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PLoS ONE, ISSN 1932-6203, 09/2011, Volume 6, Issue 9, p. e25097
Background: Neurotrophin receptors were initially identified in neural cells. They were recently detected in some cancers in association with invasiveness, but... 
MULTIPLE-MYELOMA | RECEPTOR TRKB | HUMAN NEUROBLASTOMA-CELLS | HEPATOCELLULAR-CARCINOMA | PANCREATIC-CANCER | PROSTATE-CANCER | IN-VIVO | BIOLOGY | FACTOR ACTIVATION | KINASE-B | NERVE GROWTH-FACTOR | Brain-Derived Neurotrophic Factor - genetics | Apoptosis - drug effects | Humans | Adaptor Proteins, Vesicular Transport - genetics | Apoptosis - genetics | Receptor, trkB - genetics | Receptors, Nerve Growth Factor - metabolism | Adaptor Proteins, Vesicular Transport - metabolism | Brain-Derived Neurotrophic Factor - pharmacology | Receptor, trkC - genetics | Receptor, trkB - antagonists & inhibitors | Brain-Derived Neurotrophic Factor - metabolism | Cell Membrane - metabolism | Colorectal Neoplasms - metabolism | Enzyme-Linked Immunosorbent Assay | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Receptors, Nerve Growth Factor - genetics | Indole Alkaloids - pharmacology | Fluorescent Antibody Technique | Cell Line, Tumor | Cell Proliferation - drug effects | Carbazoles - pharmacology | Receptor, trkB - metabolism | Receptor, trkC - metabolism | Tyrosine | Nerve growth factor | B cells | Colorectal cancer | Cell proliferation | Brain | Colorectal carcinoma | Neuroblastoma | Kinases | Neurotrophin 3 | Tissues | Ovarian cancer | Metastases | Proteins | Receptors | Cell growth | Penicillin | Tumor necrosis factor-TNF | TrkA protein | TrkA receptors | Autocrine signalling | Neurotrophins | Protein-tyrosine kinase | Starvation | Cell survival | Secretion | Neurons | Invasiveness | Pharmacology | Survival | Patients | Neurotrophin receptors | Brain-derived neurotrophic factor | Medical prognosis | Cell lines | Affinity | TrkB receptors | Spinal cord injuries | Receptor mechanisms | Transporter | Cytoplasm | Tumors | Apoptosis | Cancer | Cell Membrane | Receptor, trkB | Receptor, trkC | Cell Proliferation | Cellular Biology | Adaptor Proteins, Vesicular Transport | Indole Alkaloids | Receptors, Nerve Growth Factor | Life Sciences | Carbazoles | Brain-Derived Neurotrophic Factor | Colorectal Neoplasms
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 03/2012, Volume 227, Issue 3, pp. 1017 - 1025
Neurotrophins (NTs) belong to a family of growth factors that play a critical role in the control of skin homeostasis. NTs act through the low‐affinity... 
MIGRATION | IN-VITRO | PHYSIOLOGY | DENDRITIC CELLS | MYOFIBROBLAST | TISSUE-REPAIR | SKIN | RECEPTORS | NGF | EXPRESSION | NERVE GROWTH-FACTOR | CELL BIOLOGY | Brain-Derived Neurotrophic Factor - genetics | Fibroblasts - secretion | Receptor, trkA - physiology | Receptor, trkC - physiology | Receptor, Nerve Growth Factor - genetics | Receptor, trkC - secretion | Fibroblasts - physiology | Myofibroblasts - physiology | Humans | Receptor, trkB - secretion | Receptor, trkB - physiology | Cell Survival - genetics | Male | Myofibroblasts - secretion | Nerve Growth Factors - metabolism | Receptor, trkB - genetics | Cell Differentiation - genetics | Receptor, trkC - genetics | Brain-Derived Neurotrophic Factor - physiology | Guided Tissue Regeneration - methods | Wound Healing - genetics | Dermis - cytology | Nerve Growth Factors - physiology | Cell Differentiation - physiology | Cell Survival - physiology | Nerve Growth Factors - secretion | Cells, Cultured | Receptor, Nerve Growth Factor - physiology | Foreskin | Dermis - secretion | Myofibroblasts - cytology | Receptor, trkA - genetics | Fibroblasts - cytology | Wound Healing - physiology | Dermis - physiology | Receptor, trkA | Receptor, trkB | Receptor, trkC | Cell Survival | Dermis | Wound Healing | Receptor, Nerve Growth Factor | Life Sciences | Immunology | Nerve Growth Factors | Brain-Derived Neurotrophic Factor | Fibroblasts | Cell Differentiation | Myofibroblasts | Guided Tissue Regeneration
Journal Article
Cancer Discovery, ISSN 2159-8274, 04/2017, Volume 7, Issue 4, pp. 400 - 409
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies in patients with advanced or... 
REARRANGEMENT | ONCOGENE | ONCOLOGY | ANALOG SECRETORY CARCINOMA | LANDSCAPE | KINASE FUSIONS | SARCOMAS | ETV6-NTRK3 GENE FUSION | CRIZOTINIB | GENOMIC ALTERATIONS | CLINICAL-RESPONSE | Benzamides - pharmacokinetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Receptor, trkA - antagonists & inhibitors | Male | Receptor, trkB - genetics | Indazoles - administration & dosage | Protein Kinase Inhibitors - adverse effects | Mammary Analogue Secretory Carcinoma - genetics | Dose-Response Relationship, Drug | Benzamides - administration & dosage | Membrane Glycoproteins - antagonists & inhibitors | Receptor, trkC - genetics | Anaplastic Lymphoma Kinase | Melanoma - genetics | Colorectal Neoplasms - drug therapy | Receptor, trkB - antagonists & inhibitors | Aged, 80 and over | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Benzamides - adverse effects | Carcinoma, Non-Small-Cell Lung - pathology | Crizotinib | Protein Kinase Inhibitors - pharmacokinetics | Proto-Oncogene Proteins - antagonists & inhibitors | Pyridines - administration & dosage | Carcinoma, Non-Small-Cell Lung - genetics | Receptor, trkC - antagonists & inhibitors | Melanoma - pathology | Mammary Analogue Secretory Carcinoma - drug therapy | Membrane Glycoproteins - genetics | Protein Kinase Inhibitors - administration & dosage | Sequestosome-1 Protein - genetics | Pyrazoles - administration & dosage | Indazoles - pharmacokinetics | Receptor Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - genetics | Melanoma - drug therapy | Adolescent | Receptor, trkA - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Indazoles - adverse effects | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Endocrinology, ISSN 0013-7227, 06/2009, Volume 150, Issue 6, pp. 2646 - 2653
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2011, Volume 6, Issue 11, p. e27213
Background: Diffuse large B-cell lymphoma (DLBCL) is a common and often fatal malignancy. Immunochemotherapy, a combination of rituximab to standard... 
SURVIVAL | ACTIVATION | PATHWAY | BIOLOGY | P75(NTR) | ANTIBODY | RECEPTOR | EPRATUZUMAB | SORTILIN | NERVE GROWTH-FACTOR | LYMPHOCYTES | Brain-Derived Neurotrophic Factor - genetics | Receptor, Nerve Growth Factor - genetics | Humans | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Nerve Growth Factors - metabolism | Receptor, trkB - genetics | Lymphoma, Large B-Cell, Diffuse - metabolism | Immunoenzyme Techniques | Flow Cytometry | Receptor, trkC - genetics | Brain-Derived Neurotrophic Factor - metabolism | Tumor Cells, Cultured | Real-Time Polymerase Chain Reaction | Receptor, Nerve Growth Factor - metabolism | Lymphoma, B-Cell - drug therapy | Lymphoma, B-Cell - metabolism | Lymphoma, Large B-Cell, Diffuse - drug therapy | Nerve Growth Factor - metabolism | Enzyme-Linked Immunosorbent Assay | RNA, Messenger - genetics | Rituximab | Blotting, Western | Receptor, trkA - metabolism | Nerve Growth Factors - genetics | Fluorescent Antibody Technique | Receptor, trkA - genetics | Receptor, trkB - metabolism | Receptor, trkC - metabolism | Antibodies, Monoclonal, Murine-Derived - therapeutic use | Chemotherapy | Nerve growth factor | Lymphomas | B cells | Health aspects | Apoptosis | Cancer | Cell culture | Brain | Biotechnology | Colorectal cancer | Cytotoxicity | Confocal microscopy | Nervous system | Malignancy | Confocal | Kinases | Cancer therapies | Western blotting | Proteins | Signal transduction | Receptors | Remission | Tumor necrosis factor-TNF | Autocrine signalling | Neurotrophins | Systems development | Deprivation | Cell survival | Secretion | Exposure | Tumor cell lines | Survival | Lymphoma | Neurotrophin receptors | Polymerase chain reaction | Cytometry | Sensitivity | Brain-derived neurotrophic factor | Lymphocytes B | Microscopy | Cell lines | Tumors | B-cell lymphoma | Lymphoma, Large B-Cell, Diffuse | Receptor, trkA | Receptor, trkB | Receptor, trkC | Antibodies, Monoclonal, Murine-Derived | Antineoplastic Agents | Cellular Biology | Lymphoma, B-Cell | Nerve Growth Factor | Receptor, Nerve Growth Factor | Life Sciences | Nerve Growth Factors | Brain-Derived Neurotrophic Factor | RNA, Messenger
Journal Article
Handbook of experimental pharmacology, ISSN 0171-2004, 2014, Volume 220, pp. 103 - 119
The tropomyosin-related tyrosine kinase (Trk) receptors were initially described as a family of growth factor receptors required for neuronal survival. They... 
Signaling endosome | Neurotrophins | Trk receptors | Survival | Neurite outgrowth | Apoptosis | Axonal Transport | Receptor, trkA - physiology | Animals | Receptor, trkB - chemistry | Receptor, trkC - physiology | Signal Transduction | Neuronal Plasticity | Humans | Receptor, trkA - chemistry | Receptor, trkB - physiology | Receptor, trkC - chemistry
Journal Article
Pharmacology and Therapeutics, ISSN 0163-7258, 05/2017, Volume 173, pp. 58 - 66
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2014, Volume 111, Issue 52, pp. 18661 - 18666
Lung adenocarcinomas harboring activating mutations in the epidermal growth factor receptor (EGFR) represent a common molecular subset of non-small cell lung... 
Genes | Epidermal cells | Cell lines | Open reading frames | Growth factor receptors | Viability | Genetic mutation | Genetic screening | Cells | Lung neoplasms | ORF | Epidermal growth factor receptor | Non-small cell lung cancer | non-small cell lung cancer | TARGETED THERAPY | WILD-TYPE | GEFITINIB | epidermal growth factor receptor | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | KINASE INHIBITORS | TYROSINE KINASES | GROWTH-FACTOR RECEPTOR | ERLOTINIB RESISTANCE | MUTATIONS | C-SRC | Receptor, Epidermal Growth Factor - genetics | Receptor, trkB | Humans | Membrane Glycoproteins - biosynthesis | Receptor Protein-Tyrosine Kinases - biosynthesis | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Receptor, Fibroblast Growth Factor, Type 1 - genetics | MAP Kinase Signaling System | Proto-Oncogene Proteins c-mos - genetics | Receptor, trkA - biosynthesis | Protein-Tyrosine Kinases - genetics | Protein-Tyrosine Kinases - biosynthesis | Proto-Oncogene Proteins c-raf - biosynthesis | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Receptor, Epidermal Growth Factor - biosynthesis | Lung Neoplasms - enzymology | Proto-Oncogene Proteins c-raf - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Membrane Glycoproteins - genetics | Receptor, Fibroblast Growth Factor, Type 2 - biosynthesis | Gene Expression Regulation, Enzymologic | Receptor Protein-Tyrosine Kinases - genetics | Cell Line, Tumor | Receptor, trkA - genetics | Carcinoma, Non-Small-Cell Lung - enzymology | Proto-Oncogene Proteins c-mos - biosynthesis | Receptor, Fibroblast Growth Factor, Type 1 - biosynthesis | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Protein research | Oncology, Experimental | Genetic aspects | Research | Lung cancer, Non-small cell | Gene expression | Cancer | Biological Sciences
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, p. e69252
Objectives: delta-opioid receptor (DOR) activation reduced brain ischemic infarction and attenuated neurological deficits, while DOR inhibition aggravated the... 
CREB PHOSPHORYLATION | TRUNCATED TRKB | CORTICAL-NEURONS | MESSENGER-RNA | MULTIDISCIPLINARY SCIENCES | FOCAL CEREBRAL-ISCHEMIA | DEATH | HYPOXIA | K+ HOMEOSTASIS | EXPRESSION | Naltrexone - analogs & derivatives | Receptors, Opioid, delta - metabolism | Reperfusion Injury - etiology | Brain Ischemia - metabolism | Male | Infarction, Middle Cerebral Artery - metabolism | Quinolines - pharmacology | Brain - metabolism | Brain - blood supply | Naltrexone - pharmacology | Infarction, Middle Cerebral Artery - complications | Receptors, Opioid, delta - antagonists & inhibitors | Brain-Derived Neurotrophic Factor - metabolism | Reperfusion Injury - metabolism | Brain Ischemia - complications | Cerebrovascular Circulation - drug effects | Activating Transcription Factor 1 - metabolism | Rats | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Animals | Cyclic AMP Response Element-Binding Protein - metabolism | CD11b Antigen - metabolism | Receptor, trkB - metabolism | Receptors, Opioid, delta - agonists | Occlusion | Brain | Neurosciences | Phosphorylation | Traumatic brain injury | Neurobiology | Fluorescence | Reversing | Activation | Neurosurgery | Cerebrospinal fluid | Kinases | Proteins | Head injuries | Reperfusion | Ischemia | Cerebral blood flow | Rodents | Neostriatum | Inhibition | Cerebral infarction | CD11b antigen | Narcotics | Opioid receptors | Cyclic AMP response element-binding protein | Blood flow | Neurological diseases | Medicine | Studies | Signaling | Injury prevention | Brain research | Brain-derived neurotrophic factor | Hypoxia | Naltrindole | TrkB receptors | Infarction | Receptor mechanisms | Laboratory animals | Hippocampus | Brain injury | Integrative medicine
Journal Article
Journal of Molecular Biology, ISSN 0022-2836, 06/2014, Volume 426, Issue 13, pp. 2457 - 2470
The discoidin domain receptors (DDRs), DDR1 and DDR2, form a unique subfamily of receptor tyrosine kinases that are activated by the binding of triple-helical... 
crystallography | gleevec | drug design | phosphorylation | oncology | FIBROSIS | ACTIVATION | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-SURVIVAL | IDENTIFICATION | CANCER | DISCOVERY | INVASION | IMATINIB | STI-571 INHIBITION | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Molecular Sequence Data | Pyridazines - pharmacology | Discoidin Domain Receptors | Protein Kinase Inhibitors - chemistry | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptors, Collagen - genetics | Benzamides - pharmacology | Binding Sites | Receptors, Collagen - chemistry | Protein Structure, Tertiary | Amino Acid Sequence | Proto-Oncogene Proteins c-abl - genetics | Protein Structure, Secondary | Receptors, Mitogen - antagonists & inhibitors | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Discoidin Domain Receptor 1 | Pyrimidines - pharmacology | Receptors, Mitogen - chemistry | Imatinib Mesylate | Piperazines - pharmacology | Receptors, Collagen - antagonists & inhibitors | Sequence Homology, Amino Acid | Receptor Protein-Tyrosine Kinases - genetics | Protein Kinase Inhibitors - pharmacology | Receptor Protein-Tyrosine Kinases - chemistry | Receptors, Mitogen - genetics | Memory (Computers) | Collagen | Atherosclerosis | Crystals | Development and progression | Drug resistance | Structure | Phosphotransferases | CML, chronic myeloid leukemia | KID, kinase insert domain | A-loop, activation loop | ITC, isothermal titration calorimetry | TCEP, tris(2-carboxyethyl)phosphine | DDR, discoidin domain receptor | TKI, tyrosine kinase inhibitor | RTKs, receptor tyrosine kinases | TrkB, tropomyosin-related kinase B | IGF1R, insulin-like growth factor 1 receptor
Journal Article