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1 ChpArec also had a rapid rate of autodephosphorylation.
2 with phosphorylated CheY and stimulates its autodephosphorylation.
3 phorylated Spo0F, which results in increased autodephosphorylation.
4 he CheA kinase in vitro but were impaired in autodephosphorylation.
5 s the rhythm of KaiC autophosphorylation and autodephosphorylation and is an example of dynamics-driv
7 in mutants lacking CheZ, a catalyst of CheY autodephosphorylation, and severely reduced in mutants w
8 en processes in OCLs, and cyt-PTPe undergoes autodephosphorylation at Tyr-683, thus limiting Src acti
10 active-site features, the rates of catalytic autodephosphorylation for different response regulators
13 lternately stimulate autophosphorylation and autodephosphorylation of KaiC with a periodicity of appr
14 o OmpR were not affected by DNA, whereas the autodephosphorylation of OmpR-P was inhibited slightly.
15 for a systematic analysis of intermolecular autodephosphorylation of SHP-2, which revealed how confo
17 89A and CheYE89Q had autophosphorylation and autodephosphorylation properties similar to those of wil
18 active site amino acid compositions have on autodephosphorylation rate may allow manipulation of pho
19 esidue identity may be sufficient to predict autodephosphorylation rate, and hence the kinetics of th
24 o the inactive conformation might retard the autodephosphorylation reaction if the two processes are
25 ariable active site positions decreased CheY autodephosphorylation up to 40-fold and increased the Sp
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