Biphasic modulation by ACTH-like peptides of protein synthesis in a cell-free system from rat brain.
Brain protein synthesis in a cell-free system was stimulated by 10(-8) M-ACTH1-24. This stimulatory effect was completely inhibited by aurintricarboxylic acid (ATA), an inhibitor of reinitiation of new peptide chains. The N-terminal peptide sequence 4-10 exerted a biphasic modulation of cell-free protein synthesis, i.e., a stimulation at low concentrations (10(-8) and 10(-10) M) and an inhibition at a high concentration (10(-4) M). The D-isomer, ACTH4-10-7-D-phe, also showed a biphasic modulation that, however, was in a direction opposite to that shown by ACTH4-10-7-L-phe at 10(-8) M and 10(-4) M.
D000324:Adrenocorticotropic Hormone / Q000031:analogs & derivatives* / Q000494:pharmacology*; D000818:Animals; D001312:Aurintricarboxylic Acid / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002474:Cell-Free System; D003366:Cosyntropin / Q000494:pharmacology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D009419:Nerve Tissue Proteins; D010446:Peptide Fragments; D003366:Cosyntropin; D001312:Aurintricarboxylic Acid; D000324:Adrenocorticotropic Hormone; C011394:ACTH (4-10)