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Although histone modifications play major roles in processes such as transcription, replication and DNA repair, their oncogenic importance is not yet well established.
Transcription factors, enhancers, silencers, and epigenetic modifications play major roles in cancer development and may influence correlation among expression levels of hosts and targets.
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Indeed, unliganded ERs may be transcriptionally active and post-translational modifications play a major role in this context.
We conclude that Myc-induced chromatin modifications play a major role in Myc-induced exit from the stem cell compartment.
Regulation of gene expression involves multi-layered mechanisms in which epigenetic modifications such as DNA methylation and histone tail modifications play a major role[1], [2].
We conclude that Myc-induced chromatin modifications play a major role in Myc-induced exit from the stem cell compartment and differentiation into interfollicular epidermis and sebocytes.
As such, histone modifications and certain combinations of modifications play a major role in dictating the accessibility status of the chromatin.
This is in accordance with recent studies showing that epigenetic modifications including methylation, siRNA signatures, and histone modifications play a major role in vernalization [ 13, 38].
The increasing amount of experimental in vitro and in vivo data strongly supports the hypothesis that epigenetic modifications play a major role in the development not only of cancer but also of rheumatic diseases.
Although target site modifications play a major role in resistance [ 4, 5, 28, 29], other mechanisms such as insecticide biodegradation, altered transport, sequestration and modification of the insect cuticle also account for a significant part of resistance [ 6, 18, 30, 31].
Irrespectively of whether 30-nm fibers exist or not, the generic mechanisms of higher-order hierarchical folding that depend on histone substitutions or modifications are still likely to play major roles in higher order folding structures.
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