Quantitative metabolomics services for biomarker discovery and validation.
Specializing in ready to use metabolomics kits.
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Nicotinic Acetylcholine Receptor Nicotinic Acetylcholine Receptor Voltage- dependent L-type calcium channel subunit alpha-1C Myosin light chain kinase Acetylcholinesterase Myosin LC-P Myosin light chain 3 N-type calcium channel Vesicular acetylcholine transporter High affinity choline transporter 1 Choline O- acetyltransferase Calmodulin-1 Myosin light chain phosphatase Ca+ Acetylcholine Na+ Neostigmine Ca+ Choline Choline Na+ Ca+ Ca+ Acetyl-CoA Choline CoA H2O Acetic acid Manganese Ca+ Calmodulin-1 Acetylcholine Acetylcholine Muscle Contraction Muscle Relaxation Magnesium Presynaptic Neuron Motor End Plate 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 nicotinic receptors on the post-synaptic membrane 7. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 8. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Neostigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. The activated nicotinic receptor stimulates sodium ion influx, depolarizing the cell Vesicle Neostigmine is administered intravenously and diffuses into the bloodstream and travels to its target within the brain Sacroplasmic Reticulum 6. Depolarization causes a release of calcium from the sarcoplasmic reticulum. Calcium binds to calmodulin that in turn activates myosin light chain kinase. Once phosphorylated starts initiating muscle contraction Neuromuscular Junction
Unknown Unknown CACNA1C MYLK2 ACHE MYL3 MYL3 CACNB1 SLC18A3 SLC5A7 CHAT CALM1 PPP1CB Calcium Acetylcholine Sodium Neostigmine Calcium Choline Choline Sodium Calcium Calcium Acetyl-CoA Choline Coenzyme A Water Acetic acid Calcium CALM1 Acetylcholine Acetylcholine Muscle Contraction Muscle Relaxation
CACNA1C MYLK2 ACHE MYL3 MYL3 CACNB1 SLC18A3 SLC5A7 CHAT CALM1 PPP1CB Ca+ ACh Na+ Eustigm Ca+ Choline Choline Na+ Ca+ Ca+ Ac-CoA Choline CoA H2O Acoh Mn2+ Ca+ CALM1 ACh ACh Mus Con Mus Rel Mg2+ Presynaptic Neuron Motor End Plate 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 nicotinic receptors on the post-synaptic membrane 7. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 8. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Neostigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. The activated nicotinic receptor stimulates sodium ion influx, depolarizing the cell Vesicle Neostigmine is administered intravenously and diffuses into the bloodstream and travels to its target within the brain Sacroplasmic Reticulum 6. Depolarization causes a release of calcium from the sarcoplasmic reticulum. Calcium binds to calmodulin that in turn activates myosin light chain kinase. Once phosphorylated starts initiating muscle contraction Neuromuscular Junction