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By using site-directed mutagenesis, we identified two amino acid residues that likely serve as the catalytic acid/base and nucleophile as in other GH5 proteins.
Following observations provided by molecular dynamics simulation, we explore the hypothesis of interaction of these arginines with acidic residues, and using site-directed mutagenesis, we identified aspartate D307 and glutamate E308 residues as critical for the function of ICCRs.
Through structural modeling and site-directed mutagenesis, we identified several key amino acids of these UGTs that may play important roles in determining their activities and substrate regio-specificities.
From the screening of random mutagenesis, we identified an amino acid mutation (H114Y) contributing to rHuEPO binding and four amino acid mutations (R76S, A132D, A162D, and C181Y) contributing to expression of soluble rhEPOR.
Using site-directed mutagenesis, we identified Cys75 of Ubc9 as the target for S-nitrosation.
Moreover, using structural modeling and site-directed mutagenesis, we identified two proximal aromatic residues located within the WD repeat region that significantly impact m7G association.
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Moreover, using ChIP assay and direct mutagenesis we identify two TCF4-binding sites on the uch l1 promoter that are involved in this regulation.
In this report, using extensive mutagenesis we identify a novel DNA sequence that functions as a core promoter element at the second start site of the hepatitis B virus (HBV) X mRNA which we have named XCPE2 (X core promoter element 2).
Using a combination of X-ray crystallography and site-directed mutagenesis, we identify, among others, a metal-binding site adjacent to the nucleotide-binding site in the GTPase domain that involves a conserved cysteine and several glutamate residues.
Via a comprehensive mutagenesis screen, we identified transmembrane domain residues essential for latrophilin-1 basal activity and for agonist peptide response.
As part of a large-scale N-ethyl-N-nitrosourea (ENU) mutagenesis screen, we identified a mouse mutant, Mariusz, which exhibited muscle weakness along with hindlimb syndactyly.
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mutagenesis we constructed
mutagenesis we disrupted
mutagenesis we defined
mutagenesis we measured
mutagenesis we exchanged
mutagenesis we developed
mutagenesis we confirmed
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mutagenesis we obtained
mutagenesis we used
mutagenesis we asked
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mutagenesis we were
mutagenesis we mutated
mutagenesis we altered
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