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Cardiac α-myosin isolated from the hearts of homozygous transgenic mice engineered to carry the R403Q mutation showed enhanced average force, actin filament velocity and ATPase activity, consistent with a gain in myosin function [14].
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Allelic test between the G978 mutation and ebr2, which showed enhanced resistance only to blast (Campbell and Ronald 2005), was not done.
PEA3 was shown enhance cancer metastasis [ 44].
Those without the mutation showed the usual signs of deprivation.
Designed mutation shows that switching interactions enhance the rate, perhaps by destabilizing the ground state immediately before the transition state and limiting nonproductive diffusion before and after the chemical transition state, thereby reducing the activation entropy.
Likewise, the psi mutation shows less sensitivity to auxin than the wild type, and enhances the ability to maintain the auxin response in the root tip under low P supply (X.M. Wang et al., 2010).
A recent report [42] demonstrates that TRPC6 mutations previously shown to enhance channel activity lead to enhanced basal NFAT-mediated transcription in several cell lines, including cultured podocytes.
Mice carrying the P250R mutation in Fgfr1 associated with Pfeiffer syndrome were also previously shown to exhibit enhanced osteoblastic differentiation of cells within the sagittal suture [ 47].
The proposed mutation rule was shown to enhance the global and local search capabilities of the basic DE and to increase the convergence speed.
The proposed mutation rule is shown to enhance the local search ability of the basic Differential Evolution (DE) and to get a better trade-off between convergence rate and robustness.
While this mutation has been shown to enhance chemoresistance upon transfection into p53 null Saos-2 cells [56], these osteosarcoma-derived cells may not necessarily be representative for breast cancers in vivo.
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