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Balance between gene activation and repression, as well as mechanisms of maintenance and erasure of expression patterns, require fine gene tuning.
Therefore NF-Y is a fundamental switch at the heart of decision between gene activation and repression in CCAAT regulated genes.
Furthermore, the observations of abnormal DNA methylation patterns in malignant cells are becoming increasingly interesting, as new information of the link between gene activation and methylation status increase.
However, we chose to investigate METH-induced changes on histone H4 acetylated at lysine residue 5 (H4K5Ac) because a strong link exists between gene activation and acetylation of lysine residues (K5, K8, K12, and K16) of histone H4 [ 39- 42].
It is therefore possible that part of the antagonistic activity of the Cyc8 Tup1 and Swi Snf complexes is acted out at the level of histone acetylation, and that the rapid reversibility of this modification allows for the dynamic switch between gene activation and repression.
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No patient-level correlations between gene activation information and individual patient-data were performed, according to U.S. Department of Human Health Services and Federal Drug Administration regulations, and in compliance with the World Medical Association Declaration of Helsinki (http://www.wma.net/en/30publications/10policies/b3/index.html).html
Taken together, these results support a direct linkage between CBP-mediated gene activation and CpG demethylation at promoter sites of RA target genes.
This is associated with a much earlier (and higher) transcript accumulation of most XTH genes than when treated with 0.5 µL L−1 ethylene, suggesting a strong correlation between ethylene, XTH gene activation and cell separation in the AZ.
Our study establishes therefore a connection between DNA hypomethylation, CG gene activation, and cancer metastasis.
Little else is known about the relationship between the extent of gene activation and the magnitude of physiological adaptation to exercise training in humans.
DOI: http://dx.doi.org/10.7554/eLife.08009.011 To further explore the connection between LXR-dependent target gene activation and inflammatory repression, we analyzed signaling pathways downstream of TLR4 in macrophages.
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