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MicroRNAs (miRNAs) are a novel class of small non-coding RNAs (~22 bp) that are believed to regulate gene expression by directly binding with 3′UTR of target mRNAs, causing translational inhibition or mRNA degradation (Ambros, 2004; Bartel, 2004).
Tet proteins are believed to regulate gene transcription notably through the enzymatic oxidation of the repressive cytosine DNA methylation mark (5mC) into hydroxymethylcytosine (5hmC) (Pastor et al. 2013); however, the enzymatic activity of Tet proteins is unaffected in the absence of O-GlcNAcylation (Chen et al. 2012; Deplus et al. 2013; Ito et al. 2014).
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PSIP1-P75 was previously shown to be involved in cell survival [50], protection against stress [51], differentiation [52], cell fate determination [48] and is believed to regulate genes involved in development [53].
These tracts are believed to regulate contingency genes but as yet no phenotypic variation has been identified associated with many of these genes.
Each miR is believed to regulate multiple genes.
microRNAs (miRNAs) are believed to regulate their targets through posttranscriptional gene regulation and have the potential to silence gene expression via multiple mechanisms.
On the other hand, E2F5 is involved in cell cycle regulation by inhibiting c-Myc, an oncogene and a transcription factor that is believed to regulate expression of 15% of all genes [68].
These transcribed sequences fold into stem loops and are believed to regulate expression of the adjacent genes [10], [11], [13].
TR is believed to regulate overlapping but distinct target genes in different organs to effect organ-specific metamorphosis.
UCA1, short for urothelial cancer associated 1, is believed to regulate the expression of several genes involved in tumorigenesis, embryonic development, or both [ 31].
Because the diverse disease models used for these microarray experiments (including diabetes, cancer cachexia, chronic renal failure, fasting and denervation) have muscle atrophy in common, the commonly up- or downregulated genes are believed to regulate the loss of muscle components and are called atrophy-related genes or 'atrogenes' (Sacheck et al., 2007).
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