Prell H H, Harvey A M
Mol Gen Genet. 1983;190(3):427-31. doi: 10.1007/BF00331072.
A method was developed to demonstrate recA-dependent P22-repressor breakdown in vivo by SDS-polyacrylamide electrophoresis of unfractionated extracts of phage-infected, lysogenic Salmonella typhimurium strains TA1530 rec+ and TA1530 recA1-. The antirepressor of P22 is not cleaved by recA protein. Under conditions of unregulated ant-overproduction (Harvey et al. 1981) antirepressor protects c2-repressor in vivo against proteolytic cleavage by recA protein.
通过对噬菌体感染的溶源鼠伤寒沙门氏菌菌株TA1530 rec⁺和TA1530 recA1⁻的未分级提取物进行SDS-聚丙烯酰胺凝胶电泳,开发了一种方法来证明体内recA依赖性P22阻遏物的降解。P22的抗阻遏物不会被recA蛋白切割。在抗阻遏物不受调控的过量产生的条件下(Harvey等人,1981年),抗阻遏物在体内保护c2阻遏物免受recA蛋白的蛋白水解切割。