Quantitative metabolomics services for biomarker discovery and validation.
Specializing in ready to use metabolomics kits.
Your source for quantitative metabolomics technologies and bioinformatics.
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Gq protein signaling cascade Phospholipase C Protein kinase C alpha type Histamine H1 receptor Nitric oxide synthase, endothelial Myosin light chain phosphatase Voltage- dependent P/Q-type calcium channel subunit alpha-1A Voltage- dependent L-type calcium channel subunit beta-1 Voltage- dependent calcium channel subunit alpha-2/delta-2 Inositol 1,4,5- trisphosphate receptor type 1 Myosin LC-P Myosin light chain 3 Calmodulin-1 Myosin light chain kinase, smooth muscle Calmodulin-1 Histamine NO Inositol 1,4,5- trisphosphate Aripiprazole lauroxil NO Ca+ Ca+ Ca+ Aripiprazole lauroxil Phosphatidylinositol 4,5-bisphosphate L-Arginine H+ NADPH O2 H2O Citrulline NADP Calcium Heme FAD Flavin Mononucleotide Tetrahydrobiopterin Ca+ Diacylglycerol Muscle Contraction Muscle relaxation Mast Cells Release Histamine Manganese Magnesium Calcium Endoplasmic Reticulum Calcium cannot bind to calmodulin to activate the calmodulin-binding domain of nitric oxide synthase. There is an overall decrease in calcium levels in the cytosol caused by the inhibition of the Gq signaling cascade Cytosol Endothelial Cell Aripiprazole lauroxil antagonizes Histamine H1 receptors in endothelial cells, preventing histamine from activating the receptor The inhibition of Nitric oxide synthesis prevents the activation of myosin light chain phosphatase. This causes an accumulation of myosin light chain-phosphate which causes the muscle to contract. Myocyte Actin and myosin bind bringing the filaments together causing muscle contraction Actin filament Myosin filament Blood Vessel constriction Blood vessel