Disease relevance of BCHE

• Thus as a consequence of BChE inhibition both, organization of nuclear cell layers and of plexiform-like (neuropile) areas, as detected by an antibody to the fiber fasciculation protein F11, is temporally advanced by at least two days [1].
• Incidence of numerous human poisonings by quinalphos (Ekalux, Bayrusil) in agricultural areas near Belgrade initiated this study on the ability of the compound to inhibit hen brain neuropathy target esterase, acetylcholinesterase and plasma butyrylcholinesterase in vivo [2].

High impact information on BCHE

• Close relationships between acetylcholinesterase (AcChoEase; acetylcholine acetylhydrolase, true cholinesterase, EC, 3.1.1.7) and butyrylcholinesterase (BtChoEase, acylcholine acylhydrolase, pseudocholinesterase, EC, 3.1.1.8) with cell proliferation were observed in the early chicken brain [3].
• The amounts of BuchE increase progressively throughout embryonic development, independent of autonomic innervation, and in mature chick heart predominate over the much less abundant amounts of AchE [4].
• The second approach examines the influence of vagotomy and sympathetic denervation of 8-day-old chick myocardium on expression of the molecular forms of AchE, BuchE, mAchR, and beta-adrenergic receptors [4].
• The amplified segment contained 423 bp of BCHE sequence including the active site serine of the enzyme (amino acid 198) and a component of the anionic site, aspartate 70 [5].
• Results showed that the BCHE gene was present in a single copy in the genome of all these vertebrates [5].

Biological context of BCHE

• The pronounced effects of antisense 5'-BChE transfection of spheroids document a key role of BChE during the early reaggregation process of retinal cells, most likely by regulating their growth and differentiation [6].
• The differently sized glycosylation parts of brain and serum BChE may indicate that they subserve different functions [7].
• Quantitative development and molecular forms of acetyl- and butyrylcholinesterase during morphogenesis and synaptogenesis of chick brain and retina [8].
• We have inserted 577 bp of the 5' upstream region plus 106 bp of the exon 1 of the rabbit BChE gene in reverse orientation under control of an SV40 early promoter derivative in an expression vector [6].
• Butyrylcholinesterase antisense transfection increases apoptosis in differentiating retinal reaggregates of the chick embryo [9].

Anatomical context of BCHE

• Butyrylcholinesterase activity was found in the mouse and quail but not the chick brain vasculature, and appeared around Days 17 (mouse) and 15 (quail). gamma-Glutamyltranspeptidase activity was demonstrated histochemically in mouse but not in chick and quail brain capillaries, beginning at Day 15 [10].
• Because cholinesterases can regulate neurite growth in vitro by a nonenzymatic mechanism, these data strongly support that both inactive and active forms of BChE may be involved in noncholinergic communication, possibly depending on particular glycosylation patterns [11].
• Neither asymmetric AChE nor BuChE was detected in the motor neurons [12].
• Butyrylcholinesterase was found in chick sciatic nerve in four main molecular forms--G1, G2, G4 and A12--distinguishable by thier sedimentation coefficients in sucrose gradients (4.2S, 6.4S, 11.3S and 19S, respectively) [13].
• These findings suggest that some of the butyrylcholinesterase is located in the axonal mitochondria and/or axolemma [13].

Associations of BCHE with chemical compounds

• The rate at which human BChE hydrolyzes cocaine is slow, with a kcat of 3.9 min(-1) and Km of 14 microM [14].
• Brain acetylcholinesterase, acid phosphatase, and 2',3'-cyclic nucleotide-3'-phosphohydrolase and plasma butyrylcholinesterase activities in hens treated with a single dermal neurotoxic dose of S,S,S-tri-n-butyl phosphorotrithioate [15].
• Labeling of the 85- and 79-kDa bands was inhibited by butyrylcholine, suggesting that these proteins have BuChE activity [16].
• Several side activities have been attributed to butyrylcholinesterase (BChE), including aryl acylamidase (AAA) activity, which is an amidase-like activity with unknown physiological function splitting the artificial substrate o-nitroacetanilide [17].
• Taken together, these data support a hitherto unsuspected role of BChE in non-cholinergic cells, possibly in conjunction with GABA [18].

Physical interactions of BCHE

• Butyrylcholinesterase is complexed with transferrin in chicken serum [19].

Regulatory relationships of BCHE

• Chicken retinospheroids as developmental and pharmacological in vitro models: acetylcholinesterase is regulated by its own and by butyrylcholinesterase activity [20].

Analytical, diagnostic and therapeutic context of BCHE

• The amounts of AchE and BuchE molecular forms in avian heart are not measurably influenced by bilateral vagotomy for a duration of 4 days, unilateral vagotomy for a duration of 25 days, or sympathetic denervation [4].
• Effects of electrical stimulation on molecular forms of butyrylcholinesterase in denervated fast and slow latissimus dorsi muscles of newly hatched chicken [21].
• In PLD muscle, denervation performed at day 2 substantially reduced the rate of rapid decrease of BuChE specific activity which takes place during normal development, whereas in the case of ALD muscle little change was observed [21].
• The distribution of liver esterases included both monomeric (G1) and G4 BChE and a large p-nitrophenylacetate (p-NPA) esterase activity that was separated into two main peaks by density gradient ultracentrifugation [22].
• Modification of the technique by periodic redissociation of the neuronal aggregates during cell separation increased the purity of the neuronal cultures to greater than or equal to 97% as determined both by microscopic examination and by measurement of levels of butyrylcholinesterase, an enzyme present in the non-neuronal cells [23].

References