Abstract
Insulin signaling is key to the etiology of metabolic syndrome. Recent work (Luan et al., 2009) uncovers a role for beta-arrestin, previously known to control GPCR desensitization, in insulin signaling. In mouse models, beta-arrestin-2 controls whole-body insulin action by regulating assembly of a complex containing insulin receptor, c-Src, and Akt.
MeSH terms
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Animals
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Arrestins / genetics
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Arrestins / metabolism*
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Enzyme Activation
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Humans
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Insulin / metabolism*
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Metabolic Syndrome
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Mice
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Mice, Knockout
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction / physiology*
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beta-Arrestin 2
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beta-Arrestins
Substances
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ARRB2 protein, human
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Arrb2 protein, mouse
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Arrestins
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Insulin
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beta-Arrestin 2
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beta-Arrestins
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Proto-Oncogene Proteins c-akt