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Brain Research, ISSN 0006-8993, 2012, Volume 1494, pp. 1 - 8
Abstract Dexmedetomidine (Dex) has been demonstrated to provide neuroprotection against ischemia/reperfusion (I/R) injury. However, the exact mechanism of this... 
Neurology | MCAO | GSK-3β | ERK1/2 | PI3K | Dexmedetomidine | ACTIVATION | INCREASES | BRAIN-DAMAGE | MECHANISMS | FOREBRAIN ISCHEMIA | NEUROSCIENCES | NEUROPROTECTION | HIPPOCAMPUS | INSULIN | GSK-3 beta | STRESS | OCCLUSION | Protein Kinases - metabolism | Reperfusion Injury - etiology | Glycogen Synthase Kinase 3 - drug effects | Phosphatidylinositol 3-Kinase - drug effects | Cerebral Cortex - pathology | Glycogen Synthase Kinase 3 beta | Male | Mitogen-Activated Protein Kinase 1 - drug effects | CA1 Region, Hippocampal - drug effects | Brain Ischemia - enzymology | Mitogen-Activated Protein Kinase 3 - drug effects | CA1 Region, Hippocampal - pathology | Neuroprotective Agents - pharmacology | Infarction, Middle Cerebral Artery - complications | Dexmedetomidine - pharmacology | Cell Death - drug effects | Cerebral Cortex - drug effects | Phosphatidylinositol 3-Kinase - metabolism | Brain Ischemia - complications | Protein Kinases - drug effects | Reperfusion Injury - pathology | Reperfusion Injury - enzymology | Rats | Infarction, Middle Cerebral Artery - pathology | Glycogen Synthase Kinase 3 - metabolism | Rats, Sprague-Dawley | Animals | MAP Kinase Signaling System - drug effects | Reperfusion Injury - prevention & control | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Signal Transduction - physiology | Infarction, Middle Cerebral Artery - enzymology | Mitogen-Activated Protein Kinase 1 - metabolism | Brain | Cerebral infarction | Edema | Neuroprotection | Phosphorylation | Cell survival | MEK inhibitors | Cortex | Extracellular signal-regulated kinase | Glycogen synthase kinase 3 | AKT protein | Data processing | Western blotting | 1-Phosphatidylinositol 3-kinase | Reperfusion | Ischemia | Cerebral blood flow | Wortmannin | Injuries
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
by Zhang, J and Zhu, L.X and Cheng, X and Lin, Y and Yan, P and Peng, B
Journal of Dental Research, ISSN 0022-0345, 6/2015, Volume 94, Issue 6, pp. 853 - 862
Mineral trioxide aggregate is the currently recommended material of choice for clinical pulp repair despite several disadvantages, including handling... 
proto-oncogene proteins c-akt | extracellular signal-regulated MAP kinase | cell movement | focal adhesion kinase | JNK mitogen-activated protein kinase | dental pulp capping | TISSUE REGENERATION | PROLIFERATION | MESENCHYMAL STEM-CELLS | FOCAL ADHESIONS | MINERAL TRIOXIDE AGGREGATE | ENDOTHELIAL PROGENITOR CELLS | IN-VITRO | DENTISTRY, ORAL SURGERY & MEDICINE | DIFFERENTIATION | PERIODONTAL-LIGAMENT FIBROBLASTS | END FILLING MATERIALS | Receptors, Fibroblast Growth Factor - drug effects | Nanoparticles - chemistry | Stress Fibers - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Paxillin - drug effects | Pulp Capping and Pulpectomy Agents - pharmacology | Wound Healing - drug effects | Calcium Compounds - pharmacology | Silicates - pharmacology | JNK Mitogen-Activated Protein Kinases - drug effects | Dentinogenesis - drug effects | Cells, Cultured | Dental Pulp - cytology | Rats | Dental Pulp - drug effects | Materials Testing | Dentin, Secondary - drug effects | Focal Adhesion Kinase 1 - drug effects | Cell Movement - drug effects | Focal Adhesions - drug effects | Oxides - pharmacology | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Ceramics - chemistry | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Membrane Proteins - drug effects | Aluminum Compounds - pharmacology | Vinculin - drug effects | Drug Combinations | Proto-Oncogene Proteins c-akt - drug effects
Journal Article
European Journal of Cancer, ISSN 0959-8049, 2016, Volume 68, pp. 1 - 10
Abstract Purpose We performed a multi-centre phase I study to assess the safety, pharmacokinetics (PK) and pharmacodynamics (PD) of the orally available small... 
Hematology, Oncology and Palliative Medicine | Pharmacodynamics | MEK inhibitor | Phase I | Optimal biological dose | Pharmacokinetics | BRAF-MUTATED MELANOMA | MULTICENTER | SELUMETINIB PLUS DOCETAXEL | SAFETY | TRAMETINIB | CELL LUNG-CANCER | TRIAL | DOSE-ESCALATION | ONCOLOGY | DOUBLE-BLIND | AZD6244 ARRY-142886 | Lung Neoplasms - drug therapy | Pancreatic Neoplasms - metabolism | Nausea - chemically induced | Allosteric Regulation | Humans | Lung Neoplasms - metabolism | Middle Aged | Male | Fatigue - chemically induced | Ribosomal Protein S6 Kinases, 70-kDa - drug effects | Protein Kinase Inhibitors - adverse effects | Colorectal Neoplasms - drug therapy | Chromatography, Liquid | Proto-Oncogene Proteins c-akt - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Bile Duct Neoplasms - metabolism | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Administration, Oral | Carcinoma, Non-Small-Cell Lung - metabolism | Neoplasms - drug therapy | Maximum Tolerated Dose | Mesothelioma - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Anorexia - chemically induced | Glycogen Synthase Kinase 3 beta - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Neoplasms - metabolism | Phosphoproteins - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | Cholangiocarcinoma - metabolism | Chromatography, High Pressure Liquid | Diarrhea - chemically induced | Mitogen-Activated Protein Kinase 3 - drug effects | Pancreatic Neoplasms - drug therapy | Tandem Mass Spectrometry | Uterine Cervical Neoplasms - metabolism | Esophageal Neoplasms - metabolism | Adult | Female | Colorectal Neoplasms - metabolism | Bile Duct Neoplasms - drug therapy | Drug Eruptions - etiology | Abdominal Pain - chemically induced | Uterine Cervical Neoplasms - drug therapy | Glycogen Synthase Kinase 3 beta - metabolism | Mesothelioma - drug therapy | Cholangiocarcinoma - drug therapy | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Esophageal Neoplasms - drug therapy | Proto-Oncogene Proteins c-akt - drug effects | Care and treatment | Protein kinases | Mitogens | Cells | Tumors
Journal Article
Journal of Molecular Neuroscience, ISSN 0895-8696, 11/2015, Volume 57, Issue 3, pp. 335 - 351
The objective of this study is to explore the neuroprotective effect and mechanism of picroside II on ERK1/2-COX2 signal transduction pathway after cerebral... 
Neurochemistry | Neurosciences | Rats | Inflammatory reaction | Cell Biology | Neurology | Cerebral ischemia | ERK1/2 | Biomedicine | Proteomics | COX2 | Picroside II | Apoptosis | ISCHEMIA/REPERFUSION INJURY | ACTIVATED PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | AKT | MODEL | BLOOD-FLOW | NEUROSCIENCES | CISPLATIN-INDUCED APOPTOSIS | MICROGLIA | PC12D CELLS | CYCLOOXYGENASE-2 EXPRESSION | PROSTAGLANDIN E-2 | Neuroprotective Agents - therapeutic use | Iridoid Glucosides - pharmacology | Nitriles - pharmacology | Rats, Wistar | Apoptosis - drug effects | Cerebral Cortex - pathology | Male | Mitogen-Activated Protein Kinase 1 - drug effects | Cyclooxygenase 2 - biosynthesis | Mitogen-Activated Protein Kinase 3 - drug effects | RNA, Messenger - biosynthesis | Neuroprotective Agents - pharmacology | Cyclooxygenase 2 - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 3 - biosynthesis | Cyclooxygenase 2 Inhibitors - therapeutic use | Nerve Tissue Proteins - biosynthesis | Enzyme Induction - drug effects | Behavior, Animal - drug effects | Infarction, Middle Cerebral Artery - drug therapy | Drug Evaluation, Preclinical | Brain Damage, Chronic - pathology | Severity of Illness Index | Nerve Tissue Proteins - antagonists & inhibitors | Butadienes - pharmacology | Lipopolysaccharides - toxicity | Cyclooxygenase 2 Inhibitors - pharmacology | Mitogen-Activated Protein Kinase 3 - genetics | MAP Kinase Kinase Kinases - genetics | RNA, Messenger - genetics | Behavior, Animal - physiology | Cyclooxygenase 2 - drug effects | Infarction, Middle Cerebral Artery - pathology | Random Allocation | Cinnamates - pharmacology | Nerve Tissue Proteins - genetics | Mitogen-Activated Protein Kinase 1 - biosynthesis | Brain Damage, Chronic - etiology | Animals | MAP Kinase Signaling System - drug effects | MAP Kinase Kinase Kinases - biosynthesis | Signal Transduction - drug effects | Iridoid Glucosides - therapeutic use | Cinnamates - therapeutic use | Brain Damage, Chronic - prevention & control | MAP Kinase Kinase Kinases - drug effects | Care and treatment | Cellular signal transduction | Phytochemicals | Research | Health aspects
Journal Article
Toxicology Letters, ISSN 0378-4274, 2011, Volume 204, Issue 1, pp. 71 - 80
Journal Article
Gynecologic Oncology, ISSN 0090-8258, 2016, Volume 143, Issue 3, pp. 466 - 471
Abstract Objective Metformin reduces cancer incidence and improves overall survival in diabetic patients. In preclinical studies, metformin decreases... 
Hematology, Oncology and Palliative Medicine | Obstetrics and Gynecology | mTOR | Metformin | Inhibition | Endometrial cancer | Window of opportunity | RISK | PROLIFERATION | OBSTETRICS & GYNECOLOGY | DIABETIC-PATIENTS | BREAST-CANCER | TRIAL | THERAPY | ONCOLOGY | COHORT | NEOADJUVANT | Immunohistochemistry | AMP-Activated Protein Kinases - metabolism | Phosphoproteins - drug effects | Prospective Studies | Apoptosis - drug effects | Humans | Leptin - metabolism | Middle Aged | Caspase 3 - metabolism | Endometrial Neoplasms - metabolism | Endometrium - drug effects | Ki-67 Antigen - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Insulin-Like Growth Factor I - drug effects | Phosphoproteins - metabolism | AMP-Activated Protein Kinases - drug effects | Carcinoma, Endometrioid - metabolism | Mitogen-Activated Protein Kinase 3 - drug effects | Lectins - metabolism | Phosphatidylinositol 3-Kinases - drug effects | Caspase 3 - drug effects | Biomarkers, Tumor - metabolism | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Endometrium - metabolism | Cytokines - metabolism | GPI-Linked Proteins - drug effects | Metformin - pharmacology | GPI-Linked Proteins - metabolism | Hypoglycemic Agents - pharmacology | Insulin - metabolism | Cytokines - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Lectins - drug effects | Endometrial Neoplasms - pathology | Aged | Cell Proliferation - drug effects | Endometrium - pathology | Carcinoma, Endometrioid - pathology | Insulin-Like Growth Factor I - metabolism | Ki-67 Antigen - drug effects | Proto-Oncogene Proteins c-akt - drug effects | Women | Diabetics | Analysis | Oncology, Experimental | Research | Cancer
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 10, pp. H1720 - H1730
S-glutathionylation of cardiac myosin-binding protein C (cMyBP-C) induces Ca2+ sensitization and a slowing of cross-bridge kinetics as a result of increased... 
Oxidative stress | Diastolic dysfunction | Cardiac myosin-binding protein C | S-glutathionylation | Sarcomeres | BINDING-PROTEIN-C | MYOFILAMENT RESPONSE | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | sarcomeres | TROPONIN-I | CA2 | RECOMMENDATIONS | cardiac myosin-binding protein C | CARDIAC-HYPERTROPHY | MUTATION | diastolic dysfunction | PERIPHERAL VASCULAR DISEASE | ECHOCARDIOGRAPHY | oxidative stress | ALPHA-TROPOMYOSIN | Free Radical Scavengers - pharmacology | Tropomyosin - genetics | Calcium - metabolism | Cardiomyopathy, Hypertrophic, Familial - genetics | Calcium-Binding Proteins - drug effects | Male | Mitogen-Activated Protein Kinase 1 - drug effects | Carrier Proteins - drug effects | Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Female | Diastole - drug effects | Phosphorylation - drug effects | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Cardiomyopathy, Hypertrophic, Familial - physiopathology | Myofibrils - drug effects | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Cardiomyopathy, Hypertrophic, Familial - metabolism | Mice, Transgenic | Animals | Carrier Proteins - metabolism | Heart Ventricles - physiopathology | Mitogen-Activated Protein Kinase 3 - metabolism | Acetylcysteine - pharmacology | Heart Ventricles - metabolism | Mice | Myofibrils - metabolism | Oxidative Stress - drug effects | Heart Ventricles - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Complications and side effects | Care and treatment | Usage | Cardiomyopathy, Hypertrophic | Analysis | Acetylcysteine | Protein C | Influence | Genetic aspects | Genetic engineering | Research | Hypertrophy | Muscle Mechanics and Ventricular Function
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 1/2008, Volume 100, Issue 2, pp. 140 - 154
Background Patients with Birt-Hogg-Dubé (BHD) syndrome harbor germline mutations in the BHD tumor suppressor gene that are associated with an increased risk... 
COLLECTING DUCT | TUBEROUS SCLEROSIS COMPLEX | ONCOLOGY | GERMAN-SHEPHERD DOG | INTERCALATED CELLS | BHD GENE | CANCER | RENAL-CARCINOMA | GENITOURINARY TRACT | RAT MODEL | NODULAR DERMATOFIBROSIS | Immunohistochemistry | Polycystic Kidney Diseases - genetics | Protein Kinases - metabolism | Blotting, Southern | Kidney Neoplasms - genetics | Antibiotics, Antineoplastic - pharmacology | Kidney - pathology | Immunoblotting | Kidney Neoplasms - metabolism | Mitogen-Activated Protein Kinase 1 - drug effects | Polycystic Kidney Diseases - complications | Mitogen-Activated Protein Kinase 3 - drug effects | Kidney - metabolism | Polycystic Kidney Diseases - pathology | Tumor Suppressor Proteins - genetics | Germ-Line Mutation | Disease Models, Animal | Estrone - genetics | Polycystic Kidney Diseases - metabolism | Protein Kinases - drug effects | Kidney - drug effects | Gene Silencing | Kaplan-Meier Estimate | Genotype | Proto-Oncogene Proteins - genetics | Random Allocation | Reverse Transcriptase Polymerase Chain Reaction | Sirolimus - pharmacology | Syndrome | Mice, Knockout | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Fluorescent Antibody Technique | Kidney Neoplasms - pathology | Cell Proliferation - drug effects | Mice | TOR Serine-Threonine Kinases | Mitogen-Activated Protein Kinase 1 - metabolism | Cell proliferation | Gene silencing | Care and treatment | Kidney cancer | Physiological aspects | Genetic aspects | Research | Health aspects | Methods | Genetic disorders | Kidney diseases | Risk factors | Cancer | Tumors | Index Medicus
Journal Article
American Journal of Physiology - Endocrinology and Metabolism, ISSN 0193-1849, 2016, Volume 311, Issue 6, pp. E939 - E948
Previous studies have shown that very lowdose infusions of leptin into the third or the fourth ventricle alone have little effect on energy balance, but... 
Energy expenditure | Rats | Food intake | Body composition | CHOLECYSTOKININ | PHYSIOLOGY | PHOSPHORYLATION | FOOD-INTAKE | energy expenditure | BODY-WEIGHT | body composition | HINDBRAIN | NUCLEUS | IN-VIVO | ENDOCRINOLOGY & METABOLISM | NEURONS | rats | FAT DEPOTS | food intake | Phosphoproteins - drug effects | Phosphatidylinositol 3-Kinase - drug effects | Male | Mitogen-Activated Protein Kinase 1 - drug effects | Phosphoproteins - metabolism | Rhombencephalon - drug effects | Phosphatidylinositol 3-Kinases | Dose-Response Relationship, Drug | Mitogen-Activated Protein Kinase 3 - drug effects | Liver - drug effects | Fourth Ventricle | Leptin - pharmacology | Hypothalamus - drug effects | Phosphatidylinositol 3-Kinase - metabolism | STAT3 Transcription Factor - metabolism | Uncoupling Protein 1 - drug effects | Protein Tyrosine Phosphatase, Non-Receptor Type 1 - drug effects | Uncoupling Protein 1 - metabolism | Liver - metabolism | Rats, Sprague-Dawley | Blotting, Western | Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism | Animals | Hypothalamus - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | STAT3 Transcription Factor - drug effects | Suppressor of Cytokine Signaling 3 Protein - drug effects | Rhombencephalon - metabolism | Adipose Tissue, Brown - drug effects | Adipose Tissue, Brown - metabolism | Infusions, Intraventricular | Suppressor of Cytokine Signaling 3 Protein - metabolism | Energy Metabolism - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Cellular signal transduction | Genetic aspects | Genetic transcription | Health aspects | Leptin
Journal Article
Journal of Ethnopharmacology, ISSN 0378-8741, 2008, Volume 115, Issue 2, pp. 184 - 193
Journal Article