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Gq protein signaling cascade Choline O- acetyltransferase Acetylcholinesterase N-type calcium channel Vesicular acetylcholine transporter High affinity choline transporter 1 Ca+ Acetylcholine Rivastigmine Rivastigmine Ca+ Choline Choline Rivastigmine Rivastigmine Acetyl-CoA Choline CoA H2O Acetic acid Acetylcholine Muscarinic acetylcholine receptor M1 Acetylcholine Magnesium Presynaptic Neuron Post-Synaptic Neuron 2. An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions 1. Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal 3. Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis 4. Acetylcholine in the synaptic cleft activates muscarinic receptors on the post-synaptic membrane 6. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 7. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Rivastigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. M1 receptor activation stimulates the Gq signaling cascade. The downstream effects are responsible for improving learning and memory ↓ Amyloid-Beta Production ↓ Tau Phosphorylation ↑ Neuronal Survival ↑ Cerebral Blood Flow Vesicle Rivastigmine is administered orally and diffuses into the bloodstream and travels to its target within the brain Rivastigmine inhibits choline-o-acetyltransferase, leading to accumulation of acetylcholine in the synaptic cleft.
GNAQ CHAT ACHE CACNB1 SLC18A3 SLC5A7 Calcium Acetylcholine Rivastigmine Rivastigmine Calcium Choline Choline Rivastigmine Rivastigmine Acetyl-CoA Choline Coenzyme A Water Acetic acid Acetylcholine CHRM1 Acetylcholine
GNAQ CHAT ACHE CACNB1 SLC18A3 SLC5A7 Ca+ ACh Rivasti Rivasti Ca+ Choline Choline Rivasti Rivasti Ac-CoA Choline CoA H2O Acoh ACh CHRM1 ACh Mg2+ Presynaptic Neuron Post-Synaptic Neuron 2. An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions 1. Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal 3. Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis 4. Acetylcholine in the synaptic cleft activates muscarinic receptors on the post-synaptic membrane 6. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 7. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Rivastigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. M1 receptor activation stimulates the Gq signaling cascade. The downstream effects are responsible for improving learning and memory ↓ Amyloid-Beta Production ↓ Tau Phosphorylation ↑ Neuronal Survival ↑ Cerebral Blood Flow Vesicle Rivastigmine is administered orally and diffuses into the bloodstream and travels to its target within the brain Rivastigmine inhibits choline-o-acetyltransferase, leading to accumulation of acetylcholine in the synaptic cleft.
GNAQ CHAT ACHE CACNB1 SLC18A3 SLC5A7 Ca2+ ACh Rivasti Rivasti Ca2+ Choline Choline Rivasti Rivasti Ac-CoA Choline CoA H2O Acoh ACh CHRM1 ACh