Nitric oxide donor SIN-1 mediated down-regulation of the G-protein alpha-subunit in C6 glioma cells.
In C6 glioma cells, the nitric oxide (NO) donor 3-morpholinosynonimine hydrochloride (SIN-1) (0.5 mM) produced a significant decrease in the stimulatory G-protein alpha subunit (G alpha(s)) levels. Northern hydridization did not detect any differences in G alpha(s) mRNA levels after SIN-1 treatment. Furthermore SIN-1 increased endogenous and cholera toxin-catalyzed ADP-ribosylation of G alpha(s). 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) (0.5mM), a NO scavenger, had no effect on endogenous or cholera toxin-catalyzed ADP-ribosylation of G alpha(s), but reversed the increase in endogenous and cholera toxin-catalyzed ADP-ribosylation of G alpha(s) induced by SIN-1. These results suggest that increasing ADP-ribosylation may be involved in SIN-1 mediated G alpha(s) down-regulation.
Young
L T
LT
Department of Psychiatry, McMaster University, Hamilton, Ontario, Canada.
Woods
C M
CM
Wang
J F
JF
Asghari
V
V
D000246:Adenosine Diphosphate Ribose / Q000378:metabolism; D000818:Animals; D015152:Blotting, Northern; D002772:Cholera Toxin / Q000494:pharmacology; D003497:Cyclic N-Oxides / Q000494:pharmacology; D015536:Down-Regulation / Q000187:drug effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D019204:GTP-Binding Proteins / Q000378:metabolism*; D005910:Glioma / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D007093:Imidazoles / Q000494:pharmacology; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D014407:Tumor Cells, Cultured
D003497:Cyclic N-Oxides; D004791:Enzyme Inhibitors; D007093:Imidazoles; D012333:RNA, Messenger; C079391:2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide; D000246:Adenosine Diphosphate Ribose; D009569:Nitric Oxide; C002385:linsidomine; D002772:Cholera Toxin; D008981:Molsidomine; D019204:GTP-Binding Proteins