Neurotransmitters

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spinqualitylabelsall models Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image   Print3D Acetylcholine Acetylcholinesterase (EC 3.1.1.7, e.g. from Torpedo californica, TcAChE) hydrolysizes the neurotransmitter acetylcholine (ACh), producing choline and an acetate group. ACh directly binds Ser200 (via its nucleophilic Oγ atom) within the catalytic triad catalytic triad (Ser200, His440, and Glu327) of (ACh/TcAChE structure 2ace). The residues Trp84 and Phe330 are also important in the ligand recognition. After this binding acetylcholinesterase hydrolysizes ACh. Acetylcholinesterase Acetylcholinesterase: Treatment of Alzheimer's disease Torpedo californica acetylcholinesterase with bifunctional inhibitor Acetylcholinesterase: Substrate Traffic and Inhibition Acetylcholinesterase Inhibitor Pharmacokinetics Acetylcholinesterase inhibitors AChE inhibitors and substrates Human Acetylcholinesterase African Malaria Mosquito Acetylcholinesterase Acetylcholinesterase inhibited by nerve agent soman Acetylcholinesterase with DFP Acetylcholinesterase with OTMA Acetylcholinesterase with acetylcholine Acetylcholinesterase complexed with N-9-(1',2',3',4'-tetrahydroacridinyl)-1,8-diaminooctane Complex of TcAChE with an iminium galanthamine derivative Complex of TcAChE with bis-acting galanthamine derivative Cholinesterase Flexibility of aromatic residues in acetylcholinesterase Huperzine A Complexed with Acetylcholinesterase & Huperzine A Complexed with Acetylcholinesterase (Chinese) Acetylcholinesterase complexed with Tacrine, the 1st anti Alzheimer's drug Torpedo Californica Acetylcholinesterase in complex with an (R)-Tacrine-(10)-Hupyridone inhibitor Torpedo Californica Acetylcholinesterase in complex with an (S)-Tacrine-(10)-Hupyridone inhibitor Torpedo californica acetylcholinesterase with alkylene-linked tacrine dimer (5 carbon linker) Torpedo californica acetylcholinesterase with alkylene-linked tacrine dimer (7 carbon linker) Torpedo californica acetylcholinesterase with bifunctional inhibitor Tetramerization domain of acetylcholinesterase African Malaria Mosquito Acetylcholinesterase Group:SMART:Acetylcholinesterase:A Story of Substrate Traffic and Inhibition by Green Mamba Snake Toxin Treatments:AChE Inhibitor References Dopamine Dopamine Receptors Dopamine receptors 1 page Dopamine receptors 2 page Agonists Amphetamine Methamphetamine Antagonists Clebopride Nafadotride Eticlopride. Structure of the human dopamine D3 receptor in complex with the antagonist eticlopride and maltose (3pbl). Eticlopride binding site. Parkinson's disease DOPA decarboxylase is responsible for the synthesis of dopamine and serotonin from L-DOPA and L-5-hydroxytryptophan, respectively. It is highly stereospecific, yet relatively nonspecific in terms of substrate, making it a somewhat uninteresting enzyme to study. Although it is not typically a rate-determining step of dopamine synthesis, the decarboxylation of L-DOPA to dopamine by DDC is the controlling step for individuals with Parkinson's disease, the second most common neurodegenerative disorder, occuring in 1% of the population over the age of 65. The loss of dopaminergic neurons is the main cause of cognitive impairment and tremors observed in patients with the disease. The hallmark of the disease is the formation of alpha-synuclein containing Lewy bodies. Currently, treatment for the disease is aimed at DOPA decarboxylase inhibition. Since dopamine cannot cross the blood-brain barrier, it cannot be used to directly treat Parkinson's disease. Thus, exogenously administered L-DOPA is the primary treatment for patients suffering from this neurodegenerative disease. Unfortunately, DOPA decarboxylase rapidly converts L-DOPA to dopamine in the blood stream, with only a small percentage reaching the brain. By inhibiting the enzyme, greater amounts of exogenously administered L-DOPA can reach the brain, where it can then be converted to dopamine. . Unfortunately, with continued L-Dopa treatment, up to 80% of patients experience 'wearing-off' symptoms, dyskinesias and other motor complications (referred to as the "on-off phenomenon". . Clearly, a better understanding of the catalytic mechanism and enzymatic activity of DDC in both healthy and PD individuals is critical to drug design and treatment of the disease.

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Alexander Berchansky