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)

By using a picrosirius dye, sensitive and specific staining of collagens plated in microtiter wells was achieved. The range of detection was from 0.5 to 20 micrograms. Human collagen types I, III, IV, and V were tested and able to be detected by the method. The dye did not bind to acetylcholinesterase or elastin. It did bind to C1q to some extent but this is not surprising since the molecule contains some triple helical collagen-like structures. A comparison performed between this assay and a colorimetric assay for hydroxyproline using tissue culture supernatants gave similar results for both samples. Due to its simplicity and sensitivity this assay will be most useful in laboratories where large numbers of samples must be screened for collagen production.
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PMID:Microplate reader-based quantitation of collagens. 138 82

The spontaneously hypertensive rat (SHR)--animal model for human essential hypertension--develops a generalized arteriopathy. The present paper discusses the atherogenic influence of hypertensive arterial lesions. The following changes in the intima might influence its permeability and barrier function, increase the trapping effect and stimulate the smooth muscle cell proliferation: the hyper-reactivity of endothelial cells; the decreased thickness of endothelial cell periphery; the reduced intercellular junction pathways; the increase in basal lamina and glycosaminoglycan sub-endothelial material; the mononuclear cell infiltrations; the widened fenestrae in the internal elastic lamina. Some hypertensive changes of the tunica media may also interact with atherogenic process through reduced smooth muscle cell lipolytic capabilities, slowed transmural diffusion, perturbed efflux, aggravated media hypoxia, namely: the decrease in esterase and cholinesterase activities, the activations of some lysosomal enzymes, the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness and transmural passage; the modified smooth muscle cell behavior.
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PMID:[Hypertensive arteriopathy and atherogenesis: cellular and molecular interactions]. 310 95

The histological, ultrastructural, morphometrical and histochemical aspects of the arterial media were studied in young and aged SHR, and compared to normotensive Wistar Kyoto rats. The diffuse thickening was the most characteristic feature of the hypertensive media. It seems due to three processes: Early generalized hypertrophy of smooth muscle cells (smc); connective matrix neogenesis and smc proliferation, more evident in peripheral vasculature. The present paper discusses the following hypertensive tunica media changes in relation to the atherosclerotic process: the decrease in lipolytic esterase and cholinesterase activities; the activation of some lysosomal enzymes; the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness; the modified smc behavior (migration, secretion, proliferation). These alterations might positively influence arterial susceptibility to atherosclerosis through reduced smc lipolytic activity; slowed transmural diffusion; perturbed efflux and aggravated media hypoxia.
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PMID:Tunica media changes in the spontaneously hypertensive rat (SHR). 360 28

The effects of collagen-like proteins on platelets were studied in human platelet-rich plasmas. The C1q subcomponent of complement (human), acetylcholinesterase (electric eel), and elastin (bovine) had no platelet aggregating activity, despite compositional homologies with collagen in terms of hydroxyproline, hydroxylysine, proline and glycine contents. Upon preincubation with platelets, acetylcholinesterase was incapable of preventing the platelet aggregation triggered by collagen, whereas elastin exerted a weak and inconsistent blocking action. In turn, native C1q strongly inhibited collagen-induced platelet aggregation and 'aggregated' C1q, obtained by ultracentrifugation of freeze-thawed monomeric C1q, had a potentiating effect. These findings confirm the highly specific character of the platelet action of C1q.
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PMID:Effect of collagen-like substances (C1q, acetylcholinesterase and elastin) on collagen-induced platelet aggregation. 698 97

The development of rat lung from a primitive gas-exchange organ to the mature respiratory organ is in large part a postnatal phenomenon that has been well characterized by morphological and morphometric methods. The alveolarization of the lung is achieved during the first 3 weeks of life. Cholinergic innervation of rat lung also appears postnatally. We have monitored the presence or activity of several proteins during postnatal rat lung development. Newborn-rat lung contains negligible amounts of acetylcholinesterase, but the specific activity of acetylcholinesterase reaches adult values by postnatal day 10-11. Neonatal-rat lung does not contain significant amounts of beta-galactoside-binding protein [Powell (1980) Biochem. J.187, 123-129]. The activity of this endogenous lung lectin was apparent at about day 6, was maximal between days 10 and 13 before declining 8-10-fold to reach adult values. Elastin has been implicated from morphological evidence as critical to lung restructuring. We have quantified the amount of desmosine and isodesmosine per g wet wt. of lung. The concentration of elastin, by this criterion, was low and stationary until postnatal day 7; a dramatic increase in elastin concentration occurred between days 10 and 20, when adult values were reached. The peak of lung-lectin activity was coincident with the maturation of acetylcholinesterase and the beginning of rapid elastin cross-linking. The specific activities of angiotensin-converting enzyme, carbonic anhydrase, choline kinase and glucose 6-phosphate dehydrogenase were also monitored.
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PMID:Postnatal development of rat lung. Changes in lung lectin, elastin, acetylcholinesterase and other enzymes. 740 72

Deletion of the long arm of chromosome 7 is a common karyotypic finding in myeloid disorders and in particular is found in association with secondary leukaemias. We have used restriction fragment length polymorphisms and gene dosage experiments to assess the loss or retention of sequences localized to chromosome 7q in five patients with clonal myeloid disorders and a 7q deletion. The deletion was interstitial in all cases with retention of the anonymous marker pS194 located at 7q36-qter. Three out of five cases also retained the more proximal gene T-cell receptor beta (TCR beta) located at 7q35. The proximal breakpoints of all five cases were localized to 7q22 by cytogenetic analysis. In two cases the proximal breakpoint lay between the genes for elastin (ELN) and collagen type 1 alpha (COL1A2) and in three cases distal to this region between the genes for erythropoietin (EPO) and acetylcholinesterase (ACHE). The genes of ACHE, plasminogen activator inhibitor 1 (PLANH1), CCAAT displacement protein (CUTL1) and Met proto-oncogene (MET) were deleted in all cases. Molecular analysis of the 7q deletion in myeloid leukaemias demonstrates heterogeneity of the breakpoints, supporting a recessive mechanism of tumourigenesis.
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PMID:Molecular characterization of the 7q deletion in myeloid disorders. 861 79