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Based on the different spatiotemporal dynamics among caudal hindbrain nuclei, we propose Hox genes could act as a facilitator in neuronal subgroup evolution.
As shown in Figure 7A, overexpression of MSN4 or HYR1 was not sufficient to cause rapamycin sensitivity, arguing against the notion that these genes could act as putative TOR inhibitors.
These unique genes could act as a potential mine to explore.
These genes could act either autonomously in the Q cells, or non-autonomously in other cells that express MAB-5.
These genes could act separately or interact under the influence of diverse environmental and epigenetic factors [ 3, 5, 6].
Although multiple genes could act as mediators of interaction between two pathways, their relative importance can be different.
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One could speculate that the mutations identified are gain-of-function mutations that would support the concept that the PIK3CD gene could act as an oncogene in NB.
Thus, the presence of the callipyge mutation on the maternal allele results in cis-mediated enhanced expression of these noncoding genes, which could act as trans-acting repressors of the effector produced by either the CmatN or CmatCpat genotypes, thereby neutralising the influence of the effector.
Recent studies reveal several likely candidate genes that could act as intermediate regulators between the miRNAs and module 29 genes.
If the majority of genes containing HLOF variants do not have measureable phenotypic effects, this could be due to a higher than usual number of paralogues for these genes, i.e. genes belonging to the same gene family could act as a buffer on the effect.
Under our meta-QTLs, we found, for example, genes involved in auxin signaling and transport or in cell division, transcription factors expressed under abiotic stresses, and sugar metabolism genes that could act on root growth or serve as osmoprotectants.
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