Brefeldin A inhibits protein synthesis in cultured cells.
The fungal metabolite brefeldin A (BFA) is known to disrupt the Golgi apparatus resulting in redistribution of Golgi proteins to the endoplasmic reticulum and inhibition of protein secretion. BFA was found to inhibit protein synthesis in rat glioma C6 cells by up to 70% between 0.1 and 1 microgram/ml. Inhibition was both time-dependent and reversible. BFA inhibited protein synthesis to varying degrees in a number of other cell lines but not in BFA-resistant marsupial kidney cells. The same concentrations of BFA which inhibited protein synthesis, also blocked the inhibitory effects of Pseudomonas exotoxin and ricin on BFA-sensitive cells. BFA, however, was unable to block the inhibition of protein synthesis by the toxins in the resistant marsupial kidney cells.
Fishman
P H
PH
Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Curran
P K
PK
D036002:ADP Ribose Transferases; D000818:Animals; D001427:Bacterial Toxins; D020126:Brefeldin A; D016466:CHO Cells; D006224:Cricetinae; D003517:Cyclopentanes / Q000494:pharmacology*; D005098:Exotoxins / Q000494:pharmacology; D006056:Golgi Apparatus / Q000187:drug effects; D006801:Humans; D007700:Kinetics; D051379:Mice; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology*; D051381:Rats; D014407:Tumor Cells, Cultured; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A
D036002:ADP Ribose Transferases; D001427:Bacterial Toxins; D020126:Brefeldin A; D003517:Cyclopentanes; D005098:Exotoxins; D011500:Protein Synthesis Inhibitors; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A