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Exact(6)
The trapping of Dome in this 'activation' compartment in ept mutants may therefore contribute to high-level activation of the Jak-Stat pathway observed in these cells.
We predict that functional analysis of these genes with single knockout mutants may therefore be impeded due to functional redundancy in which loss of a single gene may be compensated for by expression of the co-predominantly expressed paralog, masking association of either paralog with a phenotype.
The transforming ability of mTOR mutants may, therefore, be less potent than that of v‐Ras.
The increase in 4E-BP expression observed in dFOXO mutants may therefore occur as a result of FKH-mediated transcriptional regulation.
Genome editing in fish to create double Nrp1a/b mutants may therefore be a useful next step for extended analyses of NRP1 function in angiogenesis.
The H3K36me3 patterns maintained by MES-4 in these mutants may therefore have been produced during transcription in germ cells of the wild type ancestor of the met-1 mutant many generations past.
Similar(54)
Increased activity associated with the mutant may therefore, be simply due to steric freedom achieved by the truncated version of the enzyme ordinarily accomplished by activating phosphorylations.
Detection of plaques containing mutant alleles may therefore also vary depending on the sensitivity of the PCR method employed.
The proliferation of active zones observed in neurexin mutant larvae may therefore represent developmental compensation for reduced muscle excitation.
Loss of this activity in the mutant protein may therefore contribute to neuronal loss in diseased individuals.
The difference between starved and well-fed mutant cells may therefore only become apparent in late stage egg chambers that have passed this nutrient checkpoint.
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