Insulin Induces Heterologous Desensitization of G Protein-Coupled Receptor and Insulin-Like Growth Factor I Signaling by Downregulating β-Arrestin-1

β-Arrestin-1 mediates agonist-dependent desensitization and internalization of G protein-coupled receptors (GPCRs) and is also essential for GPCR mitogenic signaling. In addition, insulin-like growth factor I receptor (IGF-IR) endocytosis is facilitated by β-arrestin-1, and internalization is necess...

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Bibliografiska uppgifter
I publikationen:	Mol Cell Biol
Huvudupphov:	Dalle, Stéphane, Imamura, Takeshi, Rose, David W., Sears Worrall, Dorothy, Ugi, Satoshi, Hupfeld, Christopher J., Olefsky, Jerrold M.
Materialtyp:	Artigo
Språk:	Inglês
Utgiven:	Taylor & Francis 2002
Ämnen:	Cell Growth and Development
Länkar:	https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC134007/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/12167719/ https://ncbi.nlm.nih.govhttps://doi.org/10.1128/MCB.22.17.6272-6285.2002
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Insulin Induces Heterologous Desensitization of G Protein-Coupled Receptor and Insulin-Like Growth Factor I Signaling by Downregulating β-Arrestin-1

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