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The JNK cascade can be inactivated by the MAPK phosphatase VHP-1, and vhp-1-null mutants cause an arrest in developmental growth at the early larval stage due to hyperactivation of the JNK pathway (Supplementary Fig. 1 17.
These autoregulatory properties are altered when p53 is mutated; thus transcription-defective p53 mutants cause an accumulation of VRK1 because its degradation mechanism can not be induced [12], an observation that has been confirmed in human lung squamous cell carcinomas containing mutations in p53, which have very high levels of endogenous VRK1 [13].
As previously shown for H3-L61W (Duina et al. 2007; Nguyen et al. 2013), the H3-L61X mutants cause an overall shift in Spt16 occupancy toward the 3′ ends of the PMA1 and FBA1 genes (see Figure 3, C and F).
In fact, when TC10 mutants were expressed, there was a significant increase in mCherry-GluA1 levels in the shafts of dendrites, suggesting that the TC10 mutants cause an accumulation of AMPAR intracellular levels in the dendritic shafts, but not in the somata, that results in the decreases in surface levels.
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We therefore tested whether the shs1-ps mutants cause a phenotype that is similar to shs1Δ.
APC mutants cause a strong activation of canonical Wnt signaling that leads to arrest prior to gastrulation [36].
In conjunction, the data from the AJ and more basal sections suggest that the mutants cause a subcellular reshuffling of endogenous protein, possibly linked with its signalling ability.
In particular, we found that these histone mutants cause a shift in the distribution of Spt16 toward the 3′ regions of the transcribed genes we investigated.
In Drosophila wing or eye epithelia, mutation of ex is sufficient to cause mild tissue overgrowth, but ex, mer double mutants cause a much stronger overgrowth phenotype, similar to hpo or wts mutants (Hamaratoglu et al, 2006).
This revealed that mago, btz, and TmIIgs mutants cause a highly significant reversal in the directional bias, with 57%–59% of particles moving anteriorly, compared to only 43% in wild-type.
These neurotransmitter deficiencies in cat-4 mutants cause a variety of subtle behavioral abnormalities, including defective locomotory rate regulation and male mating (Loer and Kenyon 1993; Sawin et al. 2000).
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