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)

This report presents evidence that human acetylcholinesterase (AChE; acetylcholine hydrolase, EC3.1.1.7) exhibits immunological cross-reactivity with the protozoan parasite Trypanosoma cruzi. The immunological probes used indicate that the cross-reactive determinant is an oligosaccharidic epitope. Antibodies to AChE were detected in a high proportion of T. cruzi-infected patients sera and during the experimental infection of BALB/c mice. Moreover, anti-idiotypic antibodies against an anti-AChE rabbit antibody or a monoclonal antibody to a parasite surface antigen of 80-85 kDa were detected in sera of patients presenting the chronic cardiac form of the disease. The antibodies were less frequently found in sera from individuals with asymptomatic chronic infection. Our data may provide a biochemical basis for denervation hypersensitivity in Chagas' disease. In addition, it may support the notion of an idiotype-anti-idiotype regulation of conducting tissue damage during the course of T. cruzi infection.
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PMID:Identification of anti-acetylcholinesterase and anti-idiotype antibodies in human and experimental Chagas' disease: pathological implications. 314 9

We have previously shown that the P19 line of embryonal carcinoma cells develops into neurons, astroglia, and fibroblasts after aggregation and exposure to retinoic acid. The neurons were initially identified by their morphology and by the presence of neurofilaments within their cytoplasm. We have more fully documented the neuronal nature of these cells by showing that their cell surfaces display tetanus toxin receptors, a neuronal cell marker, and that choline acetyl-transferase and acetyl cholinesterase activities appear coordinately in neuron-containing cultures. Several days before the appearance of neurons, there is a marked decrease in the amount of an embryonal carcinoma surface antigen, and at the same time there is a substantial decrease in the volumes of individual cells. Various retinoids were able to induce the development of neurons in cultures of aggregated P19 cells, but it did not appear that polyamine metabolism was involved in the effect. We have isolated a mutant clone which does not differentiate in the presence of any of the drugs which are normally effective in inducing differentiation of P19 cells. This mutant and others may help to elucidate the chain of events triggered by retinoic acid and other differentiation-inducing drugs.
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PMID:Retinoic acid-induced neural differentiation of embryonal carcinoma cells. 665 66

The fusion of mononucleate myoblast cells into multinucleate myotubes (myogenesis) has often been studied as a model system of terminal cellular differentiation. Although cell-surface changes during myogenesis have attracted much attention and a variety of surface antigens including the nicotinic cholinergic receptor, acetylcholinesterase and muscle lectins have been shown to be present on muscle cells, a detailed identification of markers specific to the various cell types has not been attempted. This is mainly because fibroblasts are a major contaminating cell type in primary muscle cultures and these cells have no known distinctive cell-surface antigen(s). For instance, surface fibronectin has been used to distinguish fibroblasts in the rat peripheral nervous system in vitro but has proved ineffective in the human muscle cell system. In addition, Lesley and Lennon found that Thy-1 antigen was present on myoblasts but not myotubes of the rat L6 muscle cell line and primary cultures. However, Thy-1 antigen is also present on rat fibroblasts. Thus, unequivocal identification of the major mononucleate cell types in muscle cultures, fibroblasts and myoblasts has not been possible. We report here the use of two surface antigens, Thy-1 and a muscle-specific antigen recognized by a monoclonal antibody, to identify unambiguously the four major types of cells present in human muscle cultures and to propose a model of cell-surface differentiation during human myogenesis.
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PMID:Surface antigen differentiation during human myogenesis in culture. 696 55

To test the hypothesis that the c-mpl ligand is not a primary factor in thrombocytopoiesis, we investigated the biological effects of recombinant human (rh) c-mpl ligand on differentiation of murine progenitor cells and on maturation of the cultured murine megakaryocytes under serum-free conditions on the basis of ploidy distribution, megakaryocyte/platelet-specific surface antigen CD 61 [glycoprotein (GP) IIIa], and cytoplasmic acetylcholinesterase (AchE) expression in vitro. In addition, we studied the effect of c-mpl ligand on proplatelet formation (PPF) by murine mature megakaryocytes. AchE was less strongly expressed in cultured megakaryocytic cells stimulated by c-mpl ligand than in those stimulated by recombinant murine (rm) IL-3 + rh IL-6 during the differentiation of progenitor cells. Less CD 61 was expressed by c-mpl ligand during both the differentiation of progenitor cells and the maturation of megakaryocytes compared with that by rm IL-3 + rh IL-6. Endomitosis, however, was more stimulated by c-mpl ligand than by rm IL-3 + rh IL-6 under both conditions. Furthermore, PPF of mature megakaryocytes was not stimulated by c-mpl ligand. These results indicate that c-mpl ligand stimulates the nuclear development of megakaryocytic cells but that it does not stimulate cytoplasmic maturation and PPF as much as IL-6. These data strongly suggest that c-mpl ligand is not a primary factor in platelet pro-duction. (J Histochem Cytochem 46:49-57, 1998)
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PMID:Effects of c-mpl ligand on cytoplasmic maturation of murine megakaryocytes and on platelet production. 940 94