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      CyTargetLinker app update: A flexible solution for network extension in Cytoscape

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          Abstract

          Here, we present an update of the open-source CyTargetLinker app for Cytoscape ( http://apps.cytoscape.org/apps/cytargetlinker) that introduces new automation features. CyTargetLinker provides a simple interface to extend networks with links to relevant data and/or knowledge extracted from so-called linksets. The linksets are provided on the CyTargetLinker website ( https://cytargetlinker.github.io/) or can be custom-made for specific use cases. The new automation feature enables users to programmatically execute the app’s functionality in Cytoscape (command line tool) and with external tools (e.g. R, Jupyter, Python, etc). This allows users to share their analysis workflows and therefore increase repeatability and reproducibility. Three use cases demonstrate automated workflows, combinations with other Cytoscape apps and core Cytoscape functionality. We first extend a protein-protein interaction network created with the stringApp, with compound-target interactions and disease-gene annotations. In the second use case, we created a workflow to load differentially expressed genes from an experimental dataset and extend it with gene-pathway associations. Lastly, we chose an example outside the biological domain and used CyTargetLinker to create an author-article-journal network for the five authors of this manuscript using a two-step extension mechanism.

          With 400 downloads per month in the last year and nearly 20,000 downloads in total, CyTargetLinker shows the adoption and relevance of the app in the field of network biology. In August 2019, the original publication was cited in 83 articles demonstrating the applicability in biomedical research.

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          Most cited references 13

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            The BridgeDb framework: standardized access to gene, protein and metabolite identifier mapping services

            Background Many complementary solutions are available for the identifier mapping problem. This creates an opportunity for bioinformatics tool developers. Tools can be made to flexibly support multiple mapping services or mapping services could be combined to get broader coverage. This approach requires an interface layer between tools and mapping services. Results Here we present BridgeDb, a software framework for gene, protein and metabolite identifier mapping. This framework provides a standardized interface layer through which bioinformatics tools can be connected to different identifier mapping services. This approach makes it easier for tool developers to support identifier mapping. Mapping services can be combined or merged to support multi-omics experiments or to integrate custom microarray annotations. BridgeDb provides its own ready-to-go mapping services, both in webservice and local database forms. However, the framework is intended for customization and adaptation to any identifier mapping service. BridgeDb has already been integrated into several bioinformatics applications. Conclusion By uncoupling bioinformatics tools from mapping services, BridgeDb improves capability and flexibility of those tools. All described software is open source and available at http://www.bridgedb.org.
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              Cell-type-specific repression by methyl-CpG-binding protein 2 is biased toward long genes.

              Mutations in methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome and related autism spectrum disorders (Amir et al., 1999). MeCP2 is believed to be required for proper regulation of brain gene expression, but prior microarray studies in Mecp2 knock-out mice using brain tissue homogenates have revealed only subtle changes in gene expression (Tudor et al., 2002; Nuber et al., 2005; Jordan et al., 2007; Chahrour et al., 2008). Here, by profiling discrete subtypes of neurons we uncovered more dramatic effects of MeCP2 on gene expression, overcoming the "dilution problem" associated with assaying homogenates of complex tissues. The results reveal misregulation of genes involved in neuronal connectivity and communication. Importantly, genes upregulated following loss of MeCP2 are biased toward longer genes but this is not true for downregulated genes, suggesting MeCP2 may selectively repress long genes. Because genes involved in neuronal connectivity and communication, such as cell adhesion and cell-cell signaling genes, are enriched among longer genes, their misregulation following loss of MeCP2 suggests a possible etiology for altered circuit function in Rett syndrome.
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                Author and article information

                Contributors
                Role: ConceptualizationRole: Data CurationRole: MethodologyRole: Project AdministrationRole: SoftwareRole: VisualizationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing
                Role: Data CurationRole: Formal AnalysisRole: ValidationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing
                Role: Data CurationRole: Writing – Review & Editing
                Role: ConceptualizationRole: Supervision
                Role: ConceptualizationRole: Project AdministrationRole: SupervisionRole: Writing – Original Draft PreparationRole: Writing – Review & Editing
                Journal
                F1000Res
                F1000Res
                F1000Research
                F1000Research
                F1000 Research Limited (London, UK )
                2046-1402
                13 August 2019
                2018
                : 7
                Affiliations
                [1 ]Department of Bioinformatics - BiGCaT, NUTRIM, Maastricht University, Maastricht, 6229 ER, The Netherlands
                [2 ]Maastricht Centre for Systems Biology (MaCSBio), Maastricht University, Maastricht, 6229 ER, The Netherlands
                [3 ]GKC-Rett Expertise Centre, Maastricht University Medical Center, Maastricht, 6200 MD, The Netherlands
                [1 ]Resource for Biocomputing, Visualization and Informatics, Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA, USA
                [1 ]Resource for Biocomputing, Visualization and Informatics, Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA, USA
                [1 ]GlaxoSmithKline (GSK), Brentford, UK
                Author notes

                No competing interests were disclosed.

                Competing interests: No competing interests were disclosed.

                Competing interests: No competing interests were disclosed.

                Competing interests: No competing interests were disclosed.

                Competing interests: No competing interests were disclosed.

                Competing interests: No competing interests were disclosed.

                Article
                10.12688/f1000research.14613.2
                6707396
                Copyright: © 2019 Kutmon M et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Product
                Funding
                Funded by: ELIXIR
                Funded by: Dutch Province of Limburg
                This project has been co-financed by the Dutch Province of Limburg and ELIXIR, the European research infrastructure for life-science data.
                The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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