ArticleNature communications2022
Engineering receptors in the secretory pathway for orthogonal signalling control.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond ER-Golgi trafficking: unconventional protein secretion as a new design frontier for synthetic secretion switches in mammalian cells.Communications biology · 2026Review
- Joined Signatures of Erythropoietin and Interleukin-6 Signaling by Synthetic Heterodimeric gp130:Epo Receptor Complexes.ACS synthetic biology · 2026Article
- Next-generation programmable cell therapies for precision medicine.Nature reviews. Genetics · 2026Review
- Conversion of natural cytokine receptors into orthogonal synthetic biosensors.Nature chemical biology · 2025Article
- On-demand treatment of metabolic diseases by a synthetic drug-inducible exocytosis system.Nature communications · 2025Article
- Article
- Ultrashort-Peptide-Responsive Gene Switches for Regulation of Therapeutic Protein Expression in Mammalian Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Int&in: A machine learning-based web server for active split site identification in inteins.Protein science : a publication of the Protein Society · 2024Article
- Synthetic Gene Circuits for Regulation of Next-Generation Cell-Based Therapeutics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Programmable synthetic receptors: the next-generation of cell and gene therapies.Signal transduction and targeted therapy · 2024Review
- Enabling neighbour labelling: using synthetic biology to explore how cells influence their neighbours.Development (Cambridge, England) · 2024Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synthetic receptors targeted to the secretory pathway often fail to exhibit the expected activity due to post-translational modifications (PTMs) and/or improper folding. Here, we engineered synthetic receptors that reside in the cytoplasm, inside the endoplasmic reticulum (ER), or on the plasma membrane through orientation adjustment of the receptor parts and by elimination of dysfunctional PTMs sites. The cytoplasmic receptors consist of split-TEVp domains that reconstitute an active protease through chemically-induced dimerization (CID) that is triggered by rapamycin, abscisic acid, or gibberellin. Inside the ER, however, some of these receptors were non-functional, but their activity was restored by mutagenesis of cysteine and asparagine, residues that are typically associated with PTMs. Finally, we engineered orthogonal chemically activated cell-surface receptors (OCARs) consisting of the Notch1 transmembrane domain fused to cytoplasmic tTA and extracellular CID domains. Mutagenesis of cysteine residues in CID domains afforded functional OCARs which enabled fine-tuning of orthogonal signalling in mammalian cells.
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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 OpenQuestion graph.