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Furthermore, only the control MEFs-derived iPSCs, but not the mutants, contributed to the formation of chimeric mice when injected into blastocysts (Supplementary Fig S4E).
To determine whether the loss of cell polarity and proliferative defects of scrib mutants contributed to NACT-driven tumourigeneis, we again made use of the observation that aPKCCAAXDN rescues most of the scrib mutant defects but does not stop JNK-mediated cell death.
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It was shown that the overexpression of TGase zymogen gene in the mutants contributes to the increase in TGase production.
Furthermore, we propose that changes in chromatin structure in Slbp mutants contribute to overall genomic instability.
It is also possible that defects in phragmoplast formation in these mutants contributes to, or is associated with, the observed defective PIN protein localization.
Currently, we do not know whether the massive reduction of microvasculature in the WAT of Nscl-2 mutants contributes to the phenotype.
It is therefore possible that the failure of the auxin distribution system in sterol mutants contribute to the observed aberrant ethylene responses, and suppression of the latter by ein2 in turn ameiorates the auxin transport defects.
In this respect, we found that in the context of treatment with a single drug, quiescence parameters do not influence the probability that drug resistant mutants contribute to treatment failure.
How, exactly, p53 mutants contribute to PI3K/AKT activation remains an open question.
At the very least, the authors should give more information relating to the hypothesis that suppression of pectin degradation in the triploid PEG mutants contributes to increased viability.
However, it is also possible that missorting of sphingolipid synthesis enzymes or trafficking proteins in GARP mutants contributes to the observed phenotypes.
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