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The respiratory control ratio (RCR) was calculated for each bundle of muscle fiber from the ratio of the respiration at state 3 over that at state 4. RCR is indicative of the stimulatory effect of ADP on mitochondrial respiration since the ATP synthase is consuming both ADP and the transmembrane proton gradient generated by the respiration.
At this concentration, either antagonist partly reduced the stimulating effect of ADP on thrombin peak levels in mouse and human PRP (Fig. 4A, C).
We measured the effect of ADP on ν as a function of increasing [R5P] and [ATP].
Thus, α-ketoglutarate antagonized the effect of ADP on the PII Kact.
The effect of ADP on the fluorescence signal change with ATP and the affinity of ATP were also assessed.
In order to characterize in more details the phosphorylated intermediates of HMA8 formed in the presence of ATP, we tested the effect of ADP on phosphorylation.
Similar(47)
Combined with the damage of Na+-K+ ATPase and Ca2+-Mg2+ activitiesivities and the protective effects of ADP on hemolysis, we believed that energy metabolism imbalance and ion channel dysfunction of erythrocyte membrane were largely accountable for hemolysis induced by amorphous SiNPs.
Here, we extend our focus to consider the effects of ADP on the binding of PII to ATase and NRII.
ADP also inhibits dephosphorylation of SNF1 by rabbit PP1 (data not shown), strongly suggesting that the effect of ADP is on the SNF1 complex and not on the protein phosphatase per se.
We used the TSSA mutant V1 (A(His-10/S232A/T235S 3B3DF) His-10/S232A/T235S 3B3DFDP inhibitoon on avoidydrolysis actheity.
We also used nondenaturing gel electrophoresis to investigate the effect of ADP and α-ketoglutarate on the binding of PII to ATase and NRII.
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