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Reporter-gene studies using a minimal PTF1A deletion mutant indicate that the deleted region defines a new domain that is crucial for the function of this protein.
In summary, our observations on the phenotype in the gelsolin mutant indicate that the mechanisms controlling stereocilia elongation are probably diverse involving several regulatory proteins.
The absence of either Nodal or Lefty2 in the left or right LPM, the lack of Pitx2 expression in most mutant embryos, and inappropriate right-sided expression in one mutant indicate that the transfer of laterality information from the node to the left lateral plate is disrupted.
Genetic studies using the nia1nia2 double mutant indicate that NIA is a major enzymatic source of NO formation in plants [ 47].
Furthermore, our results with the Sec-to-Cys TrxR1 mutant indicate that the Sec in the enzyme is the primary target of APR-246/MQ.
Studies conducted in this mutant indicate that the influx of Ca2+ is associated with the pleiotropic phenotype; however, the precise mechanism with regards to Ca2+ signaling is still elusive.
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Murine Mfrn rescues the defects in frs zebrafish, and zebrafish mfrn complements the yeast mutant, indicating that the function of the gene may be highly conserved.
Nested exonic RT-PCR in the mutant indicated that the short forms lacked NBD1 but contained NBD2.
The ability to rescue the destabilized mutant indicates that circularization may be a useful tool in protein engineering programs geared towards generating minimized proteins.
However, kcat/KM is higher with both substrates for the triple mutant, indicating that binding energy has been diverted from substrate binding to transition state stabilization.
For Flavodoxin, the reduced B-factors for R125C mutant indicated that the disulfide bond further stabilizes the structure (Fig. S4D).
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