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These findings define a hitherto unknown mechanism of action for arginine methylation in regulating translation of a subset of mRNAs including those encoding pivotal leukemogenic transcriptional regulators MLL1 and MLL4.
We first describe studies implicating lysine methylation in regulating early steps in the replication process.
Similarly the interaction between histone modification and DNA methylation in regulating gene expression is currently unclear, and may indeed be locus specific.
Furthermore, several observations support a direct involvement of H3 K36 methylation in regulating the timing of Cdc45 binding to replication origins.
Therefore, the role of promoter methylation in regulating MGMT expression in pituitary adenomas remains controversial.
A role for DNA methylation in regulating fibroblast phenotype during disease progression is supported in several studies.
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Considering the above findings, we wanted to test the expression and methylation status of miR-125 in CRC tissues and adjacent nontumor tissues and then to evaluate whether DNA methylation participates in regulating miR-125 expression in human CRC.
Such next-generation studies should further refine our understanding of the evidently critical role that post-translational methylation plays in regulating PP2A activity in vivo.
The involvement of the transcriptionally induced H3 K36 methylation mark in regulating the timing of Cdc45 binding to replication origins provides a novel means of how gene expression may affect origin dynamics during S-phase.
In this review, we discuss the recent progress in understanding the roles of H3K4 methylation modifiers in regulating embryonic and adult stem cells' fates.
The expression of both genes is also increased in T cells treated with the methylation inhibitor 5-azacitidine, suggesting that DNA methylation is involved in regulating the expression of these genes [ 7, 8].
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