PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23562497-2 2013 We have focussed on the observation that AChE, operating as a trophic agent independent of its enzymatic action, does indeed trigger calcium entry into neurons. Calcium 133-140 acetylcholinesterase (Cartwright blood group) Homo sapiens 41-45 9282941-0 1997 The amyloid beta-protein of Alzheimer"s disease increases acetylcholinesterase expression by increasing intracellular calcium in embryonal carcinoma P19 cells. Calcium 118-125 acetylcholinesterase (Cartwright blood group) Homo sapiens 58-78 19468687-0 2009 Calcium signaling-induced Smad3 nuclear accumulation induces acetylcholinesterase transcription in apoptotic HeLa cells. Calcium 0-7 acetylcholinesterase (Cartwright blood group) Homo sapiens 61-81 19468687-2 2009 We previously showed that cellular calcium mobilization upregulated AChE expression by modulating promoter activity and mRNA stability. Calcium 35-42 acetylcholinesterase (Cartwright blood group) Homo sapiens 68-72 19468687-3 2009 In this study, we have identified a potential Smad3/4 binding element, TGCCAGACA, located within the -601 to -571 bp fragment of the AChE promoter, as an important calcium response motif. Calcium 164-171 acetylcholinesterase (Cartwright blood group) Homo sapiens 133-137 19468687-7 2009 Calcium-induced AChE transcriptional activation was significantly blocked when the nuclear localization signal of Smad3 was destroyed. Calcium 0-7 acetylcholinesterase (Cartwright blood group) Homo sapiens 16-20 19468687-8 2009 Taken together, our data suggest Smad3 can regulate AChE transcriptional activation following calcium-induced nuclear accumulation. Calcium 94-101 acetylcholinesterase (Cartwright blood group) Homo sapiens 52-56 17728068-0 2007 The CCAAT-binding factor CBF/NF-Y regulates the human acetylcholinesterase promoter activity during calcium ionophore A23187-induced cell apoptosis. Calcium 100-107 acetylcholinesterase (Cartwright blood group) Homo sapiens 54-74 16021692-0 2005 Juliflorine: a potent natural peripheral anionic-site-binding inhibitor of acetylcholinesterase with calcium-channel blocking potential, a leading candidate for Alzheimer"s disease therapy. Calcium 101-108 acetylcholinesterase (Cartwright blood group) Homo sapiens 75-95 12027383-5 2002 Aliquots with added calcium (without the presence of Br-A23187 in DMSO) had a significantly higher erythrocyte acetylcholinesterase activity. Calcium 20-27 acetylcholinesterase (Cartwright blood group) Homo sapiens 111-131 12031351-5 2002 Acetylcholinesterase regulation of outgrowth was shown to depend on an influx of extracellular calcium specifically via the L-type voltage-gated calcium channel. Calcium 95-102 acetylcholinesterase (Cartwright blood group) Homo sapiens 0-20 20156431-2 2010 The C-terminal region of AChE has been shown to be responsible for non-cholinergic actions of AChE by binding to an allosteric site on the alpha 7-nicotinic acetylcholine receptor, thereby causing calcium influx; the resultant signal has trophic effects in immature neurons, but toxic effects in mature neurons. Calcium 197-204 acetylcholinesterase (Cartwright blood group) Homo sapiens 25-29 20156431-2 2010 The C-terminal region of AChE has been shown to be responsible for non-cholinergic actions of AChE by binding to an allosteric site on the alpha 7-nicotinic acetylcholine receptor, thereby causing calcium influx; the resultant signal has trophic effects in immature neurons, but toxic effects in mature neurons. Calcium 197-204 acetylcholinesterase (Cartwright blood group) Homo sapiens 94-98 18769671-7 2008 Moreover, inherent N-AChE-S was upregulated by stressors inducing protein misfolding and calcium imbalances, both characteristic of AD; and in cortical tissues from AD patients, N-AChE-S overexpression coincides with Tau hyper-phosphorylation. Calcium 89-96 acetylcholinesterase (Cartwright blood group) Homo sapiens 21-25 17654703-4 2007 We report that, in astroglia and in an immortalized cell line, GH4-halpha7, acute oxidative stress causes influx of extracellular calcium through L-type voltage-gated calcium channels (L-VGCC), followed by increased release of AChE into the extracellular medium. Calcium 130-137 acetylcholinesterase (Cartwright blood group) Homo sapiens 227-231 17335779-5 2007 Considering the large size of the human skin with 1.8m(2) surface area with its calcium gradient in the 10(-3)M range, our results implicate calcium-activated BuchE as a major protective mechanism against suicide inhibition of AchE by organophosphates in this non-neuronal tissue. Calcium 141-148 acetylcholinesterase (Cartwright blood group) Homo sapiens 227-231 17320203-0 2007 Calcineurin mediates acetylcholinesterase expression during calcium ionophore A23187-induced HeLa cell apoptosis. Calcium 60-67 acetylcholinesterase (Cartwright blood group) Homo sapiens 21-41 17000130-0 2007 Regulation of acetylcholinesterase expression by calcium signaling during calcium ionophore A23187- and thapsigargin-induced apoptosis. Calcium 49-56 acetylcholinesterase (Cartwright blood group) Homo sapiens 14-34 17000130-0 2007 Regulation of acetylcholinesterase expression by calcium signaling during calcium ionophore A23187- and thapsigargin-induced apoptosis. Calcium 74-81 acetylcholinesterase (Cartwright blood group) Homo sapiens 14-34 17000130-3 2007 During apoptosis, treatment of HeLa and MDA-MB-435s cells with the calcium ionophore A23187 resulted in a significant increase in acetylcholinesterase mRNA and protein levels. Calcium 67-74 acetylcholinesterase (Cartwright blood group) Homo sapiens 130-150 9282941-7 1997 To examine the possibility that the increase in AChE expression was mediated by an influx of calcium through voltage-dependent calcium channels (VDCCs), drugs acting on VDCCs were tested for their effects. Calcium 93-100 acetylcholinesterase (Cartwright blood group) Homo sapiens 48-52 9282941-13 1997 The results suggest that the increase in AChE expression around amyloid plaques could be due to a disturbance in calcium homeostasis involving the opening of L-type VDCCs. Calcium 113-120 acetylcholinesterase (Cartwright blood group) Homo sapiens 41-45 2561349-2 1989 It was revealed, that under conditions promoting DS (hyperpolarization, muscle warming, rise of calcium concentration as well as treatment by the DS--potentiating agent--proadifen) decrease of the postsynaptic membrane sensitivity to the acetylcholine can develop after few multiquantal end-plate currents--and when acetylcholinesterase is inhibited--during the response to a single quantum of acetylcholine. Calcium 96-103 acetylcholinesterase (Cartwright blood group) Homo sapiens 316-336 8899663-2 1996 Glutamate (GLU), kainate and AMPA, as well as glycine (GLY) evoked dose-related, calcium-dependent liberation of soluble forms of AChE from both slices and synaptosomes. Calcium 81-88 acetylcholinesterase (Cartwright blood group) Homo sapiens 130-134 1913783-0 1991 Calcium and ionophore A23187 stimulates deposition of extracellular matrix and acetylcholinesterase release in cultured myotubes. Calcium 0-7 acetylcholinesterase (Cartwright blood group) Homo sapiens 79-99 1913783-2 1991 We demonstrate here than increases in intracellular calcium concentration induce a time- and concentration-dependent deposition of extracellular matrix and an increase in acetylcholinesterase secretion. Calcium 52-59 acetylcholinesterase (Cartwright blood group) Homo sapiens 171-191 1913783-3 1991 Scanning and transmission electron-microscopy revealed that treatment with the calcium ionophore A23187, or high extracellular Ca2+ levels (5 mM to 15 mM) produce significant deposits of extracellular matrix around the myotubes, as well as a marked increase in the acetylcholinesterase reaction-product. Calcium 79-86 acetylcholinesterase (Cartwright blood group) Homo sapiens 265-285 1511329-2 1992 The subset of neurons particularly sensitive to AChE are characterized by functionally active apical dendrites extending into the pars reticulata and generating a powerful calcium conductance. Calcium 172-179 acetylcholinesterase (Cartwright blood group) Homo sapiens 48-52 30411689-9 2019 Molecular docking study indicated that the spirocyclohexadienone, 9e (IC50 = 0.12 microM), a mixedtype AChE inhibitor, showed a good interaction at active site of the enzyme, including the cationic (CAS) and the peripheral site (PAS). Calcium 199-202 acetylcholinesterase (Cartwright blood group) Homo sapiens 103-107 6834035-4 1983 The local evoked release of acetylcholinesterase and of total protein differed in the extent to which they were calcium-dependent. Calcium 112-119 acetylcholinesterase (Cartwright blood group) Homo sapiens 28-48 5532277-0 1970 [Effect of lithium and calcium ions on erythrocyte acetylcholinesterase activity]. Calcium 23-30 acetylcholinesterase (Cartwright blood group) Homo sapiens 51-71 6108954-4 1981 In untreated inside-out vesicles, 3.76 +/- 1.44 nmol of calcium/min/unit of acetylcholinesterase were transported, compared with 10.57 +/- 2.05 (+/- S.D. Calcium 56-63 acetylcholinesterase (Cartwright blood group) Homo sapiens 76-96 30567381-7 2018 Similarly docking studies predicted interaction of the most active compounds with both CAS and PAS of either AChE or BChE with mixed type of enzyme inhibition confirmed by kinetic studies. Calcium 87-90 acetylcholinesterase (Cartwright blood group) Homo sapiens 109-113 24059317-7 2014 During "Cisplatin-CAS site of AChE enzyme" interaction, it was found that out of the three amino acids constituting the catalytic triad (S203, H447 and E334), two amino acid residues namely S203 and H447 interact with Cisplatin by hydrogen bonding and hydrophobic interaction, respectively. Calcium 18-21 acetylcholinesterase (Cartwright blood group) Homo sapiens 30-34 27967267-8 2017 New AChE inhibitors with polypharmacology or dual inhibitory activity have also emerged as highlighted by new AChE inhibitors with dual activity at L-type calcium channels, GSK-3, BACE1 and H3, although most only show low micromolar activity, thus further research is warranted. Calcium 155-162 acetylcholinesterase (Cartwright blood group) Homo sapiens 4-8 27967267-8 2017 New AChE inhibitors with polypharmacology or dual inhibitory activity have also emerged as highlighted by new AChE inhibitors with dual activity at L-type calcium channels, GSK-3, BACE1 and H3, although most only show low micromolar activity, thus further research is warranted. Calcium 155-162 acetylcholinesterase (Cartwright blood group) Homo sapiens 110-114 24473150-0 2014 Copper, aluminum, iron and calcium inhibit human acetylcholinesterase in vitro. Calcium 27-34 acetylcholinesterase (Cartwright blood group) Homo sapiens 49-69 24473150-6 2014 However, aluminum, cupric, ferric and calcium ions were able to inhibit AChE via noncompetitive mechanism of inhibition. Calcium 38-45 acetylcholinesterase (Cartwright blood group) Homo sapiens 72-76