Aura 2

Post-transcriptional regulation of gene expression (PTR) has been object of a rising interest in the latest years, gaining wide recognition as the most important determinant of protein levels and cell phenotypes. In consequence to this interest, huge amounts of data have been and are being collected every day primarily thanks to the advent of the new high-throughput techniques such as polysomal profiling, ribosome footprinting, and protein-RNA interaction mapping methods such as RIP, CLIP and its several variants.This massive quantity of information cannot be exploited at its best, due to the fact that most of it lies isolated and scattered throughout several databases, or in published papers reporting single PTR interactions. The lack of a comparative platform hampers the possibility to obtain a comprehensive view of the multiple factors binding to UTRs, which could both enlighten about the biological meaning of their combination and allow us to trace regulatory networks. Integrating complementary data types could therefore generate a relevant potential for the discovery of PTR circuits, significantly contributing to the advancement of the field. The solution we envisaged was to build a unified warehouse for PTR data, augmented with clever data mining tools. We thus originally developed AURA, the Atlas of UTR Regulatory Activity, which we now present in a widely extended and improved second version, AURA 2. AURA 2 is a meta-database of post-transcriptional regulatory interactions, centered on untranslated regions (UTRs) of mRNAs and relying on experimental data as its sole source of information. We decided to exclude predictions (except for two kinds of them, see below) so to give strength to insights and to sustain clues derived from the data integration tools. AURA 2 includes, to mention a few, data such as RBPs and ncRNA binding sites on UTRs, ciselements like AU-Rich Elements, RNA epigenetics data such as m5C and m6A profiles, alternative polyadenylation profiles and variation profiles such as SNPs and somatic mutations in cancer. The result is an environment in which widely different aspects of the same process, PTR, can be observed side by side and employed to derive new functional insights on the regulation