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Developmental trajectories of early brain network formation are genetically programmed and can be modified by epigenetic and environmental influences.
An individual cancer phenotype is the result of cell-specific, developmental stage-specific, and metabolism-related changes in gene expression selectively occurring at a time and modified by epigenetic interactions [6].
Recent studies have suggested that apart from SNPs, the expression of CGB genes might be modified by epigenetic mechanisms (29, 30).
Collectively, MLL, RUNX1 and PU.1 were closely interacted, and these interactions were modified by epigenetic regulation at the gene regulatory region, such as PU.1 URE or RUNX1 intronic enhancer, suggesting MLL fusions might interfere the myeloid differentiation caused by RUNX1 and PU.1 in different manner.
The growth advantage of dysplastic cells over their normal neighbours leads to progressive cytological and architectural derangement, and individual cancer phenotypes are the result of cell-specific, developmental stage-specific, and metabolism-related changes in gene expression that occur selectively at specific times and are modified by epigenetic interactions [ 3].
The impact of disease genotypes may also be modified by epigenetic and environmental factors, allowing both for synergistic and antagonistic interactions resulting in highly individualized contributions to the phenotype (whether deleterious or protective) that will variously perturb the balance of specific biological pathways so as to give rise to disease.
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miRNA expression may also be modified by targeting epigenetic mechanisms such as through reversal of hypermethylation.
However, whether an influence of methyl donor intake is modified by polymorphisms in such epigenetic regulators has not previously been studied in relation to CRC.
RNA is heavily modified by methylation and many other epigenetic tags, so the current Oxford Nanopore RNA-sequencing preadsol reans an mRNA with an attached cDNA.
DNA methylation patterns may thus be modified by altered expression or activity of epigenetic regulators such as TET.
Our discovery of an epigenetic pathway that had been modified by Hv-miR-420 indicates that some variables regarding Hv-miR-420 and HMT su var)3 9 in the dual stages of HzNV-1 may need to be taken into consideration in the future.
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