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

Localization of choline-acetyltranspherase (CHAT 2. 3. 1. 6) and acetylcholinesterase (ACHE 3. 1. 1. 7) in the neuronal plexus of the main artery in the cat brain has been studied. It has been stated that CHAT is mainly revealed in preterminal and terminal fibres of the plexus, while AXE--along the whole length of the fibre. ACHE activity is higher than that of Chat.
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PMID:[Choline acetyltransferase in the nerve plexuses of the basilar artery of the cat brain]. 66 80

In the brain of the hagfish Myxine glutinosa the distribution of acetylcholinesterase has been studied in serial cryostat sections. High activity was found in the motor column of the brain stem, in the pars ventralis thalami and in the primordium hippocampi. In the hemispheres and the olfactory bulb the ACHE-content is low.
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PMID:The distribution of acetylcholinesterase in the cyclostome brain. II. Myxine glutinosa. 114 87

Characterization of genomic clones encoding mouse acetylcholinesterase enabled us to identify a restriction fragment length polymorphism that distinguishes between the progenitor strains for the recombinant inbred strain sets AKXD and BXD. The strain distribution pattern for this polymorphism indicates that Ache is located on distal mouse chromosome 5.
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PMID:Assignment of the gene for acetylcholinesterase to distal mouse chromosome 5. 135 6

To establish the chromosomal location of the human ACHE gene encoding the acetylcholine hydrolyzing enzyme acetylcholinesterase (ACHE, acetylcholine acetylhydrolase, E.C. 3.1.1.7), a human-specific polymerase chain reaction (PCR) procedure that supports the selective amplification of ACHE DNA fragments from human genomic DNA was employed with 19 human-hamster somatic cell hybrids carrying one or more human chromosomes. Informative ACHE-specific PCR fragments were produced from two cell lines, both of which include human chromosome 7, but not with DNA from 17 cell hybrids carrying various combinations of all human chromosomes other than 7. Fluorescent in situ hybridization of biotinylated ACHE DNA with metaphase chromosomes from human peripheral blood lymphocytes revealed prominent labeling on the 7q22 position. Therefore, further tests were performed to confirm the chromosome 7 location. DNA samples from the two cell lines including chromosome 7 and the ACHE gene were positive with PCR primers informative for the human cystic fibrosis CFTR gene, known to reside at the 7q31.1 position, but negative for the ACHE-related butyrylcholinesterase (BCHE, acylcholine acylhydrolase, E.C. 3.1.1.8) gene, mapped at the 3q26-ter position, confirming that these lines contain chromosome 7 but not chromosome 3. In contrast, three other cell lines including chromosome 3, but not 7, were BCHE-positive and ACHE-negative. In addition, genomic DNA from a sorted chromosome 7 library supported the production of ACHE- but not BCHE-specific PCR products, whereas with DNA from a sorted chromosome 3 library, the BCHE but not the ACHE fragment was amplified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mapping the human acetylcholinesterase gene to chromosome 7q22 by fluorescent in situ hybridization coupled with selective PCR amplification from a somatic hybrid cell panel and chromosome-sorted DNA libraries. 138 Apr 83

In 20 unselected autopsy cases tissue blocks from the hippocampus with adjacent entorhinal cortex and neocortex were stained for acetylcholinesterase (AChE). From five brains shown to have large numbers of senile plaques tissue, adjacent to that taken for AChE tissue blocks, was embedded in paraffin and sections were immunostained for the A4 protein. The morphological aspects were compared. Equivalent types of plaques and plaque-like structures were observed in the A4- and ACHE-stained sections. On selected tissue blocks from patients with many senile plaques two immediately adjacent cryostat sections were stained, one for AChE and one for A4 protein. The same individual plaques could be identified on the two sections. These findings suggest that high AChE activity is intimately associated with the process of A4 protein formation and accumulation in plaques and that this association already occurs at a very early stage of plaque formation.
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PMID:Senile plaques: staining for acetylcholinesterase and A4 protein: a comparative study in the hippocampus and entorhinal cortex. 170 83

1. Various hybridization approaches were employed to investigate structural and chromosomal interrelationships between the human cholinesterase genes CHE and ACHE encoding the polymorphic, closely related, and coordinately regulated enzymes having butyrylcholinesterase (BuChE) and acetylcholinesterase (AChE) activities. 2. Homologous cosmid recombination with a 190-base pair 5' fragment from BuChEcDNA resulted in the isolation of four overlapping cosmid clones, apparently derived from a single gene with several introns. The Cosmid CHEDNA included a 700-base pair fragment known to be expressed at the 3' end of BuChEcDNA from nervous system tumors and which has been mapped by in situ hybridization to the unique 3q26-ter position. In contrast, cosmid CHEDNA did not hybridize with full-length AChEcDNA, proving that the complete CHE gene does not include AChE-encoding sequences either in exons or in its introns. 3. The chromosomal origin of BuChE-encoding sequences was further examined by two unrelated gene mapping approaches. Filter hybridization with DNA from human/hamster hybrid cell lines revealed BuChEcDNA-hybridizing sequences only in cell lines including human chromosome 3. However, three BuChEcDNA-homologous sequences were observed at chromosomal positions 3q21, 3q26-ter, and 16q21 by a highly stringent in situ hybridization protocol, including washes at high temperature and low salt. 4. These findings stress the selectivity of cosmid recombination and chromosome blots, raise the possibility of individual differences in BuChEcDNA-hybridizing sequences, and present an example for a family highly similar proteins encoded by distinct, nonhomologous genes.
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PMID:Human acetylcholinesterase and butyrylcholinesterase are encoded by two distinct genes. 201 62

Cholinesterases are ubiquitous carboxylesterase type B enzymes capable of hydrolyzing the neurotransmitter acetylcholine which are transiently expressed in multiple germline, embryonic, and tumor cells. The acute poisoning effects of various organophosphorous compounds are generally attributed to their irreversible covalent interaction with cholinesterases and block of their catalytic activities. We have recently found a de novo inheritable amplification of a CHE gene encoding defective butyrylcholinesterase (acylcholine acyl hydrolase; EC 3.1.1.8) in a family under prolonged exposure to the agricultural organophosphorous insecticide methyl parathion. Further analysis revealed that both the CHE and the ACHE genes, encoding acetylcholinesterase (acetylcholine acetyl hydrolase; EC 3.1.1.7), are amplified in leukemias and platelet disorders and that the tumorigenic expression of these genes in ovarian carcinomas is associated with their frequent coamplification in these tumors. The amplification of CHE and ACHE genes in normal and tumor tissues might be analogous to the well-known amplification of other genes encoding target proteins to toxic compounds. As such, it could provide cells a selection advantage when exposed to organophosphorous poisons. Further, since cholinesterases appear to play developmentally important roles in multiple cell types, the amplification and overexpression of their corresponding genes might affect fertility, be related to the progression of various tumor types, and bear upon the ecological and clinical risks involved with the common use of organophosphorous poisons.
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PMID:Amplification of butyrylcholinesterase and acetylcholinesterase genes in normal and tumor tissues: putative relationship to organophosphorous poisoning. 240 80

The effect of conventional antidotal therapy of oral intoxication due to organophosphorus insecticide Neguvon in male mice is compared to the effect of peritoneal dialysis. As a dialysate, the combination of ACHE reactivator with atropine, distilled water and ACHE preparation has been used. In order to evaluate treatment results, the clinical course of intoxication and the increase of blood ACHE activity inhibited with perorally Neguvon were investigated. The highest increase in activity of inhibited blood ACHE has been stated by the peritoneal dialysis with ACHE preparation. Furthermore, the effects of two dialysates were compared. The first one consisted in ACHE reactivator with atropine, and the second one in ACHE preparation, respectively. The ACHE containing dialysate showed better therapeutical results. The mentioned acetylcholinesterase is stated to be inhibited through the treatment with 50% of Neguvon dosage applied to the experimental animals. Thus the actual dose of Neguvon inducing proper intoxication was reduced to its half amount.
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PMID:[Methods of treating experimental Neguvon poisoning and a comparison of their effects]. 264 Mar 62

Prenatal diagnosis is primarily the task of the obstetrician and clinical geneticist, but it must concern the pediatrician as well. It may give advance warning of postnatal problems and yield information that is valuable in the care of the newborn. Moreover, the pediatrician may be called upon to judge the prognosis of a child with a prenatally detected anomaly and prenatal therapy might be considered. Recent progress in prenatal diagnosis concerns sonography, including fetal blood sampling and biopsy; early detection of neural tube defects by alpha-fetoprotein and acetylcholinesterase determination (ACHE test); first trimester diagnosis of chromosome anomalies and inborn errors of metabolism; and prenatal DNA analysis. Technical progress in prenatal diagnosis improves the reliability of prognosis and genetic counselling, but also adds to existing ethical problems and may create new ones.
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PMID:[Progress in prenatal diagnosis]. 265 18

The present study's aim was to examine the behavioral and neurochemical effects of damage limited to intrinsic neurons of the frontal cortex in rats. Specifically, it was of interest to evaluate the effects of N-methyl-D-aspartic acid-induced lesions of discrete frontal cortical loci on passive avoidance memory and on cortical cholinergic neurochemical markers (choline acetyltransferase--CAT and acetylcholinesterase--ACHE). The present study also compared the behavioral and neurochemical effects produced by frontal cortical damage with those effects produced by lesions of the nucleus basalis of Meynert (nbM). Results indicated that nbM lesions and lesions to a rostral frontal cortical site produced severe passive avoidance memory impairments when subjects were tested 72 hours after training. Cortical, but not hippocampal, levels of CAT and ACHE were depleted in nbM animals only. These data were interpreted as providing support for the view that intrinsic frontal cortical neurons contribute to memory.
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PMID:Infusion of NMDA into the nucleus basalis of Meynert, frontal cortex or lateral ventricle in rats: effect on memory and cholinergic brain neurochemistry. 268 74


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