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Previously, a prdB mutant was shown to have a decreased growth rate compared to the parent strain22.
GAG silencing by this mutant was shown in a murine seeding model of human cancer cells, whereby a greatly reduced number of liver metastases was detected when the animals were treated intravenously with 1 mg/kg CXCL12α (Δ8 L29K V39K) before cancer cell application.
Furthermore, the Ghd10 locus of the ghd10 mutant was shown to be allelic to Ehd2/RID1/OsID1.
A tps1/tps1 mutant was shown to be deficient in trehalose synthesis and was extremely sensitive to H2O2 exposure [19].
Once the ENU mutant was shown to be heritable, it was mapped by crossing to the D2 strain.
The K557R mutant was shown to be more sensitive to citrate inhibition than the K617A mutant; they exhibited Ki values of 0.3 mM and 0.5 mM, respectively.
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The comparison result of the amino acid sequences of native protein and mutant was showed in Fig. 2A, where 27 mutation positions were highlighted.
The secondary structures of wt hAID and the N51A mutant are shown in gray.
The apparently different responses of the chip to the complementary strand and the single-base mutant are shown under electric potential control.
The 11-aa deletion (aa332 342) in the vWFA domain of the mutant is shown with dashes.
Data from the W36K mutant are shown in Fig. 4E.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com