Location of Repository

miTALOS v2: Analyzing Tissue Specific microRNA Function.

By Martin Preusse, Fabian J Theis and Nikola S Mueller


MicroRNAs are involved in almost all biological processes and have emerged as regulators of signaling pathways. We show that miRNA target genes and pathway genes are not uniformly expressed across human tissues. To capture tissue specific effects, we developed a novel methodology for tissue specific pathway analysis of miRNAs. We incorporated the most recent and highest quality miRNA targeting data (TargetScan and StarBase), RNA-seq based gene expression data (EBI Expression Atlas) and multiple new pathway data sources to increase the biological relevance of the predicted miRNA-pathway associations. We identified new potential roles of miR-199a-3p, miR-199b-3p and the miR-200 family in hepatocellular carcinoma, involving the regulation of metastasis through MAPK and Wnt signaling. Also, an association of miR-571 and Notch signaling in liver fibrosis was proposed. To facilitate data update and future extensions of our tool, we developed a flexible database backend using the graph database neo4j. The new backend as well as the novel methodology were included in the updated miTALOS v2, a tool that provides insights into tissue specific miRNA regulation of biological pathways. miTALOS v2 is available at http://mips.helmholtz-muenchen.de/mitalos

Topics: Medicine, R, Science, Q
Publisher: Public Library of Science (PLoS)
DOI identifier: 10.1371/journal.pone.0151771
OAI identifier: oai:doaj.org/article:9dc1b27bcb9d4794a4cdf059160ac399
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://mips.helmholtz-muenchen... (external link)
  • https://doaj.org/toc/1932-6203 (external link)
  • http://europepmc.org/articles/... (external link)
  • https://doaj.org/article/9dc1b... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.