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Decoy database searches are used to filter out false positive protein identifications derived from search engines, but there is no consensus about which decoy is "the best". We evaluate nine different decoy designs using public data sets from samples of known composition. Statistically significant performance differences were found, but no single decoy stood out among the best performers. Ultimately, we recommend peptide level reverse decoys searched independently from the target.

This article provides an overview of publicly available proteomic data repositories in a single document with a particular focus on the latest developments, many of which are not announced through traditional publications. The review is intended to inform the proteomics practitioner of the options for storage and dissemination of their MS/MS data in the public domain, and to help those who want to mine proteomic data generated by others. The latter area has arguably seen the most development in recent times, as repositories have sprouted new tools for data analysis, visualisation and experimental design. We also highlight key biological datasets available at each repository, including standard datasets. Finally, we touch upon areas of significant challenge and future directions.

Recognition of virus infection by innate pattern recognition receptors (PRRs), including membrane-associated toll-like receptors (TLR) and cytoplasmic RIG-I-like receptors (RLR), activates cascades of signal transduction pathways leading to production of type I interferons (IFN) and proinflammatory cytokines that orchestrate the elimination of the viruses. Although it has been demonstrated that PRR-mediated innate immunity plays an essential role in defending virus from infection, it also occasionally results in overwhelming production of proinflammatory cytokines that cause severe inflammation, blood vessel leakage and tissue damage. In our efforts to identify small molecules that selectively enhance PRR-mediated antiviral, but not the detrimental inflammatory response, we discovered a compound, RO 90–7501 (‘2’-(4-Aminophenyl)-[2,5′-bi-1H-benzimidazol]-5-amine), that significantly promoted both TLR3 and RLR ligand-induced IFN-β gene expression and antiviral response, most likely via selective activation of p38 mitogen-activated protein kinase (MAPK) pathway. Our results thus imply that pharmacological modulation of PRR signal transduction pathways in favor of the induction of a beneficial antiviral response can be a novel therapeutic strategy.