ArticleeLife2024
Genetic code expansion, click chemistry, and light-activated PI3K reveal details of membrane protein trafficking downstream of receptor tyrosine kinases.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Site-Specific Protein Bioconjugation Through Cellular Incorporation of Noncanonical Amino Acids.Angewandte Chemie (International ed. in English) · 2026Review
- The multifaceted significance of phosphoinositides in endocytic trafficking.FEBS letters · 2026Review
- Scalable Flow Synthesis of Genetically Encodable Tetrazine Amino Acids.Organic process research & development · 2026Article
- Oncogenic Alterations in PI3K Signaling Emulated Optogenetically Recapitulate Some Phenotypic Changes in Mammary Epithelia.ACS synthetic biology · 2026Article
- Tuning Encodable Tetrazine Chemistry for Site-Specific Protein Bioorthogonal Ligations.Angewandte Chemie (International ed. in English) · 2025Article
- Quantitative Protein Labeling in Live Cells by Controlling the Redox State of Encoded Tetrazines.Journal of the American Chemical Society · 2025Article
- Fluorescence labeling strategies for cell surface expression of TRPV1.The Journal of general physiology · 2024Article
- Fluorescence labeling strategies for the study of ion channel and receptor cell surface expression: A comprehensive toolkit for extracellular labeling of TRPV1.bioRxiv : the preprint server for biology · 2024Article
- Ginsenoside Rg1 exerts anti-arrhythmic effect by inhibiting IScience progressArticle
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Authors and funding
12 authors.
Funding
Abstract
Ligands such as insulin, epidermal growth factor, platelet-derived growth factor, and nerve growth factor (NGF) initiate signals at the cell membrane by binding to receptor tyrosine kinases (RTKs). Along with G-protein-coupled receptors, RTKs are the main platforms for transducing extracellular signals into intracellular signals. Studying RTK signaling has been a challenge, however, due to the multiple signaling pathways to which RTKs typically are coupled, including MAP/ERK, PLCγ, and Class 1A phosphoinositide 3-kinases (PI3K). The multi-pronged RTK signaling has been a barrier to isolating the effects of any one downstream pathway. Here, we used optogenetic activation of PI3K to decouple its activation from other RTK signaling pathways. In this context, we used genetic code expansion to introduce a click chemistry noncanonical amino acid into the extracellular side of membrane proteins. Applying a cell-impermeant click chemistry fluorophore allowed us to visualize delivery of membrane proteins to the plasma membrane in real time. Using these approaches, we demonstrate that activation of PI3K, without activating other pathways downstream of RTK signaling, is sufficient to traffic the TRPV1 ion channels and insulin receptors to the plasma membrane.
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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.