ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Kinase-mediated quasi-dimers of EGFR.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- EGFR Mutations and Tyrosine Kinase Inhibitors: Structural Insights and Therapeutic Advances.ACS omega · 2026Review
- Optogenetic clustering and membrane translocation of the BcLOV4 photoreceptor.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Epiregulin is a dendritic cell-derived EGFR ligand that maintains skin and lung fibrosis.Science immunology · 2022Article
- Fluorescence Imaging of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Review
- Structural Insight and Development of EGFR Tyrosine Kinase Inhibitors.Molecules (Basel, Switzerland) · 2022Review
- Allosteric activation of preformed EGF receptor dimers by a single ligand binding event.Frontiers in endocrinology · 2022Article
- Expanding the Disorder-Function Paradigm in the C-Terminal Tails of Erbbs.Biomolecules · 2021Review
- Oncostatin M Receptor-Targeted Antibodies Suppress STAT3 Signaling and Inhibit Ovarian Cancer Growth.Cancer research · 2021Article
- Comprehensive Model for Epidermal Growth Factor Receptor Ligand Binding Involving Conformational States of the Extracellular and the Kinase Domains.Frontiers in cell and developmental biology · 2020Article
- Kinase-Inactivated EGFR Is Required for the Survival of Wild-Type EGFR-Expressing Cancer Cells Treated with Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2019Article
- Rethink of EGFR in Cancer With Its Kinase Independent Function on Board.Frontiers in oncology · 2019Article
- Allosteric regulation of epidermal growth factor (EGF) receptor ligand binding by tyrosine kinase inhibitors.The Journal of biological chemistry · 2018Article
- Inhibitor-induced HER2-HER3 heterodimerisation promotes proliferation through a novel dimer interface.eLife · 2018Article
- Studying the Conformation of a Receptor Tyrosine Kinase in Solution by Inhibitor-Based Spin Labeling.Angewandte Chemie (International ed. in English) · 2017Article
- HER2-HER3 dimer quantification by FLIM-FRET predicts breast cancer metastatic relapse independently of HER2 IHC status.Oncotarget · 2016Article
- Analysis of the Role of the C-Terminal Tail in the Regulation of the Epidermal Growth Factor Receptor.Molecular and cellular biology · 2015Article
- A point mutation in the extracellular domain of KIT promotes tumorigenesis of mast cells via ligand-independent auto-dimerization.Scientific reports · 2015Article
- Article
- Effect of phosphorylation on EGFR dimer stability probed by single-molecule dynamics and FRET/FLIM.Biophysical journal · 2015Article
- Efficacy and mechanism of action of the tyrosine kinase inhibitors gefitinib, lapatinib and neratinib in the treatment of HER2-positive breast cancer: preclinical and clinical evidence.American journal of cancer research · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Ligand-induced dimerization of the epidermal growth factor receptor (ErbB-1/EGFR) involves conformational changes that expose an extracellular dimerization interface. Subsequent alterations within the cytoplasmic kinase domain, which culminate in tyrosine phosphorylation, are less understood. Our study addressed this question by using two strategies: a chimeric receptor approach employed ErbB-3, whose defective kinase domain was replaced by the respective part of EGFR. The implanted full-length kinase, unlike its subdomains, conferred dimerization and catalysis. The data infer that the kinase function of EGFR is restrained by the carboxyl tail; once grafted distally to the ectopic tail of ErbB-3, the kinase domain acquires quasi-dimerization and activation. In an attempt to alternatively refold the cytoplasmic tail, our other approach employed kinase inhibitors. Biophysical measurements and covalent cross-linking analyses showed that inhibitors targeting the active conformation of EGFR, in contrast to a compound recognizing the inactive conformation, induce quasi-dimers in a manner similar to the chimeric ErbB-3 molecule. Collectively, these observations unveil kinase domain-mediated quasi-dimers, which are regulated by an autoinhibitory carboxyl tail. On the basis of these observations, we propose that quasi-dimers precede formation of ligand-induced, fully active dimers, which are stabilized by both extracellular and intracellular receptor-receptor interactions.
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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.