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Insight into this question is provided from studies by Sonenberg and colleagues [22] showing that expression of a dominant negative PKR (DN-PKR) variant or of an eIF2α -Ser51Ala mutant in mouse NIH3T3 cells induced transformation.
Another M. tuberculosis mutant which produced a reduced level of SOD using antisense-sodA was sensitive to killing by hydrogen peroxide which led to attenuation of the mutant in mouse lungs and spleen [37].
Nonetheless, it cannot be excluded that the pgm locus encodes other virulence factors required for bubonic production since it was recently shown that a pgm negative mutant had a greater loss of virulence than the Ybt biosynthetic mutant in mouse model of pneumonic plague [11].
We have shown that the expression of a dominant-negative ROCK mutant in mouse stromal ST2 cells induced osteoblastic differentiation, whereas the expression of a constitutively active ROCK mutant attenuated osteoblastic differentiation.
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The deletion of the transcriptional regulator for this apparatus creates a non-pathogenic mutant in mice and is of interest in studying the host response.
The chi-squared test with larger contingency tables was used to analyze the protective efficacy of the mutant in mice [61].
In this work we compare both the transcriptome and the proteome of M. tuberculosis wild type with a phoP mutant to characterize the PhoP regulon, and we test the antigenic capacity and persistence of the phoP mutant in mice model.
Our results show no evidence of enhanced virulence of wild-type M. tuberculosis strains or a deletion mutant in mice or guinea pigs after mouse passaging or reduced virulence in strains that have not been passaged.
The growth deficiency of our tpx mutant in mice suggests that thiol peroxidase is essential for the bacterium to initiate growth and to persist in the face of host innate and acquired immunity.
Moreover, NSC319726 suppresses growth of tumor xenografts expressing the p.R175H mutant in mice.
For high FVIs, the fly model, thus, cannot well predict the virulence class of any mutant in mice.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com