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The cdk9T212A mutation rendered the kinase insensitive to stimulation by Csk1 in vitro, and phenocopied csk1Δ in both its cold-sensitivity and poor growth on the minimal medium EMM [20].
The fact that no red fluorescent colonies are visible supports the conclusion that the mutation rendered the promoter nonfunctional.
This mutation rendered the allele MICA*008 resistant to UL142-mediated inhibition of type I transmembrane MICA proteins.
At AA sequence differences of 22% between the native capsid protein and either replacement, only one of two transgenic genomes was viable; however, a single mutation rendered the second transgenic genome viable.
More recently, a genetic polymorphism was described in mice in which the proline residue at position 451 of the P2X7R CT is replaced by a leucine residue; this single-amino-acid mutation rendered the P2X7R still capable of performing as a cation channel, but largely attenuated pore formation (Adriouch et al., 2002; Le Stunff et al., 2004).
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The M766D mutation renders the enzyme incapable of supporting the temperature-sensitive strain at a non-permissive temperature.
The Bsdr1 mutation renders the plant shorter with fewer tillers, but not severely abnormal as is common with many gain-of-resistance mutants in Arabidopsis (Shirano et al. 2002; Vogel and Somerville 2000).
This mutation renders the enzyme inactive, since Asp102 is a catalytic residue.
This mutation renders the clock arrhythmic and the SDS-PAGE analysis indicates that KaiCI430A is hyper-phosphorylated (Fig. 3).
This insertion mutation renders the GH receptor nonfunctional and causes severe GH resistance, leading to suppression of peripheral IGF-1 and insulin levels.
Here, I show that mice engineered to carry a germline point mutation rendering the propeptide protease-resistant exhibit increases in muscle mass approaching those seen in mice completely lacking myostatin.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com