作者: E. Papini , D. Sandoná , R. Rappuoli , C. Montecucco
DOI: 10.1002/J.1460-2075.1988.TB03207.X
关键词:
摘要: Diphtheria toxin (DT) in acidic media forms ion-conducting channels across the plasma membrane and inhibits protein synthesis of both highly poorly DT-sensitive cell lines. This results loss potassium entry sodium protons with a concomitant rapid lowering potential. The pH dependency permeability changes is similar to that inhibition synthesis. DT-induced ion close when external medium returned neutrality cells recover their normal monovalent cation content. Similar were induced by two DT mutants defective either enzymatic activity or binding, but not mutant translocation. implication these findings for mechanism translocation discussed.