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Thus, it is likely that the metabolic pathways for a phenotypic trait or disease involve multiple interacting gene products and regulatory loci that could generate a complex network of genetic actions and interactions [3], [4].
The potent suppression of a single gene transcript using electroporation prompted us to examine whether this approach would be useful for targeting multiple transcripts simultaneously and thereby enable the perturbation of multiple interacting gene products in the RB and p53 pathways.
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However, in three cases, multiple interacting genes were found for one deficiency (two deficiencies contained two interacting genes each, and one deficiency contained three interacting genes), suggesting that the stronger phenotype of the deficiency may arise in part from the reduction of multiple interacting genes.
Many crop traits are quantitative, complex, and controlled by multiple interacting genes.
The genetic susceptibility of an individual to such a disease appears not to be the result of a single causative gene but rather arises from multiple interacting genes.
In addition to the processes acting on individual genes, large-scale gene duplication events (for example, whole genome duplication) may have occurred and produced multiple interacting genes together creating an additional retention mechanism.
We tested this by attempting to target multiple interacting genes simultaneously in the RB and p53 pathways to achieve the phenotypic endpoint of cell cycle reentry in mature post mitotic islet cells.
In addition to the processes acting on individual genes described above, large-scale gene duplication (segmental, whole chromosome, and whole genome) events duplicate multiple interacting genes together creating an additional retention mechanism (Papp et al. 2003; Aury et al. 2006; Hughes et al. 2007).
The best approach may be to transform hosts with target Wolbachia genes and assess whether a CI phenotype can be induced, as has been performed for ankyrin repeat-encoding genes previously [ 38], although if multiple interacting Wolbachia genes are required to produce the CI phenotype the use of individual genes in this way may not clearly reveal their role.
Complex phenotypes are often the result of a response of multiple functionally interacting genes.
We present a computational framework for Bayesian statistical inference of target genes of multiple interacting TFs from high-throughput gene expression time-series data.
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