| 1. | Our work elucidates the formation of the feedback inhibition site . point mutations reveal that amino acid replacements at phel44 , leul75 , leul79 , phe209 and val221 partially or completely relieve the feedback inhibition of arog addressed by 1 mm phenylalanine . combined with the 3d structure of arog , our results demonstrate that the feedback inhibition site consists of asp6 , asp7 , ile10 , ile13 , pro150 , gln151 , leul75 , leu179 , serl80 , phe209 , ser211and val221
实验结果表明：在1mm苯丙氨酸的存在下， 1 )野生型arog受到90以上的反馈抑制； 2 ) pro150leu , leu179ala , phe209ala和val221ala这四种点突变在保持与野生型arog相近的比活的同时，解除了80 100的反馈抑制； 3 )点突变phe144ala仅解除反馈抑制约30 ，同时保持与野生型相当的比活； 4 )突变体leu175ala仅能够解除18的反馈抑制， leul75gln能够解除44的反馈抑制， leu175asp解除了84的反馈抑制，并且比活都比野生型高。 |
