Title : Effects of hexamethonium, phenothiazines, propranolol and ephedrine on acetylcholinesterase carbamylation by physostigmine, aldicarb and carbaryl: interaction between the active site and the functionally distinct peripheral sites in acetylcholinesterase.

Pub. Date : 1998 Jan

PMID : 9568379






12 Functional Relationships(s)
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1 Effects of hexamethonium, phenothiazines, propranolol and ephedrine on acetylcholinesterase carbamylation by physostigmine, aldicarb and carbaryl: interaction between the active site and the functionally distinct peripheral sites in acetylcholinesterase. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
2 Effects of hexamethonium, phenothiazines, propranolol and ephedrine on acetylcholinesterase carbamylation by physostigmine, aldicarb and carbaryl: interaction between the active site and the functionally distinct peripheral sites in acetylcholinesterase. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
3 Physostigmine, aldicarb and carbaryl were potent inhibitors of acetylcholinesterase (AChE). Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
4 Physostigmine, aldicarb and carbaryl were potent inhibitors of acetylcholinesterase (AChE). Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
5 The physostigmine-inhibited AChE fluoresced at 300 nm excitation and 500 nm emission wavelengths, but the aldicarb and carbaryl inhibited enzyme did not. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
6 The fluorescence intensity of physostigmine-inhibited AChE decreased with increasing the substrate (acetylthiocholine) concentration, thus indicating that physostigmine binding to the active site is essential for the development of fluorescence. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
7 The fluorescence intensity of physostigmine-inhibited AChE decreased with increasing the substrate (acetylthiocholine) concentration, thus indicating that physostigmine binding to the active site is essential for the development of fluorescence. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
8 Thus, the physostigmine-inhibited AChE fluoresces due to the binding of trimethylpyrrolo[2,3-b]indol (TMPI) moiety, formed by the hydrolysis of physostigmine, to a peripheral site in AChE. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
9 Thus, the physostigmine-inhibited AChE fluoresces due to the binding of trimethylpyrrolo[2,3-b]indol (TMPI) moiety, formed by the hydrolysis of physostigmine, to a peripheral site in AChE. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
10 Thus, the physostigmine-inhibited AChE fluoresces due to the binding of trimethylpyrrolo[2,3-b]indol (TMPI) moiety, formed by the hydrolysis of physostigmine, to a peripheral site in AChE. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
11 Thus, the physostigmine-inhibited AChE fluoresces due to the binding of trimethylpyrrolo[2,3-b]indol (TMPI) moiety, formed by the hydrolysis of physostigmine, to a peripheral site in AChE. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens
12 Hexamethonium protected AChE from inhibition by carbamates and decreased the fluorescence intensity of the physostigmine-inhibited AChE. Physostigmine acetylcholinesterase (Cartwright blood group) Homo sapiens