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β-Arrestins Regulate Mitogenic Signaling and Clathrin-mediated Endocytosis of the Insulin-like Growth Factor I Receptor

Open access
Lin, Fang-Tsyr, Daaka, Yehia, Lefkowitz, Robert J.·1998·Journal of Biological Chemistry

Abstract

beta-Arrestins mediate agonist-dependent desensitization of G protein-coupled receptors and target the receptors to clathrin-coated pits for internalization. Here we report an expanded role of beta-arrestins in promoting clathrin-mediated endocytosis of a tyrosine kinase growth factor receptor, i.e. the insulin-like growth factor I (IGF-1) receptor. beta-Arrestins bind to the ligand-occupied IGF-1 receptors, promote their endocytosis, and enhance IGF-1-dependent mitogen-activated protein kinase phosphorylation and DNA synthesis. Our results suggest a role for beta-arrestins in regulating mitogenic signaling and clathrin-mediated endocytosis of receptors not classically coupled to G proteins.

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Metadata

Authors
Lin, F.-T., Daaka, Y., & Lefkowitz, R. J.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1998-11
Volume
273
Issue
48
Pages
31640-31643
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2163304919
Cited by
182
References
0
FWCI
2.25
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: β-Arrestins Regulate Mitogenic Signaling and Clathrin-mediated Endocytosis of the Insulin-like Growth Factor I Receptor. https://app.cochat.ai/papers/10.1074/jbc.273.48.31640
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Lin, F.-T., Daaka, Y., & Lefkowitz, R. J. (1998). β-Arrestins Regulate Mitogenic Signaling and Clathrin-mediated Endocytosis of the Insulin-like Growth Factor I Receptor. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.273.48.31640

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.