Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nerve growth factor (NGF)-potentiating effect of K vitamins on PC12D cells was investigated. Treatment of PC12D cells with vitamin K(1) or K(2) in the presence of NGF significantly enhanced the proportion of neurite-bearing cells and acetylcholinesterase activity compared with NGF treatment alone. The K vitamins-enhanced neurite outgrowth on PC12D cells was completely blocked by a protein kinase A (PKA) inhibitor or mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059, whereas a protein kinase C inhibitor chelerythrine chloride did not significantly inhibit the enhancing effect of the K vitamins. These results suggest that the K vitamins enhance neurite outgrowth via the activation of PKA and MAPK-mediated signaling pathways in PC12D cells.
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PMID:Novel effect of vitamin K(1) (phylloquinone) and vitamin K(2) (menaquinone) on promoting nerve growth factor-mediated neurite outgrowth from PC12D cells. 1191 78

This study is to explore the involvement of muscarinic acetylcholine receptors/protein kinase C cascade and the mitogen-activated protein kinase pathway in the effect of huperzine A on the secretory amyloid precursor protein-alpha. Upregulation of secretory amyloid precursor protein-alpha by huperzine A was attenuated by muscarinic acetylcholine receptor antagonist (specifically by M1-muscarinic acetylcholine receptor antagonist), and markedly blocked (-37.7%) by protein kinase C inhibitor as well. Meanwhile, huperzine A can activate the phosphorylation of mitogen-activated protein kinase and, accordingly, partly restored PD98059-decreased secretory amyloid precursor protein-alpha secretion. In addition, huperzine A largely inhibited (-55.4%) acetylcholinesterase activity of the cell line. Our results suggest that activated M1-muscarinic acetylcholine receptor/protein kinase C pathway and mitogen-activated protein kinase signaling are involved in the process of huperzine A enhancing the secretory amyloid precursor protein-alpha secretion.
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PMID:Involvement of M1-muscarinic acetylcholine receptors, protein kinase C and mitogen-activated protein kinase in the effect of huperzine A on secretory amyloid precursor protein-alpha. 1742

The major pathological changes in Alzheimer's disease are beta amyloid deposits and cognitive impairment. Calycosin is a typical phytoestrogen derived from radix astragali that binds to estrogen receptors to produce estrogen-like effects. Radix astragali Calycosin has been shown to relieve cognitive impairment induced by diabetes mellitus, suggesting calycosin may improve the cognitive function of Alzheimer's disease patients. The protein kinase C pathway is upstream of the mitogen-activated protein kinase pathway and exerts a neuroprotective effect by regulating Alzheimer's disease-related beta amyloid degradation. We hypothesized that calycosin improves the cognitive function of a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway. Various doses of calycosin (10, 20 and 40 mg/kg) were intraperitoneally injected into APP/PS1 transgenic mice that model Alzheimer's disease. Calycosin diminished hippocampal beta amyloid, Tau protein, interleukin-1beta, tumor necrosis factor-alpha, acetylcholinesterase and malondialdehyde levels in a dose-dependent manner, and increased acetylcholine and glutathione activities. The administration of a protein kinase C inhibitor, calphostin C, abolished the neuroprotective effects of calycosin including improving cognitive ability, and anti-oxidative and anti-inflammatory effects. Our data demonstrated that calycosin mitigated oxidative stress and inflammatory responses in the hippocampus of Alzheimer's disease model mice by activating the protein kinase C pathway, and thereby improving cognitive function.
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PMID:Calycosin improves cognitive function in a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway. 2923 34

Great effort is put into seeking a new and effective strategies to control insect pests. One of them is to combine natural products with chemical insecticides to increase their effectiveness. In the study presented, menthol which is an essential oil component was evaluated on its ability to increase the efficiency of bendiocarb, carbamate insecticide. A multi-approach study was conducted using biochemical method (to measure acetylcholinesterase enzyme activity), electrophysiological technique (microelectrode recordings in DUM neurons in situ), and confocal microscopy (for calcium imaging). In the electrophysiological experiments, menthol caused hyperpolarization, which was blocked by an octopamine receptor antagonist (phentolamine) and an inhibitor of protein kinase A (H-89). It also raised the intracellular calcium level. The effect of bendiocarb was potentiated by menthol and this phenomenon was abolished by phentolamine and H-89 but not by protein kinase C inhibitor (bisindolylmaleimide IX). The results indicate that menthol increases carbamate insecticide efficiency by acting on octopamine receptors and triggering protein kinase A phosphorylation pathway.
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PMID:Menthol Increases Bendiocarb Efficacy Through Activation of Octopamine Receptors and Protein Kinase A. 3163 51