Autophagy is a catabolic pathway in which cytoplasmic vesicles engulf cellular components to transport them to the lysosome for digestion. The autophagy process is critical for maintaining cell homeostasis, and for dealing with stress-inducing conditions. Hence, defects in this pathway can lead to a wide range of pathologies. Utilizing the NCBI’s Gene Expression Omnibus (GEO) database we obtained gene expression signatures from autophagy-related studies. Up and down gene sets from over 100 studies were compiled and compared with gene sets extracted from literature-based databases including autophagy-related gene sets from Geneshot, the Gene Ontology, and KEGG. Studies with significant overlap with autophagy-related literature-based gene sets were utilized to determine which of the expression signatures are most relevant to autophagy. Once the consensus signature was generated, the data was queried against the L1000 resource to identify potential novel small molecules that could induce autophagy, and against ChEA3 to determine transcriptional regulators that may control the autophagy process. Treating cells with the predicted small molecules, and genetically perturbing the predicted transcription factors, will be experimentally tested in autophagy induction functional studies in the near future. This presentation is by Alessandra LaRocco, an undergraduate student at Yale University. Alessandra describes her summer research project with the BD2K-LINCS DCIC in the Ma'ayan Lab at the Icahn School of Medicine at Mount Sinai.
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