Rohrbach M S, Bodley J W
J Biol Chem. 1976 Feb 25;251(4):930-3.
Escherichia coli Elongation Factor G is inhibited ireversibly by the chemical modification of 1 cysteine residue with N-ethylmaleimide. At pH 5.2, this cysteine is approximately 130 times more reactive than beta-mercaptoethanol toward N-ethylmaleimide. Inhibition is not prevented by either the ribosome or GTP alone at concentrations approximately equal to that of Elongation Factor G, but in combination they reduce the inhibition by 50%. Increasing the stability of the Elongation Factor G-ribosome-GDP complex by the addition of fusidec acid, completely protects against N-ethylmaleimide inhibition. The modified protein cannot form either the Elongation Factor G-ribosome-GMP-P(CH2)P or the Elongation Factor G-ribosome-GDP-fusidic acidcomplex. However, the modification had no effect on its ability to form the Elongation Factor G-ribosome complex. These results suggest that the cysteine residue modified by N-ethylmaleimide is at or near the nucleotide binding site.
大肠杆菌延伸因子G可被N - 乙基马来酰亚胺对1个半胱氨酸残基的化学修饰不可逆地抑制。在pH 5.2时,该半胱氨酸对N - 乙基马来酰亚胺的反应活性比β - 巯基乙醇高约130倍。单独的核糖体或GTP在浓度约等于延伸因子G时均不能阻止抑制作用,但它们共同作用可使抑制作用降低50%。通过添加夫西地酸增加延伸因子G - 核糖体 - GDP复合物的稳定性,可完全防止N - 乙基马来酰亚胺的抑制作用。修饰后的蛋白质既不能形成延伸因子G - 核糖体 - GMP - P(CH2)P复合物,也不能形成延伸因子G - 核糖体 - GDP - 夫西地酸复合物。然而,这种修饰对其形成延伸因子G - 核糖体复合物的能力没有影响。这些结果表明,被N - 乙基马来酰亚胺修饰的半胱氨酸残基位于核苷酸结合位点或其附近。