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However, similar to the model in scheme 2, it fails to consistently produce a bump in the Off response (Figure S2B).
Our hypothesis is illustrated in Scheme 3. If the model in Scheme 1A operates, 1 cannot acylate the active site cysteine.
The key characteristic of the kinetics model in Scheme 1 is the emergence of branched pathways from the initial encounter complex, having Michaelis states of differing reactivity.
Our recent investigation with a mutant of PhaECAv in which the active site cysteine was replaced with a serine revealed noncovalent intermediates (dimers and trimers) providing evidence in support of the model in Scheme 1B.
However, if the model in Scheme 1B is operative, HBCH2CoA would extend the sT chain to generate a methylene analogue of [H]-saturated tetrameric-CoA ([H]-sTet-CH2-CoA, 17, Scheme 3), and further elongation would not be possible.
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Differentiation of two mechanistic models in Scheme 1 has been difficult as with both class I and III synthases the rate of chain elongation is much faster than that of chain initiation.
The stopped-flow transients in Figures 1 and 2 were globally fit to the kinetic model shown in Scheme 2.
The stereochemical course of the reaction can be explained by means of the model proposed in Scheme 13.
The observed electrical characteristics correlate well with the three phase sintering model described in Scheme 2 and illustrate the importance of the fusion process to the electron mobility.
The stereochemical course of this stereodivergent reaction can be explained on the basis of the transition state model depicted in Scheme 18.
We have globally fitted (62) the binding model shown in Scheme 1 to the direct and reverse titrations (see Experimental Procedures).
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