RNA methylation adds a second layer of genetic information that dictates the post-transcriptional fate of RNAs. Although various methods exist that enable the analysis of RNA methylation in a site-specific or transcriptome-wide manner, whether biophysical approaches can be employed to such analyses is unexplored. In this study, Fourier-transform infrared (FT-IR) and circular dichroism (CD) spectroscopy are employed to examine the methylation status of both synthetic and cellular RNAs.
View Article and Find Full Text PDFTrends Cell Biol
October 2024
Targeting RNA mA marks in apoptosis-related transcripts holds promise for RNA therapeutics. However, pathway-specific RNA mA sites on pro- or antiapoptotic transcripts have not been fully unveiled, let alone characterized. This article summarizes the current knowledge and gaps in the cellular response modulated by apoptotic stimulus-specific RNA mA marks.
View Article and Find Full Text PDFBackground/aim: Cancer is a complex disease that involves both genetic and epigenetic factors. While emerging evidence clearly suggests that changes in epitranscriptomics play a crucial role in cancer pathogenesis, a comprehensive understanding of the writers, erasers, and readers of epitranscriptomic processes, particularly under apoptotic conditions remains lacking. The aim of this study was to uncover the changes in the expression of mA RNA modifiers under apoptotic conditions across various cancer cell lines.
View Article and Find Full Text PDFEpitranscriptomic mechanisms, which constitute an important layer in post-transcriptional gene regulation, are involved in numerous cellular processes under health and disease such as stem cell development or cancer. Among various such mechanisms, RNA methylation is considered to have vital roles in eukaryotes primarily due to its dynamic and reversible nature. There are numerous RNA methylations that include, but are not limited to, 2'-O-dimethyladenosine (mAm), -methylguanosine (mG), -methyladenosine (mA) and -methyladenosine (mA).
View Article and Find Full Text PDFTumor necrosis factor-α (TNF-α) is a ligand that induces both intrinsic and extrinsic apoptotic pathways in HeLa cells by modulating complex gene regulatory mechanisms. However, the full spectrum of TNF-α-modulated epitranscriptomic mA marks is unknown. We employed a genomewide approach to examine the extent of mA RNA modifications under TNF-α-modulated apoptotic conditions in HeLa cells.
View Article and Find Full Text PDFCisplatin (CP), which is a conventional cancer chemotherapeutic drug, induces apoptosis by modulating a diverse array of gene regulatory mechanisms. However, cisplatin-mediated changes in the mA methylome are unknown. We employed an mA miCLIP-seq approach to investigate the effect of mA methylation marks under cisplatin-mediated apoptotic conditions on HeLa cells.
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