JQuery

Alternative polyadenylation (APA) is a widespread mechanism that contributes to the sophisticated dynamics of gene regulation. Approximately 50% of all protein-coding human genes harbor multiple polyadenylation (PA) sites; their selective and combinatorial use gives rise to transcript variants with differing length of their 3' untranslated region (3'UTR). Shortened variants escape UTR-mediated regulation by microRNAs (miRNAs), especially in cancer, where global 3'UTR shortening accelerates disease progression, dedifferentiation and proliferation.

RNA secondary structure analysis often requires searching for potential helices in large sequence data.

Protein-protein interactions (PPIs) and microRNA (miRNA)-target interactions are important for deciphering the mechanisms of tumorigenesis. However, current PPI databases do not support cancer-specific analysis. Also, no available databases can be used to retrieve cancer-associated miRNA-target interactions. As the pathogenesis of human cancers is affected by several miRNAs rather than a single miRNA, it is needed to uncover miRNA synergism in a systems level.

Mammalian genomes encode for thousands of microRNAs, which can potentially regulate the majority of protein-coding genes. They have been implicated in development and disease, leading to great interest in understanding their function, with computational methods being widely used to predict their targets. Most computational methods rely on sequence features, thermodynamics, and conservation filters; essentially scanning the whole transcriptome to predict one set of targets for each microRNA.