ArticleProceedings of the National Academy of Sciences of the United States of America2003
Beta -Arrestin 1 down-regulation after insulin treatment is associated with supersensitization of beta 2 adrenergic receptor Galpha s signaling in 3T3-L1 adipocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 42 citations in OpenAlex.
- GPCRs in the regulation of the functional activity of multipotent mesenchymal stromal cells.Frontiers in cell and developmental biology · 2022Review
- A kinase-independent role for unoccupied insulin and IGF-1 receptors in the control of apoptosis.Science signaling · 2010Article
- G protein-coupled receptor kinase 2 plays a relevant role in insulin resistance and obesity.Diabetes · 2010Article
- Beta-arrestin inhibits CAMKKbeta-dependent AMPK activation downstream of protease-activated-receptor-2.BMC biochemistry · 2010Article
- Amino acid-sensing mTOR signaling is involved in modulation of lipolysis by chronic insulin treatment in adipocytes.American journal of physiology. Endocrinology and metabolism · 2009Article
- Adipocyte CREB promotes insulin resistance in obesity.Cell metabolism · 2009Article
- Beta-Arrestin-1 mediates glucagon-like peptide-1 signaling to insulin secretion in cultured pancreatic beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Anti-beta1-adrenergic receptor autoantibodies in patients with chronic Chagas heart disease.Clinical and experimental immunology · 2007Article
- Activated N-formyl peptide receptor and high-affinity IgE receptor occupy common domains for signaling and internalization.Molecular biology of the cell · 2007Article
- Genetic pleiotropy between asthma and obesity in a community-based sample of twins.The Journal of allergy and clinical immunology · 2005Article
- beta-arrestin-1 competitively inhibits insulin-induced ubiquitination and degradation of insulin receptor substrate 1.Molecular and cellular biology · 2004Article
- GRK2 is an endogenous protein inhibitor of the insulin signaling pathway for glucose transport stimulation.The EMBO journal · 2004Article
- Antidiabetic effect of novel modulating peptides of G-protein-coupled kinase in experimental models of diabetes.Diabetologia · 2004Article
- Multifaceted roles of beta-arrestins in the regulation of seven-membrane-spanning receptor trafficking and signalling.The Biochemical journal · 2003Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
beta-Arrestin 1 is required for internalization and mitogen-activated protein (MAP) kinase activation by the beta2 adrenergic receptor (beta2AR). Our previous studies have shown that chronic insulin treatment down-regulates cellular beta-arrestin 1 levels, leading to a marked impairment in G protein-coupled receptor and insulin-like growth factor-1 receptor-mediated MAP kinase and mitogenic signaling. In this study, we show that chronic insulin-treated, beta-arrestin 1depleted 3T3-L1 adipocytes display (i) increased isoproterenol-induced cAMP generation (53 +/- 38% at 1.5 min, 25 +/- 19% at 5 min, 63 +/- 14% at 30 min, and 59 +/- 2% at 60 min), a Galpha(s)-associated pathway; (ii) impaired isoproterenol-induced beta2AR internalization (reduced by 98 +/- 4%), which is required for MAP kinase signaling, a Galpha(i)-associated pathway; and (iii) increased beta-arrestin 1 phosphorylation at Ser-412. Taken together, these findings represent a hitherto unknown mechanism (degradation and phosphorylation of beta-arrestin, whereby the activation of the insulin receptor, belonging to the family of receptor tyrosine kinases, causes supersensitization of Galpha(s)-associated signaling and inhibition of Galpha(i)-associated signaling by the beta2AR, a prototypical G protein-coupled receptor.
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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.