Ethanol-induced growth inhibition in embryonic chick brain is associated with changes in cytoplasmic cyclic AMP-dependent protein kinase regulatory subunit.
Several lines of research have suggested that ethanol-induced changes in the adenylate cyclase/protein kinase cascade may contribute to the growth retardation observed in infants exposed to ethanol in utero. Based on studies with an embryonic chick model, the data presented here suggest that chronic ethanol treatment significantly lowered the binding of cyclic AMP by protein kinase regulatory subunit (RII) and reduced the level of phosphorylation of RII by the endogenous cytoplasmic protein kinase catalytic subunit. Furthermore, ethanol treatment altered the phosphorylation of at least one other brain cytosolic protein (molecular weight = 62-65 kD).
Beeker
K
K
Department of Biochemistry, ECU School of Medicine, Greenville, NC 27834.
Deane
D
D
Elton
C
C
Pennington
S
S
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000196:embryology* / Q000201:enzymology; D002352:Carrier Proteins / Q000032:analysis / Q000378:metabolism*; D002642:Chick Embryo; D000242:Cyclic AMP / Q000378:metabolism*; D000431:Ethanol / Q000494:pharmacology*; D047908:Intracellular Signaling Peptides and Proteins; D010766:Phosphorylation; D011485:Protein Binding; D011494:Protein Kinases / Q000378:metabolism*
D002352:Carrier Proteins; D047908:Intracellular Signaling Peptides and Proteins; C015482:protein kinase modulator; D000431:Ethanol; D000242:Cyclic AMP; D011494:Protein Kinases