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Cytokine and Growth Factor Reviews, ISSN 1359-6101, 04/2019, Volume 46, pp. 10 - 16
All organisms display circadian rhythms which are under the control of the circadian clock located in the hypothalamus at the suprachiasmatic nucleus, (SCN).... 
Circadian clock | TGF | p38 | TNF | IMMUNE-RESPONSE | KAPPA-B ACTIVATION | SLEEP | MELATONIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | CELL BIOLOGY | ROLES | GENE-EXPRESSION | TNF-ALPHA | NIGHT-SHIFT WORK | BINDING | Somatotropin | Medical colleges | Tumor necrosis factor | Genes | Physiological aspects | Genetic transcription | Transforming growth factors | Tumors | Necrosis
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 06/2014, Volume 89, Issue 4, pp. 453 - 463
Osteosarcoma is the most common primary malignancy of bone and is characterized by a high malignant and metastatic potential. Transforming growth factor alpha... 
Osteosarcoma | TGF-α | Migration | TGF-alpha | ADHESION MOLECULES | HUMAN CHONDROSARCOMA CELLS | BREAST-CANCER CELLS | HEPATOCELLULAR-CARCINOMA | GASTRIC-CANCER | COLORECTAL-CANCER | PI3K-AKT PATHWAY | PHARMACOLOGY & PHARMACY | NF-KAPPA-B | TRANSGENIC MICE | Osteosarcoma - drug therapy | Receptor, Epidermal Growth Factor - agonists | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Male | NF-kappa B - metabolism | Antineoplastic Agents - therapeutic use | Bone Neoplasms - pathology | Proto-Oncogene Proteins c-akt - genetics | Bone Neoplasms - metabolism | Receptor, Epidermal Growth Factor - metabolism | Lung Neoplasms - secondary | RNA Interference | Antineoplastic Agents - pharmacology | Bone Neoplasms - drug therapy | Proto-Oncogene Proteins c-akt - metabolism | Transforming Growth Factor alpha - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Osteosarcoma - metabolism | Recombinant Proteins - metabolism | NF-kappa B - antagonists & inhibitors | Second Messenger Systems - drug effects | Transforming Growth Factor alpha - antagonists & inhibitors | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Mice, SCID | Transforming Growth Factor alpha - genetics | Phosphatidylinositol 3-Kinase - chemistry | Up-Regulation - drug effects | Xenograft Model Antitumor Assays | Cell Movement - drug effects | Intercellular Adhesion Molecule-1 - metabolism | Animals | Intercellular Adhesion Molecule-1 - chemistry | Lung Neoplasms - prevention & control | NF-kappa B - genetics | Phosphatidylinositol 3-Kinase - genetics | Tumor Burden - drug effects | Intercellular Adhesion Molecule-1 - genetics | Proto-Oncogene Proteins c-akt - agonists | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Osteosarcoma - secondary | Osteosarcoma - pathology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Metastasis
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2015, Volume 10, Issue 9, p. e0138372
The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-alpha has been shown to cause adverse left ventricular remodeling and... 
CTGF EXPRESSION | NADPH OXIDASE | INDUCED HYPERTENSION | XANTHINE-OXIDASE | NAD(P)H OXIDASE | CARDIAC RESTRICTED OVEREXPRESSION | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | GENE-EXPRESSION | BLOOD-PRESSURE | TRANSGENIC MICE | Tumor Necrosis Factor-alpha - metabolism | MAP Kinase Signaling System - physiology | Oxidative Stress - physiology | Collagen Type III - metabolism | NADPH Oxidases - metabolism | Male | NF-kappa B - metabolism | Fibrosis - metabolism | RNA, Messenger - metabolism | Myocardium - metabolism | Blood Pressure - drug effects | Blood Pressure - physiology | p38 Mitogen-Activated Protein Kinases - metabolism | Heart - physiopathology | Angiotensin II - pharmacology | Collagen Type I - metabolism | Ventricular Remodeling - physiology | Hypertension - physiopathology | Hypertension - metabolism | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Receptor, Angiotensin, Type 1 - metabolism | Heart - drug effects | Signal Transduction - physiology | Mice | Fibrosis - pathology | Oxidative Stress - drug effects | Transforming Growth Factor beta - metabolism | Ventricular Remodeling - drug effects | Connective Tissue Growth Factor - metabolism | Cardiomegaly - metabolism | Oxidases | Hypertension | Heart | Oxidative stress | RNA | Heart enlargement | Transforming growth factors | Necrosis | Tumor necrosis factor | Collagen | Angiotensin | Bone morphogenetic proteins | Tumors | Veterinary colleges | Reactive oxygen species | Collagen (type I) | Crosstalk | Body weight | Collagens | mRNA | Kinases | Remodeling | NAD(P)H oxidase | Infusion | Signal transduction | Etanercept | Tumor necrosis factor-TNF | Blood pressure | Angiotensin II | Heart diseases | NF-κB protein | Collagen (type III) | MAP kinase | Connective tissue growth factor | JNK protein | Tumor necrosis factor-α | Gene expression | Signaling | Nitric oxide | Fibrosis | Ventricle | Hypertrophy
Journal Article
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 12/2018, Volume 506, Issue 4, pp. 901 - 906
Journal Article
Journal Article