The involvement of VEGF receptors and MAPK in the cannabinoid potentiation of Ca²⁺ flux into N18TG2 neuroblastoma cells

Keyphrases

• Cannabinoids 100%
• Potentiation 100%
• Neuroblastoma Cells 100%
• Vascular Endothelial Growth Factor Receptor (VEGFR) 100%
• Ca2+ Flux 100%
• N18TG2 100%
• Stimulatory Effect 66%
• Protein Kinase 66%
• Ca2+ Influx 66%
• Novel Mechanism 33%
• CB1 Receptor 33%
• Inhibitory Effect 33%
• Mediating Effect 33%
• Phosphorylation 33%
• MAPK Cascade 33%
• PD98059 33%
• Transactivation 33%
• Receptor Tyrosine Kinase 33%
• Pertussis Toxin 33%
• Cellular Level 33%
• ERK2 33%
• GTP-binding Proteins 33%
• Protein Kinase C Inhibitor 33%
• Phenanthroline 33%
• Tissue Inhibitor of metalloproteinase-1 (TIMP-1) 33%
• Mitogen-activated Protein Kinase Inhibitor 33%
• Immunobloting 33%
• MAPK Activation 33%
• Chelerythrine 33%
• SR141716A 33%
• Dual Mechanism 33%
• Synthetic Cannabinoid Receptor Agonists 33%
• Oxindole 33%

Neuroscience

• Cannabinoid 100%
• Mitogen-Activated Protein Kinase 100%
• Neuroblastoma 100%
• VEGF Receptors 100%
• Protein Kinase C 75%
• Cannabinoid 1 Receptor 25%
• Receptor Agonists 25%
• MEK Inhibitor 25%
• G Protein 25%
• Pertussis Toxin 25%
• Metalloprotease Inhibitor 25%
• Mitogen Activated Protein Kinase 3 25%
• Tyrosine 25%
• Transactivation 25%
• Cannabinoid Receptor 25%
• Chelerythrine 25%
• Rimonabant 25%