | Neuroprotective Agents - pharmacology | Spinal Cord - pathology | Microcephaly - pathology | Neuroepithelial Cells - virology | Nucleosides - pharmacology | Fetus - virology | Cell Death - drug effects | Phosphorylation - drug effects | Neurons - drug effects | Protein-Serine-Threonine Kinases - metabolism | Zika Virus - pathogenicity | Proto-Oncogene Proteins - metabolism | Zika Virus - ultrastructure | Neurons - virology | Virus Replication - drug effects | Neuroepithelial Cells - ultrastructure | Immunity, Innate - drug effects | Zika Virus Infection - pathology | Neural Stem Cells - virology | Zika Virus - physiology | Zika Virus - drug effects | Mitochondria - metabolism | Mitochondria - drug effects | Receptor Protein-Tyrosine Kinases - metabolism | Neural Stem Cells - enzymology | Centrosome - metabolism | Mitosis - drug effects | Brain - pathology | Protein Kinase Inhibitors - pharmacology | Neuroglia - virology | Neuroepithelial Cells - drug effects | Neurons/pathology | Zika Virus/pathogenicity | Mitochondria/metabolism | Virus Replication/drug effects | Microcephaly/pathology | Neurons/drug effects | Protein-Serine-Threonine Kinases/metabolism | Neural Stem Cells/immunology | Neuroglia/ultrastructure | Neuroepithelial Cells/drug effects | Neuroepithelial Cells/virology | Life Sciences | Brain/pathology | Zika Virus/drug effects | Brain/embryology | Mitochondria/drug effects | Fetus/virology | Neocortex/pathology | Neuroglia/pathology | Cell Death/drug effects | Mitosis/drug effects | Transcription, Genetic/drug effects | Nucleosides/pharmacology | Neural Stem Cells/enzymology | Neural Stem Cells/ultrastructure | Neuroepithelial Cells/ultrastructure | Receptor Protein-Tyrosine Kinases/metabolism | Microcephaly/virology | Proto-Oncogene Proteins/metabolism | Neuroprotective Agents/pharmacology | Zika Virus/ultrastructure | Neuroepithelial Cells/immunology | Brain/virology | Immunity, Innate/drug effects | Spinal Cord/pathology | Zika Virus/physiology | Neuroglia/virology | Microbiology and Parasitology | Zika Virus Infection/pathology | Neurons/virology | Zika Virus Infection/virology | Neural Stem Cells/virology | Centrosome/drug effects | Protein Kinase Inhibitors/pharmacology | Centrosome/metabolism | Phosphorylation/drug effects
Journal Article
Journal Article
Nature (London), ISSN 1476-4687, 2017, Volume 546, Issue 7658, pp. 431 - 435
Therapies that target signalling molecules that are mutated in cancers can often have substantial short-term effects, but the emergence of resistant cancer cells is a major barrier to full cures(1,2... 
METASTATIC MELANOMA | BRAF INHIBITOR | SUBPOPULATIONS | CHROMATIN | MULTIDISCIPLINARY SCIENCES | SINGLE MAMMALIAN-CELLS | STATE | MECHANISMS | MUTATIONS | VEMURAFENIB | PLASTICITY | Transcription, Genetic - drug effects | Humans | Male | Transcription Factor AP-1 - metabolism | DNA-Binding Proteins - metabolism | Melanoma - genetics | Female | Indoles - pharmacology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Single-Cell Analysis | Cellular Reprogramming - genetics | ErbB Receptors - metabolism | In Situ Hybridization, Fluorescence | Nuclear Proteins - metabolism | Signal Transduction - genetics | Melanoma - pathology | Sulfonamides - pharmacology | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Genetic Markers - drug effects | Vemurafenib | Drug Resistance, Neoplasm - genetics | Animals | Signal Transduction - drug effects | Genetic Markers - genetics | Cell Line, Tumor | Oncogene Protein p65(gag-jun) - metabolism | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Antimitotic agents | Cell interaction | Dosage and administration | Antineoplastic agents | Drug resistance | Observations | Health aspects | Subpopulations | Transcription factors | Substance abuse treatment | Variability | Activator protein 1 | Melanoma | Genomes | Kinases | Gene expression | Sox10 protein | Signal transduction | Signaling | Converting | Population | Mutation | Differentiation | Deoxyribonucleic acid--DNA | Cancer
Journal Article
British Journal of Cancer, ISSN 0007-0920, 01/2016, Volume 114, Issue 2, pp. 177 - 187
Background: Oestrogen receptor-negative (ER-) breast cancer is intrinsically sensitive to chemotherapy. However, tumour response is often incomplete, and... 
CELLS | REDUCES TUMOR-GROWTH | STAT1 | DNA-DAMAGE | chemotherapy | IFN | THERAPY | NEOADJUVANT CHEMOTHERAPY | ONCOLOGY | ER-negative breast cancer | GENE-EXPRESSION | RESISTANCE | PATHWAY ANALYSIS | predictive signature | XENOGRAFTS | Caspase 7 - metabolism | Immunohistochemistry | Receptors, Estrogen - metabolism | Cytoskeletal Proteins - genetics | Humans | Intracellular Signaling Peptides and Proteins - drug effects | Caspase 3 - metabolism | Gene Expression Profiling | Intracellular Signaling Peptides and Proteins - metabolism | Interferon-gamma - metabolism | Carrier Proteins - drug effects | Mitochondrial Proteins - drug effects | STAT1 Transcription Factor - metabolism | Mitochondrial Proteins - metabolism | Caspase 3 - genetics | Interferon-beta - genetics | Cytokines - genetics | Intracellular Signaling Peptides and Proteins - genetics | Real-Time Polymerase Chain Reaction | Ubiquitins - metabolism | Caspase 7 - drug effects | Antigens - drug effects | Caspase 7 - genetics | Membrane Proteins - genetics | Myxovirus Resistance Proteins - drug effects | Capecitabine - pharmacology | STAT1 Transcription Factor - genetics | Breast Neoplasms - drug therapy | Blotting, Western | Breast Neoplasms - genetics | Interferon-beta - metabolism | Signal Transduction - drug effects | Mice, Nude | Membrane Proteins - drug effects | Mice | Myxovirus Resistance Proteins - genetics | Ubiquitins - drug effects | Antigens - genetics | Neoplasm Transplantation | Phosphorylation | Ubiquitins - genetics | Gene Expression Regulation, Neoplastic | Interferon-gamma - drug effects | STAT1 Transcription Factor - drug effects | Mitochondrial Proteins - genetics | Interferon-beta - drug effects | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Breast Neoplasms - metabolism | In Situ Hybridization | Caspase 3 - drug effects | Cytoskeletal Proteins - metabolism | Female | Cytoskeletal Proteins - drug effects | Membrane Proteins - metabolism | Interferon-gamma - genetics | Cytokines - metabolism | Antigens - metabolism | Cisplatin - pharmacology | Xenograft Model Antitumor Assays | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Cytokines - drug effects | Myxovirus Resistance Proteins - metabolism | Life Sciences | Computer Science | Translational Therapeutics
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Cardiovascular Neurohormonal Regulation
Journal Article
Leukemia, ISSN 0887-6924, 07/2011, Volume 25, Issue 7, pp. 1064 - 1079
... of genetic alterations in critical components in this pathway as well as mutations at upstream growth factor receptors... 
mTOR | translation | sensitivity | PI3K | therapy | resistance | TUMOR-SUPPRESSOR CANDIDATE | PROTEIN-KINASE | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | GROWTH-FACTOR RECEPTOR | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | AKT/PROTEIN-KINASE-B | ACUTE LYMPHOBLASTIC-LEUKEMIA | HEMATOPOIETIC STEM-CELLS | CHRONIC LYMPHOCYTIC-LEUKEMIA | HEMATOLOGY | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Neoplasm Proteins - physiology | PTEN Phosphohydrolase - physiology | Apoptosis - genetics | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Gene Expression Regulation, Leukemic - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Transcription Factors - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | PTEN Phosphohydrolase - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | TOR Serine-Threonine Kinases - physiology | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Leukemia - genetics | Multiprotein Complexes - drug effects | PTEN Phosphohydrolase - genetics | Proteins - physiology | Transcription Factors - physiology | RNA, Messenger - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - physiology | Multiprotein Complexes - physiology | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Pseudogenes | Signal Transduction - drug effects | Phosphatidylinositol 3-Kinases - physiology | Proteins - drug effects | RNA, Neoplasm - genetics | Protein Biosynthesis - drug effects | MicroRNAs - genetics | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Genes | Leukemia | Physiological aspects | Development and progression | Genetic aspects | Research | Antineoplastic agents | Drug therapy | Health aspects
Journal Article
PLoS biology, ISSN 1545-7885, 2007, Volume 5, Issue 2, pp. e34 - 0189
The mammalian circadian timing system consists of a master pacemaker in neurons of the suprachiasmatic nucleus (SCN) and clocks of a similar molecular makeup... 
RAT-LIVER | REVEALS PERSISTENT | SUPRACHIASMATIC NUCLEUS | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEAT-SHOCK RESPONSE | MOUSE | BIOLOGY | GENE-EXPRESSION | TIME | PERIPHERAL-TISSUES | BINDING | INDIVIDUAL FIBROBLASTS | Male | Biological Clocks - drug effects | DNA-Binding Proteins - metabolism | Hepatocytes - cytology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Liver - drug effects | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Hepatocytes - drug effects | Hepatocytes - physiology | Nuclear Receptor Subfamily 1, Group D, Member 1 | ARNTL Transcription Factors | Basic Helix-Loop-Helix Transcription Factors - genetics | Cell Cycle Proteins - metabolism | Circadian Rhythm - genetics | Mice, Transgenic | Nuclear Proteins - metabolism | Receptors, Cytoplasmic and Nuclear - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Period Circadian Proteins | Gene Expression Regulation - drug effects | Transcription Factors - metabolism | Animals | Biological Clocks - genetics | Chronobiology Phenomena | Liver - physiology | Protein Array Analysis | Doxycycline - pharmacology | Anti-Bacterial Agents - pharmacology | Liver - cytology | Mice | Circadian Rhythm - drug effects | Receptors, Cytoplasmic and Nuclear - metabolism | Circadian rhythm | Kinases | Experiments | Liver | Binding sites | Neuroscience | Molecular Biology | Computational Biology | Genetics and Genomics | Mus (Mouse) | Biochemistry | Physiology | Mammals | Cell Biology
Journal Article
The Lancet (British edition), ISSN 0140-6736, 2009, Volume 373, Issue 9678, pp. 1905 - 1917
...) expression, raised macrophage migration inhibitory factor, and increased P-glycoprotein-mediated drug efflux... 
Internal Medicine | RHEUMATOID-ARTHRITIS | MEDICINE, GENERAL & INTERNAL | OBSTRUCTIVE PULMONARY-DISEASE | HISTONE DEACETYLASE ACTIVITY | MIGRATION INHIBITORY FACTOR | ULCERATIVE-COLITIS | REGULATORY T-CELLS | RECEPTOR-BETA | RELATIVE CORTICOSTEROID INSENSITIVITY | BLOOD MONONUCLEAR-CELLS | RESPIRATORY-DISTRESS-SYNDROME | Transcription Factor AP-1 - drug effects | Glucocorticoids - therapeutic use | Transcriptional Activation - genetics | Transcription Factor AP-1 - genetics | Humans | Macrophage Migration-Inhibitory Factors - immunology | Transcriptional Activation - drug effects | Transcription Factor AP-1 - immunology | Histone Deacetylases - immunology | Transcriptional Activation - immunology | ATP-Binding Cassette, Sub-Family B, Member 1 - drug effects | Calcineurin Inhibitors | Macrophage Migration-Inhibitory Factors - genetics | Inflammation - drug therapy | Phosphodiesterase 4 Inhibitors | Anti-Inflammatory Agents - therapeutic use | Mitogen-Activated Protein Kinases - immunology | Genetic Predisposition to Disease - genetics | NF-kappa B - antagonists & inhibitors | Histone Deacetylases - genetics | Macrophage Migration-Inhibitory Factors - drug effects | Repressor Proteins - genetics | Histone Deacetylase 2 | Drug Resistance - drug effects | Inflammation - immunology | Asthma - drug therapy | ATP-Binding Cassette, Sub-Family B, Member 1 - immunology | Drug Resistance - genetics | ATP-Binding Cassette, Sub-Family B, Member 1 - genetics | Drug Resistance - immunology | Repressor Proteins - immunology | Histone Deacetylases - drug effects | Mitogen-Activated Protein Kinases - genetics | Repressor Proteins - drug effects | Mitogen-Activated Protein Kinases - drug effects | Pulmonary Disease, Chronic Obstructive - drug therapy | Corticosteroids | Dosage and administration | Inflammation | Research | Drug resistance | Drug therapy | Health aspects | Complications and side effects | Risk factors | Inflammatory bowel disease | Proteins | Respiratory distress syndrome | Asthma | Steroids
Journal Article