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Beta-endorphin Adenylate cyclase type 2 Voltage- dependent L-type calcium channel subunit beta-1 G protein- activated inward rectifier potassium channel 3 Mu-type opioid receptor Neuronal acetylcholine receptor subunit beta-2 Acetylcholine Trimebutine Na+ Acetylcholine Na+ Ca+ Ca+ Na+ Na+ ATP cAMP PPi Trimebutine GTP Neuronal acetylcholine receptor subunit alpha-4 nAchR Smooth Muscle Contraction Guanine nucleotide- binding protein G(i) subunit alpha-1 Magnesium Less nicotinic acetylcholine receptors are actiavted. Contraction of GI muscle is reduced, motility and secretion decreases. Neuromuscular Junction Smooth Muscle Myocyte Decreased calcium levels lead to decreased neurotransmitter release. Less acetylcholine is available in the synapse to bind to post synaptic muscarinic receptors on the muscle. Trimebutine activates mu opioid receptors inhibiting the N-type calcium channels on the neuron. This prevents calcium to enter the neuron and depolarize. Mu opioid receptor is coupled to Go and Gi proteins. When diphenoxylate activates the mu opioid receptor, the Gi cascade causes inhibition of adenylate cyclase and the Go signaling pathway causes inhibition of Ca2+ channels and activation of K+ channels. Pre-Synaptic Neuron Cytosol With the inhibition of adenylate cyclase, it is unable to synthesize cAMP which further prevents calcium from entering the neuron and depolarization of the neuron Synaptic Vesicle K+ channel is activated allowing K+ to enter the neuron and sodium to leave the neuron. This results in hyperpolarization, reducing the ability of the neuron to fire. Trimebutine is taken orally or intravenously
Unknown ADCY2 CACNB1 KCNJ9 OPRM1 GNB1 GNG2 Unknown Acetylcholine Trimebutine Sodium Acetylcholine Sodium Calcium Calcium Sodium Sodium Adenosine triphosphate cAMP Pyrophosphate Trimebutine Guanosine triphosphate Unknown nAchR Smooth Muscle Contraction GNAI1
ADCY2 CACNB1 KCNJ9 OPRM1 GNB1 GNG2 ACh Trime Na+ ACh Na+ Ca+ Ca+ Na+ Na+ ATP cAMP PPi Trime GTP