Insights into protein interaction networks reveal non-receptor kinases as significant druggable targets for psoriasis

• Implementation of systems biology approach to predict drug targets for psoriasis
• Comparison of differential gene expression profiles of psoriatic lesion and non-lesion skin
• Construction of protein interaction network based on the differentially expressed genes
• Confirmation of the modularity of the network based on the topological metrics
• Enrichment of kinases, the signaling mediators from the sub-networks

Psoriasis is a chronic disease of the skin characterized by hyper proliferation and inflammation of the epidermis and dermal components of the skin. T-cell-dependent inflammatory process in skin governs the pathogenesis of psoriasis. An in-silico search strategy was utilized to identify psoriatic therapeutic drug targets. The gene expression profiling of psoriatic skin identified a total of 427 differentially expressed genes (DEGs). Gene ontology investigation of DEGs identified genes involved in calcium binding, apoptosis, keratinisation, lipid transportation and homeostasis apart from immune mediated processes. The protein interaction networks identified proteins involved in various signaling mechanisms with high degree of interconnections. The gene modules derived from the main network were enriched with rich kinome. These sub-networks were dominated by the presence of non-receptor kinase family members which are major signal transmitters in immune response. The computational approach has aided in the identification of non-receptor kinases as potential targets for psoriasis drug development.