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The site specific mutants of the thermophilic P450 (P450 175A1 or CYP175A1) were designed to introduce residues that could act as acid base catalysts near the active site to enhance the peroxidases activity.
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In order to investigate the role of multidrug efflux systems as bacterial defense mechanism, wild type and gene-specific mutants of the following bacterial species were analyzed: Erwinia amylovora 1189 (wild type), Escherichia coli TG1 (wild type) [ 22], Pseudomonas syringae DC3000 (wild type) [ 23] as well as the respective mutants with deletions in acrAB, tolC, or mexAB [ 24- 28].
Specific mutants of Tyr235 increase the Km for substrate (l-Trp) and lower Km for cofactor (BH4) [46].
A tumor-specific mutant of the EGFR, EFGR variant III (EGFRvIII), causes constitutive activation of the receptor's tyrosine kinase activity and is frequently expressed in primary GBM (∼33%).
This suggests that the pro-fibrotic effects associated with this specific mutant of PPARγ in the presence of increased AngII levels are distinct from mechanisms driving cardiac hypertrophy at least under these experimental conditions, in contrast to previous studies.
The observation that ductal carcinoma-specific mutants of CK1ε promote the Wnt/Rac1/JNK and NFAT pathways and, on the other hand, inhibit the Wnt/β-catenin pathway are in good agreement with some clinical observations.
The site-specific mutants of pRL-VEGF-Con1 and pRL-VEGF-Con2 were also established by using Takara MutanBEST Kit (Takara Corp., Dalian, PRC) according the method provided by the manual.
In particular, approximately 60% of the consistently appearing central mutants are related to the knockout of a highly conserved gene in contrast to the environment-specific mutants of which approximately 30% correspond to highly conserved genes.
This dual detection allows normalizing the abundance of one qTag (representing chromosomal DNA from one specific mutant) to the total number of all qTags (which corresponds to chromosomal DNA from all strains) present in the same reaction.
As evidenced through site specific mutants, binding of cAMP to the A domain is crucial for the enhanced stability.
Using specific mutants in the Walker boxes of RFS-1, which are compromised for stimulating strand exchange, we demonstrate that filament remodeling is critical for RFS-1/RIP-1 mediactivityivity.
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