Abstract
Cellular functions are regulated through the gene expression program by the transcription of new messenger RNAs (mRNAs), alternative RNA splicing, and protein synthesis. To this end, the post-translational modifications (PTMs) of proteins add another layer of complexity, creating a continuously fine-tuned regulatory network. ADP-ribosylation (ADPr) is an ancient reversible modification of cellular macromolecules, regulating a multitude of key functional processes as diverse as DNA damage repair (DDR), transcriptional regulation, intracellular transport, immune and stress responses, and cell survival. Additionally, due to the emerging role of ADP-ribosylation in pathological processes, ADP-ribosyltransferases (ARTs), the enzymes involved in ADPr, are attracting growing interest as new drug targets. In this review, an overview of human ARTs and their related biological functions is provided, mainly focusing on the regulation of ADP-ribosyltransferase Diphtheria toxin-like enzymes (ARTD)-dependent RNA functions. Finally, in order to unravel novel gene functional relationships, we propose the analysis of an inventory of human gene clusters, including ARTDs, which share conserved sequences at 3′ untranslated regions (UTRs).
Highlights
The activation of gene expression programs serves the cell to ensure coordinated cellular processes and fate resolutions [1]
Conclusions been reviewed, highlighting the RNA processes known to date that are under its control
The maintenance of cell horange of effects that lead to enzyme inactivation, change regulatory in subcellular meostasis is gained through well inter-connected processeslocalization, that are finely or by post-translational modifications (PTMs)
Summary
The activation of gene expression programs serves the cell to ensure coordinated cellular processes and fate resolutions [1]. This coordination can be achieved both at the transcriptional and post-transcriptional levels. The PTMs of proteins have been established to play a pivotal role in mediating cell response upon specific inputs, contributing to the arrangement of a continuously fine-tuned regulatory network [2]. The dysregulation of some of the ADPr enzymes is causative of pathological mechanisms, providing evidence of the need of an efficient gene expression regulatory network. The evaluation of novel therapeutic pharmacological opportunities targeting the ADPr reaction is suggested
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