Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to find out if a cell line of glial origin possesses sigma and/or phencyclidine (PCP) binding sites. Binding of [3H]1,3-di-o-tolyl-guanidine (DTG), a highly selective ligand for sigma binding sites, and of [3H]N-[1-(2-thienyl)cyclohexyl] piperidine ([3H]TCP), a radioligand specific for PCP receptors, to C6-BU-1 glioma cells was investigated. Binding of [3H]DTG to C6-BU-1 cell membranes was reversible, saturable (Bmax = 10.5 pmol/mg protein), and of high affinity (KD = 26 nM). C6-BU-1 cells do not possess PCP receptors as indicated by negligible specific binding of [3H]TCP to C6-BU-1 cell membranes. Specific binding of [3H]DTG was reduced in the presence of Ca2+ and to a lesser extent by Mg2+. The rank order of potency of various PCP and sigma ligands was DTG > (+)3-[(3-hydroxy-phenyl)-N-n-propyl-piperidine] [(+)3-PPP] > haloperidol > pentazocine > (-)3-PPP > PCP > metaphit > dextromethorphan > (-)butaclamol > (+)butaclamol > (-)N-allylnormetazocine [(-)SKF 10,047] > MK801 > (+)SKF 10,047 > ketamine. The drug specificity, confirmed by a reversed stereoselectivity for the benzomorphan opiate SKF 10,047, indicated that these sites correspond to a subtype of sigma binding sites, the so-called sigma 2 binding site. Thus, the C6-BU-1 cell line is the first glial cell line demonstrated to have sigma 2 binding sites.
 ...
PMID:Characterization of specific binding sites for [3H]-1,3-di-o-tolyl-guanidine (DTG) in the rat glioma cell line C6-BU-1. 146 57

When added to intact C6 glioma cells in the micromolar range of concentrations, ADP and ATP induce an inhibition of the isoproterenol-elicited cAMP responses. ATP is rapidly hydrolyzed by the ectonucleotidases present on these cells, with an apparent Km of 50 microM and a Vmax of 1.1 nmol/min/10(6) cells. cAMP responses are also inhibited by millimolar concentrations of either ATP in the presence of an ATP-regenerating system to prevent ADP accumulation or AMP-PCP. These observations show that, in C6 glioma cells, ADP is a more potent inhibitor of cAMP production than ATP, the latter acting indirectly, via its rapid hydrolysis to ADP. The additive inhibition of isoproterenol-elicited cAMP responses induced, on one hand, by the treatment of the cells with a phorbol ester and by addition of ADP to the cells, and, on the other hand, by the progressive disappearance of the effects of ADP and ATP when cells are treated with increasing concentrations of Pertussis toxin, demonstrate that ADP and ATP exert their action in C6 glioma cells via a P2 purinoceptor probably negatively coupled to adenylate cyclase and a G regulatory protein.
 ...
PMID:ADP and, indirectly, ATP are potent inhibitors of cAMP production in intact isoproterenol-stimulated C6 glioma cells. 255 Dec 69