ArticleProceedings of the National Academy of Sciences of the United States of America2004
Finding new components of the target of rapamycin (TOR) signaling network through chemical genetics and proteome chips.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 245 citations in OpenAlex.
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- Phenotype and target-based chemical biology investigations in cancers.National science review · 2019Article
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- Selective Usage of Isozymes for Stress Response.ACS chemical biology · 2018Article
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- Chemical Biology Strategies to Study Autophagy.Frontiers in cell and developmental biology · 2018Review
- Systematic Identification ofMolecular & cellular proteomics : MCP · 2017Article
- A novel dual luciferase based high throughput assay to monitor autophagy in real time in yeastBiochemistry and biophysics reports · 2017Article
- Protein Array-based Approaches for Biomarker Discovery in Cancer.Genomics, proteomics & bioinformatics · 2017Review
- Relations between Effects and Structure of Small Bicyclic Molecules on the Complex Model SystemFrontiers in pharmacology · 2017Article
- Integrated Strategies to Gain a Systems-Level View of Dynamic Signaling Networks.Methods in enzymology · 2017Article
- The Potentials and Pitfalls of Microarrays in Neglected Tropical Diseases: A Focus on Human Filarial Infections.Microarrays (Basel, Switzerland) · 2016Review
- Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The TOR (target of rapamycin) proteins play important roles in nutrient signaling in eukaryotic cells. Rapamycin treatment induces a state reminiscent of the nutrient starvation response, often resulting in growth inhibition. Using a chemical genetic modifier screen, we identified two classes of small molecules, small-molecule inhibitors of rapamycin (SMIRs) and small-molecule enhancers of rapamycin (SMERs), that suppress and augment, respectively, rapamycin's effect in the yeast Saccharomyces cerevisiae. Probing proteome chips with biotinylated SMIRs revealed putative intracellular target proteins, including Tep1p, a homolog of the mammalian PTEN (phosphatase and tensin homologue deleted on chromosome 10) tumor suppressor, and Ybr077cp (Nir1p), a protein of previously unknown function that we show to be a component of the TOR signaling network. Both SMIR target proteins are associated with PI(3,4)P2, suggesting a mechanism of regulation of the TOR pathway involving phosphatidylinositides. Our results illustrate the combined use of chemical genetics and proteomics in biological discovery and map a path for creating useful therapeutics for treating human diseases involving the TOR pathway, such as diabetes and cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.